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CtDNA DYNAMIC II clinical trial

CtDNA DYNAMIC II clinical trial

DocTalk
2022
Dr. Tie
ctDNA
Stage II
Trials

In this DocTalk recorded August 2022, Dr. Jeanne Tie from The Walter & Eliza Hall Institute of Medical Research in Australia discusses her ctDNA DYNAMIC II trial with PALTOWN Scientific Director, Dr. Manju George.

Table of contents

00:00: Introduction
04:29: Minimal residual disease (MRD)
06:06: Duke’s staging
07:11: AJCC TNM staging
07:50: Adjuvant treatment for early-stage CRC & challenges
08:53: Things tried in stage II Colon cancer
11:00: Better risk stratification in stage II colon cancer
11:59: Clinical dilemma in stage II colon cancer
13:50: Other challenges
15:55: How to move the field forward?
16:30: Circulating tumor DNA, what is it?
18:12: CtDNA detects MRD
19:19: CtDNA dynamic reflects tumor burden in CRC
20:04: Post-op ctDNA detection and what it means
23:29: CtDNA dynamics — Real-time monitoring & its value
25:18: Serial ctDNA — What info does it provide about adjuvant chemo?
26:35: GALAXY trial results: Role of adjuvant chemo?
27:50: The DYNAMIC II trial
30:00: DYNAMIC II — CtDNA assay used
31:02: DYNAMIC II — Main study results
31:35: DYNAMIC II — Additional results
32:25: DYNAMIC II — Summary
35:00: DYNAMIC III — Design
36:19: Post-treatment ctDNA, role?
37:25: Trials for CtDNA positivity after Adj treatment
40:00: Q & A

Manju George 0:00
Hello everyone. Welcome to DocTalks. I’m Dr Manju George, the Scientific Director at PALTOWN Development Foundation, the nonprofit that supports COLONTOWN. And today we have the pleasure of having Dr. Scott Kopetz with us, who’s going to tell us about the BREAKWATER trial. But before we start, Dr. Kopetz can you tell us how you got interested in doing clinical trials and working in GI oncology?

Dr. Scott Kopetz 0:25
Most certainly. So I think, like many, I had personal reasons to get into oncology. I lost my mother to cancer at a young age, and so I was motivated to tackle this, and ended up in GI oncology, because I just fell in with a wonderful mentor, Paul, who was here at MD Anderson at the time, and was working in colorectal cancer and just kind of fell in love with the clinical problems and the wonderful patients of course, and really have been inspired ever since by all of our patients.

Manju George 1:08
Thank you for sharing. So then, do you want to share your screen?

Dr. Scott Kopetz 1:11
Yep, absolutely. Yeah. So just delighted. This is always so much fun. And I just start by saying, really a delight to be able to discuss and to share some of the updates here, and want to touch on some of the efforts that are ongoing. I know it’s been a little while since we’ve had an update, and so I’ll start with a little bit of background, and then dive into where the field is now and where we’re going. So some conflicts: very involved in a lot of these companies that are involved in developing novel therapies for BRAF. So kind of a key point I always like to start off with, and so apologies for those of you that have seen this slide a dozen times before. But the idea is that this is a cancer that when we have a BRAF mutation, it results in activation of growth factors, or a growth signaling pathway, right? This is a normal, healthy pathway in your body. When you cut your skin, your epithelium- your skin cells, turn it on to grow and repair, and then it gets turned off. The problem when there’s a mutation in the pathway like BRAF is that it’s constantly on and these cells are then growing. And what we found, though, is that these cancer cells like to be in this state, and that when you inhibit BRAF, with a medicine like encorafinib, that you indeed can shut down that pathway. The growth turns off, but the tumor adapts. The cancer likes this state. And then in cancer terms, we talk about this as homeostatic regulation. It’s like the thermostat: If it’s hot or cold, things get turned on or off with your heat or AC to adjust, and it’s the same thing with with cancer cells. And so there’s a transient inhibition, but the tumor adapts, has all these feedback mechanisms. The wiring that turns on other things upstream through the EGFR receptor is one of the prominent ones, and then what happens is that same signaling pathway gets turned back on.

Dr. Scott Kopetz 1:11
So the fundamental concept, and why we are using combination therapy and BRAF is because when you inhibit that second node, the EGFR, then you can shut down that adaptive mechanism, and so the combination provides benefit where either one alone doesn’t. So of course, this is the rationale behind the BEACON study, which looked at the encorafinib, the cetuximab, the BRAF and EGFR, compared it to chemotherapy control, then and looked at both triplet with a MEK, which didn’t provide any benefit, or the doublet with the BRAF and EGFR, which showed very nice results and improved overall survival, increased response rate, was a nice building block then for us to now become a standard of care, but also recognizing ways that we want to improve.

Dr. Scott Kopetz 2:42
So one way to look at this is to say it’s clearly active providing benefit from patients. There’s a subset of patients who can be on this regimen for a really long time. There’s also a number of patients that get some benefit for several months, and then the tumor adapts and progresses. So one of the questions is, well, why is that? And one of the areas that we’ve been able to characterize is really understanding these mechanisms of resistance. This is a complex slide, but what I want to do is just to have you visually look at the control and looking for any red mark, and a red mark means there’s some acquired event in the tumor. You can see very little evidence of red but when you look at the treatments with the BRAF and EGFR, you see all of these red marks. These red marks are predominantly around RAS mutations. There’s some other ones. But really, this idea that KRAS and NRAS can get mutated, the tumor mutates those in order to maintain that addiction to that growth signaling. And so, there’s an example here of a case study. And this is something I reported last year at ESMO. And this is a patient that was on the trial and at the time of progression, after about eight months on treatment that we looked in the tumor by circulating tumor DNA. So all of these KRAS mutations. These are all present in different subclones. And this is a real challenge, right?

Dr. Scott Kopetz 2:42
How do we prevent these subclones from growing out and developing resistance to the therapies? So put a pencil on that -we’ll come back to that, and some interesting hypotheses coming on that, but just acknowledging that, that’s one of the limitations that we’re dealing with. So where’s the field going? This is a good foundation, as I mentioned, and I’ll talk about some of the studies here briefly, and not really focusing a bit on BREAKWATER study, which is our first-line trial, really trying to understand how we best utilize this.

Dr. Scott Kopetz 2:42
So first, let me share some of the preclinical data that’s ongoing, and asking, “Can we do better? Is the idea of targeted therapy and more traditional chemotherapy, can we combine those and get more benefit out of that?”. Well, one of the findings that we had when we looked at this in our mice work is–in the mouse, we can generate the tumors, we can treat them with one therapy, and then move into second-line in the mouse, and then, compare this to when we do it altogether. And what we can see is that this interesting phenomenon. We think about chemotherapy and targeted therapy is two different things, but the reality is that there is some degree of cross-resistance between them, meaning that when a tumor develops resistance to chemotherapy, itcan sometimes develop resistance to the BRAF inhibitor, even though it’s never seen the BRAF inhibitor, and then vice versa. So these are kind of complex figures, but I think the way to look at it is to say, here is the benefit of encoafinib in this model, when you give encorafinib and cetuximab in first-line, the tumor has never seen a chemotherapy. However, if you give chemotherapy first, wait for the tumor to progress, and then give the BRAF and EGFR, you don’t get as much benefit. So these models aren’t under control for as long. And interesting– the same with the chemotherapy, so the prior targeted therapy may impact that. So the question is that sequential may not always be optimal in that situation. And so when we look at this and say, ‘Well, what if we put them together? What if we put the chemotherapy together with this?’.

Dr. Scott Kopetz 2:42
If you’re not used to looking at these mouse model graphs, what you’re looking for are tumors that are shrinking, going below the lines. And here you can see in the blue, these are the lowest, the best, and the combination of the targeted therapy and chemotherapy may actually induce more activity. So some of the conceptual rationale behind the BREAKWATER study: This is a large international phase III study that’s ongoing, and I’ll show you some of the data from the safety lead-in which was just ensuring, as we thought, that this would be safe to combine chemo, either FOLFOX or FOLFIRI, with the encorafinib and cetuximab. The ongoing study from phase III has three arms currently as you can see here. We don’t have any results from that, so nothing I can share yet on the randomized portion. Well, I’ll share some of the really promising data on this safety lead-in. First we should reflect and remember that chemotherapy alone in first-line gives us about a 40% response rate, the targeted therapy about a 20% in the later lines. And so we’re looking at some of these response rates, now the combination and seeing in first-line now 68/75% of the patients are having their tumors shrink down by more than half in volume. And even in second-line, where we expect maybe a 10% activity of the chemotherapy, you can see really promising, 40 or so percent shrinkage. and that duration of response is really fairly long. So remembering that with encorafenib-cetuximab we’re seeing duration of responses in under six months or so, we seem going much higher. The other way we can look at it is these progression-free survival curves where we’re seeing PFS’s that are really promising here, even in second-line, where medium PFS is somewhere in that four to six months with our current standard of care now, these small cohorts see really promising data. So, just acknowledging encouraging numbers, these are small cohorts, but I think giving us in the field a lot of enthusiasm that we’re going to see benefit with these combinations.

Dr. Scott Kopetz 2:42
Alright, so let’s go back to this–what about the mechanisms of resistance? So, a little complex– throwing a lot of scientific terms out here, but you we can actually look and see what’s changing in the tumor. And the bottom line is that when tumors progress on chemotherapy or targeted therapy or the combination, they actually have a very different pattern. And you see a number of different changes that suggest that we’re constraining the potential mechanisms of resistance, and that when you give the cancer fewer opportunities to progress there are fewer solutions to the problem of how to grow it in this regimen, what we see is that means that the tumors have a longer period of disease control. So I think the biology is really suggesting that.

Dr. Scott Kopetz 2:42
Now, interestingly, if we look at not BRAF colorectal cancer tumors, but if we look at patients that don’t have a BRAF mutation or a RAS mutation, these are ones that would benefit from the EGFR inhibition alone. There’s some data that we presented just recently in 2 JCO papers that reflect on the fact that RAS mutations occur in 40 and 20% KRAS and NRAS of patients treated with an EGFR inhibitor alone, but when you combine that in first-line with chemotherapy, it turns out that less than 10% of patients develop one of these secondary alterations. So we’re going for more than 50% like we see in BEACON, acquiring these secondary alterations. Now, when we combine it with chemotherapy earlier on, you don’t see the tumors picking that mechanism of resistance of acquiring RAS mutations. So we don’t know, I think it’s going to be really interesting to find out, but the same could occur, right? Can the combined chemotherapy prevent some of these acquired RAS mutations? Now this kind of makes sense, if we recognize that RAS mutations actually don’t result in resistance to chemotherapy, right? So RAS mutations may be the easy way out for developing resistance to the BRAF, but when you’re giving a combination, the tumor has got to find a way to grow through the BRAF inhibitor and the EGFR inhibitor, and through the chemotherapy. And if the acquired RAS mutations doesn’t result in resistance to the cytotoxic chemotherapy. Well, that’s not a solution to the tumor to grow. It’s got to find a harder way an alternate way. So this conceptually makes sense, that we’re cutting off pathways of resistance that may occur. Now the other question that we’ve asked is, well, this combination chemotherapy, we know that at some point with oxaliplatin, we need to stop the oxaliplatin. We use these maintenance regimens. So how do we do that optimally?

Dr. Scott Kopetz 14:26
And and the mouse modeling at least, suggests, probably what we would think makes sense, which is, you can’t just do maintenance with encorafenib. You need both encorafenib and cetuximab, and then also that you may get some benefit by continuing some of that 5-FU alone with it, as we had been alluding to, resulting in some of the alternate mechanisms. So we really think that the maintenance regimens, and this is how it’s written in the study, should be like a 5FU, encorafinib, and cetuximab, once a patient has received a maximal amount of oxaliplatin.

Dr. Scott Kopetz 10:19
All right, so where else is the field going? I’ll share a little bit about some of the updates in the IO space here. And this is building on some nice data that MAPK pathway inhibition, can enhance some of the immune responses in BRAF patients. And so this is that actually, from Ryan Corcoran’s group, looking at – these are old studies that we have done in years past, looking at, in responding patients, it turns out that you see an evidence of immune infiltration. And when you look at paired biopsies from patients who were gracious enough to consent to those, you see this increase in these these T cells. So we know that even though there’s no immunotherapy given in these figures, that just the targeted therapy alone may drive an immune response. And so there was nice data for those interested, looking at a BRAF, MEK, PD-L1 that is in that prior publication, thinking about how do we build on encorafinib and cetuximab, a nice trial led by Van Morris in our group looking at this, saying, “Can you add a PD-1 on top of this, even in microsatellite stable?”, so a small study but encouraging 50% response rate, which favorably compares the 20% we’d expect with the encorafinib-cetuximab alone. And then increasing the durability of this, and I think really seeing some patients that are having amazing durability to their disease.

Dr. Scott Kopetz 16:43
So that is an ongoing randomized study that’s currently enrolling nationwide for patients in second or third-line to be randomized, encorafinib-cetuximab, with or without nivolumab. So two to one randomization, so every three people enrolled, two get the nivolumab and one with the encorafinib-cetuximab. I will mention as an aside that there’s some data suggest maybe the PD-1 can rescue resistance in some settings. So there is a study, or now a cohort, that’s open– encorafenib-cetuximab-nivolumab at our institution, even if patients that had prior encorafenib and cetuximab, there are openings there. So it’s an option to consider.

Dr. Scott Kopetz 1:11
The final study I’ll mention is the rare subset of patients that have MSI high, which is more immune-sensitive and a BRAF mutation. And this is a trial ongoing that’s randomizing an initial first line setting; Pembro or PD-1 with or without the encorafenib, cetuximab to try to again, show that synergy between immunotherapy and targeted therapy. All right, so with that, just to conclude, I think this group knows: BRAF mutations, poor prognosis. We should be testing for it. We should make sure that this is a known status and that combination strategies are certainly successful, the encorafenib-cetuximab’s, the current standard of care. But hopefully I convince you that there’s some good rationale, pre-clinically and preliminary data from our first 60 patients, of potential benefit when we combine chemotherapy with encorafenib-cetuximab, and that study is ongoing, the BREAKWATER study, but there’s really interesting biology suggesting that you may be influencing and constraining the mechanisms of resistance. So if we can really shut off some of those RAS mutations, for example, that would be a substantial benefit. A lot of other areas, I don’t have time to go through all of them, but just updating where we are with the PD-1 combination: There’s work going on in neoadjuvant in the UK and adjuvant settings here in the US, a number of novel combinations are ongoing, including – I’d highlight this really interesting data that came out of an unbiased screening study with BET inhibition which is a epigenetic modifier in BRAF-mutated colorectal cancer models that was presented at AACR this year, and there’s actually a trial through the NCI network that will be opening up here the next few months to test that in patients who’ve previously been treated with encorafenib and cetuximab. So with that, thanks, as always, for your time and interest.

Manju George 19:37
Thank you very much. So, I think I will ask the first question. For a newly diagnosed patient who is BRAF mutated, with all these trials available, what do you think – if they have access to all the trials, what would be the good sequence for them to enroll?

Dr. Scott Kopetz 20:01
I think if they have MSI-H tumor, about 20% of BRAF patients will, the SEAMARK study, the last one that I showed is a great one, thinking about, how do we combine immunotherapy and targeted therapy. In patients who have microsatellite stable, 80% of BRAF patients, those are ones that we really think the BREAKWATER study is a great one to participate in. I think it is really an exciting study. We really hope it will be beneficial there. After that, if after patients have been exposed to encorafenib and cetuximab in some way, again, thinking about, can immunotherapy rescue that, as Dr. Morris’ study here is exploring, but then thinking also about how these other novel therapies, deeper inhibition of MAP kinase pathway and others may play a role.

Manju George 21:01
So basically, you’re saying that – it’s really nice that, Dr. Morris’ study is now accepting patients with encorafenib and cetuximab, right? Because that was something that people were concerned about. And then the other thing is that, so you really believe that the combination plus chemo is better instead of waiting and then, having that separately and then getting on, say, for example, the Van Morris trial?

Dr. Scott Kopetz 21:27
Yeah, so the SWOG study. Right – and I think, and for patients that are maybe on the control arm, for example, of BREAKWATER, I think the SWOG study is a great one. I think your point’s a good one. Just participating in clinical trials is important, and not all trials will be available to all sites, but we really do think that these are some of the more compelling directions that the field could go.

Manju George 22:00
Annie has a question, “Have you seen responses in BRAF patients with peritoneal mets?”

Dr. Scott Kopetz 22:05
Hi Annie, great, great question, as always. So yes, we have. You know, peritoneal disease is sometimes hard to measure and so response rates kind of get a little murky. Without getting too detailed, peritoneal is a, kind of a strip more, kind of across a surface of a tumor. The way that the guidance is to measure tumors, is that you measure the longest dimension of the tumor. So if you think of a strip of cancer, you’ve got to kind of measure that the long dimension. So even if the tumor kind of shrinks down this way, it doesn’t really get reflected. So you will see lower response rates. But part of that’s a bit of a function, a little artificial, just how we quantify the responses, and so you don’t always appreciate the extent of that, but yes, we can see responses in that setting.

Manju George 23:07
OK. I have a question about the schema of BREAKWATER. It seems that they have many cohorts, some of them, I think the main studies, like FOLFIRI plus encorafenib, plus cetuximab, and then they have an additional cohort, like a side one cohort D or something, where they are combining with FOLFOX. And then I also heard that there is some kind of prioritization that patients would be first enrolled into the encorafenib plus cetuximab arm. So, these are some of the questions that patients have, if I’m a newly diagnosed patient and I’m considering BREAKWATER, what are my chances of getting into each of these arms? Because, for example, if I’m just going to get into encorafenib plus cetuximab and I won’t get into a combination arm, then patients are thinking whether that’s a good strategy for them first, to get exposed to it, because then you can’t get on, it shouldn’t narrow down the options that are available to them later.

Dr. Scott Kopetz 24:01
Yeah, right. Yeah, it is. And I think it is important things to understand; So a little clarification: There are some amendments coming to BREAKWATER, really to focus that down a little bit more. And what we’re seeing is that the FOLFIRI component will be evaluated in a bit of a later point, and won’t be part of the initial randomization. So it’s still going to be a FOLFOX based chemotherapy backbone. Just to say, there are some changes coming that will make it a little more condensed and I think a little more patient friendly. Because I think the arms that we really are interested in is, how much does the combination of chemotherapy and targeted therapy compare to what right now is considered the standard of care, which is the chemotherapy alone. So that’s the main question. And I think the goal of really trying to get to that question as soon as possible.

Manju George 25:08
Okay, okay… okay – we will see if there are other questions. I think Annie had maybe one more.

Dr. Scott Kopetz 25:15
Oh yeah, how full SWOG 2107 is right? So, yeah, it’s enrolling. There’s still openings. And I suspect at least over the next six months or so, we’ll have openings there as well.

Manju George 25:33
Then she’s asking about class two and class three mutations.

Dr. Scott Kopetz 25:37
Yeah, great. Yeah, the class two and class three. So class one, is the BRAF V600E. The other mutations in BRAFget separated out into two different classes of therapies. There were some low levels of activity that were presented with a number of different trials. It was a little heterogeneous across many different kinds of settings. Not a great home run evidence of activity in colorectal cancer there. So I’m not sure we have a great solution to those yet, but the rationale is still there. I think part of the problem is that these are very heterogeneous, like not all class twos behave the same, not all class threes behave the same. So it is a little hard to sort out, and they are a bit rare, but we’re learning. We’re making progress. There’s hints of activity, but not any amazing responses yet.

Manju George 26:45
There’s a question from Katie, are you able to get into the BREAKWATER trial, as a second line of treatment?

Dr. Scott Kopetz 26:52
So not into the BREAKWATER. Even though I showed some data from the safety lead-in that included second-line patients, that was just in the safety lead-in. Right now, in the randomized phase III portion it’s patients that are previously untreated that are entering. So the second-line would be more the SWOG 2107 study, enco-cetux with or without PD-1.

Manju George 27:18
Yeah, I think Annie has a question. We had a few patients on the BREAKWATER trial, what is the best next treatment? I think you had mentioned some in your talk, right?

Dr. Scott Kopetz 27:26
Yeah, good question. If they were on the chemotherapy arm, they could then go over to the SWOG study, for example. If they were on the encorafenib-cetuximab, or the combination arm with chemotherapy and encorafenib-cetuximab, then, at that point, you’re right thinking about, if they were just on encorafenib-cetuximab, you could certainly think about chemotherapy at that point. Or, like mentioned, there are clinical trials ongoing in that setting to try to explore.

Manju George 27:27
With the safety lead-in, there were some differences in results with FOLFOX and FOLFIRI, right? So, I’ve heard some people ask, with FOLFIRI, there were some interactions, and the drug availability was less… or something. And then the main randomized portion of the trial is now with FOLFOX, but then the long term data show that FOLFIRI as acombination has been better, right?

Dr. Scott Kopetz 28:35
Yeah, so, we don’t really know for sure, I think it’s fair to say. I hate to make too much out of these cohorts of 10 or 15 patients and try to combine in one or the other way. So I think I would be a little more cautious there. There’s a little bit of a PK interaction as I was mentioning, so you don’t get the same exposure to the drugs as you would normally. But not sure that’s playing a big deal based on the results that we’re seeing. Like you said, it was certainly encouraging. So I think that the data really suggests that there’s substantial benefit with the FOLFOX out of the safety lead-in so I’ve been very comfortable in recommending that to the patients. I don’t think we’re missing an opportunity necessarily, on the right partner.

Manju George 29:31
Okay, okay. And then once they finish the chemo plus the Encorafenib+Cetuximab potion, then are you thinking that, say for example, if they don’t have access, we have many – because BREAKWATER is open worldwide, we are fortunate to have the SWOG 2107 right? But many other countries, they don’t. The the idea of combining encorafenib plus cetuximab with nivolumab isn’t that common. So do you think that in that case, they can get LONSURF+bev, or once they progress on the trial, what options could they consider?

Dr. Scott Kopetz 30:08
Right, yeah, so, there’s always the alternate side of toxic regimens that may make a difference. LONSURF+bev I think certainly is reasonable as well. So we do, you’re right, just kind of lean back on what kind of works in general, in colorectal cancer.

Manju George 30:23
Okay, and then, when you look at the resistance mutations, there are so many met amplifications and things like that. Do you think STIVARGA (regorafenib) has worked for people? I’ve seen that some people prefer to use STIVARGA when they get progression on encorafenib plus cetuximab. So what is your personal —

Dr. Scott Kopetz 30:44
–Yeah – we don’t – It’s not great data on that, necessarily. I think it’s a reasonable option, but I don’t know that it’s not something we’ve seen pan out in our preclinical studies, that we’re driving towards a more sensitive phenotype to regorafenib, but certainly a reasonable option.

Dr. Scott Kopetz 31:05
Okay. Were there any learnings from ANCHOR CRC trial regarding PFS or OS to those without peritoneal mets?

Dr. Scott Kopetz 31:14
Yeah, so ANCHOR was a study looking at the encorafenib plus cetuximab plus a MEK inhibitor, and that was running in parallel with BEACON, and we learned from BEACON that the MEK was adding more toxicity, not adding as much benefit. So it’s a little harder to extrapolate some of the ANCHOR data otherwise, but I think what we recognized is that the PFS was kind of in the same range as what we’d expect with the chemotherapy alone and the OS, likewise, looked encouraging, but it was non-randomized for the OS, which makes it hard to interpret. So, the breakdown by with/without, peritoneal metastasis is not really well laid out.

Manju George 32:00
Okay. And then could you say something more about that BET inhibitor trial?

Dr. Scott Kopetz 32:11
Sure. So, this is through an unbiased screen where we asked, ‘if you have a patient or a tumor on encorafenib-cetuximanb, and we screen 1000s of different nodes for ways to modify and we find a node that really tends to be a vulnerability of the cancer, and that turns out to be a bromodomain, which is a regulator ofgene expression. And so there is actually an inhibitor of bromodomain, so we were able to then show the benefits there and bring that together into a clinical trial. So there’s a bromodomain inhibitor plus encorafenib and cetuximab. What it’s doing is, really for those aficionados, is deeper inhibition of the MAP kinase, as well as shutting down MYC signaling, which is a key survival mechanism. So it’s a really way to inhibit MYC, which is one of the key oncogenes.

Manju George 33:09
Okay, I think it’s sort of hard to get the word out to BRAF folks about this trial. Has enrollment been fairly brisk at NCI centers and academic centers worldwide?

Dr. Scott Kopetz 33:22
Uh, let’s see. So I’m not sure which trial?

Manju George 33:27
I think BREAKWATER.

Dr. Scott Kopetz 33:28
Oh, BREAKWATER, yes, it is. It’s going, you know, first-line studies are a little harder, because a lot of times we don’t always know the BRAF status by the time that patients start treatment. So it’s not quite as fast as BEACON but it’s going reasonably well. We’ll get it done. Not always as fast as we like, but we’ll get it done. And I think we’re kind of on track on projections at the moment.

Manju George 33:57
Yeah, yeah. I think that we are working with Pfizer to get, in COLONTOWN University, we are going to be having a featured trial, we’re doing that for BREAKWATER. So my other question would be, since you have those mouse lines that seemed very interesting, where you’re doing sequential treatment and testing, what kind of resistance develops. Are you also doing experiments where you’re doing the encorafenib plus cetuximab plus FOLFOX and seeing what else you can give those mice?

Dr. Scott Kopetz 34:25
Right, so, we haven’t pursued that. I think it’s an interesting area to say, ‘how do you even improve upon where the BREAKWATER is going to be’, right? But no, we haven’t started that type of work yet. But I like the way you’re thinking, let’s take a step ahead.

Manju George 34:44
Yeah, because I’m sure that in a year or two, then you’ll have lots of enrollment, and then people are going to be asking, ‘what next?’.

Dr. Scott Kopetz 34:53
So that’s right, – have something ready – because that’s right… we’re looking for good post docs to do that. If anyone knows of some good post docs out there, let us know.

Manju George 35:02
Okay, okay, yeah. So Annie says it was great to see that there was an epithelial to mesenchymal transition in preclinical research. Is that showing up in BREAKWATER patients too?

Dr. Scott Kopetz 35:15
Good question. We don’t know. You know, we don’t have progression biopsies on patients on BREAKWATER, orany biopsies, for that matter. So as phase III, they tend to not have that same degree of translational research. So we’ll have blood, but we can’t always assess some of these transition states, like you mentioned Annie, in some of the samples that we’re collecting. So we’re going to rely on other ancillary, smaller phase II studies or preclinical models.

Manju George 35:48
Okay, I think we have gone through this really fast.

Dr. Scott Kopetz 35:53
Wonderful. Yeah, no, that’s great. Well, thanks so much to everyone for the time and interest and happy to answer any other questions that come up offline.

Manju George 36:03
Thank you so much.

Dr. Scott Kopetz 36:06
Thanks.

Manju George 36:07
Bye

Dr. Scott Kopetz 36:08
Bye bye.

DocTalk
2022
Dr. Tie
ctDNA
Stage II
Trials

In this DocTalk recorded August 2022, Dr. Jeanne Tie from The Walter & Eliza Hall Institute of Medical Research in Australia discusses her ctDNA DYNAMIC II trial with PALTOWN Scientific Director, Dr. Manju George.

Table of contents

00:00: Introduction
04:29: Minimal residual disease (MRD)
06:06: Duke’s staging
07:11: AJCC TNM staging
07:50: Adjuvant treatment for early-stage CRC & challenges
08:53: Things tried in stage II Colon cancer
11:00: Better risk stratification in stage II colon cancer
11:59: Clinical dilemma in stage II colon cancer
13:50: Other challenges
15:55: How to move the field forward?
16:30: Circulating tumor DNA, what is it?
18:12: CtDNA detects MRD
19:19: CtDNA dynamic reflects tumor burden in CRC
20:04: Post-op ctDNA detection and what it means
23:29: CtDNA dynamics — Real-time monitoring & its value
25:18: Serial ctDNA — What info does it provide about adjuvant chemo?
26:35: GALAXY trial results: Role of adjuvant chemo?
27:50: The DYNAMIC II trial
30:00: DYNAMIC II — CtDNA assay used
31:02: DYNAMIC II — Main study results
31:35: DYNAMIC II — Additional results
32:25: DYNAMIC II — Summary
35:00: DYNAMIC III — Design
36:19: Post-treatment ctDNA, role?
37:25: Trials for CtDNA positivity after Adj treatment
40:00: Q & A

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KRAS therapies for CRC

KRAS therapies for CRC

DocTalk
2022
Dr. Kopetz
KRAS

Dr. Scott Kopetz from MD Anderson discusses the latest KRAS-directed therapies for colorectal cancer with Paltown Scientific Director Dr. Manju George. Recorded in April 2022.

Table of contents

0:00 Introduction
1:46 What is adaptive resistance?
3:45 Lessons learned from BRAF inhibition in CRC
4:16 Targeting MAPK signaling & adaptive resistance
5:19 Pathways to resistance
7:33 KRAS mutations by tumor type
9:00 KRAS G12C inhibition
11:35 Sotorasib in CRC
12:18 Adagrasib in CRC
13:00 Adaptive resistance to KRAS G12C
23:00 How to combat adaptive resistance?
25:45 CodeBreak 101
27:00 Common mechanisms of resistance to G12C inhibitors
28:40 Summary so far
30:04 Combinations with KRAS G12C inhibitors
31:52 Beyond KRAS G12C
33:05 Clinical development of RAS inhibitors
35:19 KRAS G12D inhibitor- preclinical data
39:15 Other approaches
42:49 Conclusions
45:30 Q & A

Manju George 0:00
Hello Everyone, Welcome to DocTalks. I’m Dr Manju George, the Scientific Director of PALTOWN, the nonprofit that supports COLONTOWN. I organize DocTalks, which are Zoom video talks from expert clinicians from the field on topics that are relevant to colorectal cancer patients and caregivers. Today, we have Dr. Christopher Lieu with us. He’s the Associate Director of Clinical Research and the Co- Director of Gastrointestinal Medical Oncology at the Colorado Cancer Center. He’s also the Vice Chair of the NCI Colon Task Force. Very excited to have you with us, Dr. Lieu, and he’s going to tell us about CtDNA tests for cancer screening and about the CIRCULATE-US trial. Welcome.

Dr. Christopher Lieu 0:43
Thanks so much, Dr. George, and thank you so much for the opportunity to talk to you all today about circulating tumor DNA and an upcoming trial, or newly opened trial called CIRCULATE-US, where we’re trying to utilize this new technology to change the way we treat earlier stage colorectal cancer. So thanks for taking the time. These are my disclosures: I do want to mention that there is a contracting agreement between Natera and my institution, University of Colorado, and in regards to Natera, just mainly because they’re one of the companies that produce CtDNA assays.

Dr. Christopher Lieu 1:17
All right, so what are we going to talk about over the next 30 minutes? We’re going to go back. I know that you have already had great talks from Dr. Cohen and Dr. Kopetz in regards to circulating tumor DNA, and we’re going to build on that, but we’re going to take a little bit of a step back. I’m sure you’ve talked about circulating tumor DNA, or heard of it in terms of earlier stage, or even the utilization of this type of technology in later stage colorectal cancer. But what about screening and primary prevention of colorectal cancer? What we mean by that is essentially anybody who hasn’t ever been diagnosed with colorectal cancer, we want to prevent those cases. So where can blood based tests really make a difference? We’re going to talk about screening just in general initially, and we’re going to talk about screening rates within the United States, but we’re going to start then to talk about where CtDNA may be appropriate in primary prevention of any cancer. Of course, this includes colorectal cancer, and of course we want to follow up with a discussion about what CIRCULATE-US is in regards to the utilization of CtDNA for stage III colon cancer.

Dr. Christopher Lieu 2:24
So this is going to be a big background that everybody already knows about colorectal cancer, because this group that’s listening to this talk is, – you guys are really the experts, but it is good to go back to the basics and talk about, what is the landscape of the epidemiology to risk factors and screening for colorectal cancer. We know that this is the third most common cancer diagnosed in the United States, and the estimates for the number of colorectal cancer cases in 2022 are over 100,000 new cases of colon cancer and over 40,000 new cases of rectal cancers. So this is a tremendously big problem, and certainly something that this group knows a lot about. And of course, the risk factors for colorectal cancer include risk factors for a lot of cancers, including being overweight or obese, having physical inactivity. A little bit different than a lot of other cancers is this idea that a diet high in red meats, processed meats, or cooking meats at very high temperatures, is a risk factor for colorectal cancer. And of course, these are some foods that a lot of people like a lot. So if you eat barbecue, it is a risk factor for colorectal cancer. This isn’t an announcement to say, “don’t eat barbecue”. But of course, it does mean that we certainly want to limit how many processed meats, or red meats or high cooked or high temperature meats we eat on a daily basis.

Dr. Christopher Lieu 3:41
Smoking and alcohol use are significant risk factors for a lot of different cancers, but of course, we always worry about genetic risk and hereditary genes impacting our ability to develop a colorectal cancer. But this still is a vast minority of cases of colorectal cancer that have a genetic component to it. Familial Adenomatous Polyposis is only 1% of the population. Lynch Syndrome, which is the most common inherited cancer risk profile for colorectal cancer, is only 2 to 4%. So these are some really interesting charts in regards to the incidence of colorectal cancer by age. And so when you look at the population that’s 55 and older, you can see these dramatic decreases in the incidence of colorectal cancer. And this really speaks to the power of primary prevention. This idea that if you screen for colorectal cancer, if you get a colonoscopy and remove polyps, you can really reduce the incidence of colorectal cancer. That’s the big take home message. Of course, this group is also very familiar with the fact of the incidence in our younger population. So what you’re looking at here are graphs from 20 to 49 and you can see this inflection point in the 1980s and the 1990s where the rates of young onset colorectal cancer really started to increase, and then it increased year over year. Many of the people in this group and listening, and certainly the physicians and providers, would tell you that seeing young patients with colorectal cancer is really obviously still devastating, but it’s becoming, unfortunately, more common.

Dr. Christopher Lieu 5:13
Another way to look at this data is to look at colorectal cancer incidence rates by birth cohort, and you can again, see this inflection point that those born 1960 to 65 and then onwards. You can see this incidence increasing. Now I do have to tell you that early onset colorectal cancer is, of course, still rare, but if it increases by 2 or 3% every single year, then you can tell that even though it’s still a rare event, it’s becoming, unfortunately, more frequent. The United States is not the only country documenting an increase in early onset colorectal cancer, and those countries highlighted in red are showing similar trends. So this is a worldwide phenomenon, and not solely restricted to the United States. So the first take home point that everybody here already knows is that the incidence of colorectal cancer, particularly rectal cancer in young patients, is increasing. And this figure that you see here shows the duration of bleeding of having seen blood in the toilet before diagnosis, and this is stratified by the stage of diagnosis. When you look at older adults, the onset of bleeding to diagnosis of cancer is usually about 25 to 28 days. Here, if you look at some of the patients that were diagnosed with stage IV disease, on average, they were waiting over a year between the time that they had their initial symptoms and the time that they were actually diagnosed. And the longer that time takes, the more likely it is that you’re going to have advanced colorectal cancer, as opposed to an early stage colorectal cancer. So how do we prevent colorectal cancer? We don’t always talk a lot about screening as oncologists, because we’re usually taking care of patients after they’ve been diagnosed. But the problem with this is that there’s so many guidelines out there that it can be very confusing in terms of what patients should actually do. But of course, the American Cancer Society several years ago actually was very forward thinking and they actually decreased their age to start colorectal cancer screening from the age of 50 to 45 and I showed you the data as to why they wanted to change that. For people ages 76 to 85 the decision to be screened should be based on a lot of different factors, including how healthy that individual is. And the recommendation is that people over 85 should no longer get colorectal cancer screening.

Dr. Christopher Lieu 7:29
In terms of what tests that people offer, there’s stool-based tests and there’s visual tests. The stool-based tests include looking for blood in the stool, and that’s called a FIT Test or Fecal Immunochemical Test. We have this general fecal occult blood test, and there’s even a stool DNA test, which we’ll talk about. But of course, the gold standard is colonoscopy, because not only can you visually look at the colon, you can also remove polyps that may eventually turn into a cancer. There’s also CT imaging that’s available, and a flexible sigmoidoscopy looks at the first third of the colon, but cannot reach the last two thirds of the colon. The United States Preventative Services Task Force also has guidelines. This is our most conservative guideline group because their expectation for the level of evidence is quite high. So they really, really look at the data and say, well, the data doesn’t support certain screening, then they don’t recommend it. But if it does, then they do recommend it. Their Grade A recommendation is still for adults age 50 to 75, but the big update here in 2021 was a Grade B recommendation for 45 to 49 which means that these patients likely really should be screened. And, the more patients that get screened, the more we can prevent cancer. So your second take-home point: everybody should start screening at age 45 or 10 years before the youngest case in the immediate family. So if a first degree family member was diagnosed at the age of 40, then you would start screening at the age of 30. For patients 76 to 85: just consider the patient’s health. Then a colonoscopy is the gold standard, because it’s preventative and potentially treatable as well.

Dr. Christopher Lieu 9:10
Just a quick note from Dr. George that if you guys have any questions as the presentation comes in, feel free to put it into the chat. In all honesty, feel free to just unmute and ask the question even as I’m speaking. I’d love for this to be as interactive as possible. All right.

Manju George 9:26
Dr Lieu, then I have a question.

Dr. Christopher Lieu 9:28
Sure

Manju George 9:28
So my question is, what about polyps in the family, and how does that affect when you have to screen?

Dr. Christopher Lieu 9:36
So it really depends on the type of polyp. It’s such a great question, because I think that this really gets overlooked. If you have your typical tubular adenoma, and you get those things clipped off, and then the risk of having colorectal cancer, from a familial standpoint, is quite low. There are some times that patients have really, really advanced polyps, basically these polyps that have really high grade dysplasia and you can tell that in the next one or two years, you can tell that that patient is actually going to develop a colorectal cancer. And that’s why it’s actually so critically important to know that if you have a very advanced polyp that has significant malignant potential, we should treat those patients as if they already had a colon cancer. So, kind of complex. It’s certainly one of those things that when you get a colonoscopy, you get a polyp removed, it is good to ask, “Hey, was it a really benign polyp, or was this a really scary looking polyp?” And if it’s a scary looking polyp, then you go and tell your entire family. Great, great, great question!

Manju George 10:32
Okay, thank you.

Dr. Christopher Lieu 10:33
Absolutely! When you look at colorectal cancer screening across the country, there are disparities here. And actually, one of the questions I really wanted to ask the group was, well, what is the biggest predictor of getting colorectal cancer screening? You’ll find the answer as we go through the next several slides. But is it race and ethnicity? Is it income? Is it even geographic distribution? You can tell that your rate of colorectal cancer screening actually differs by by state. So if you’re living in Texas, for instance, then the rates are 62% which is obviously much lower than we want it to be. If you look into northeast: Rhode Island, Massachusetts, New Hampshire, Maine, they have 75 to 76% screening rates. And the goal here is, obviously would be 100% but in all honesty, even having 80% would be really, really, tremendously impactful, and you can see that there’s a difference across the entire country. Well, what about sex? So if you’re male or female, does that make a difference? In here, there’s a little bit of a difference between females and males, but for the most part, it’s relatively the same, and has stayed that way over time. What about age? It does make sense that as you get older, there’s increased use of screening. Maybe there are some other health factors, you’re seeing your doctor more frequently. But it is interesting that as you go from 50 to 64 and then from 65 to 70, there is a pretty significant jump in terms of who’s getting screened. What about race and ethnicity? It’s interesting because I thought that the disparity gap here would be wider. It’s not quite as bad as I thought there would be, but there is a disparity gap, and so even when you look at our Native American population and our Asian population, interestingly, those are some of lower rates of screening compared to some of the other groups that you’re seeing here. But for the most part, there isn’t a huge difference. But what I’ll tell you seems to be the biggest discrepancy, or disparity between colorectal cancer screening and groups is actually your insurance status. And I think that that’s actually one of the big take home points, is that if you’re insured, you’re going to get screened, and if you’re uninsured or underinsured, only half of those patients are actually getting screened. So it does tell you that a lot of these things, you can actually have an impact on. But it is interesting data.

Dr. Christopher Lieu 12:43
All right. Well, what about tumor DNA-based screening approaches for colorectal cancer? We’re here to talk about circulating tumor DNA, and we’re going to talk about — I see the question from Annie about right versus left sided primaries and screening methods. So that’s such a great, great question, and I’m actually going to answer that a little bit later over the course of the talk, because for these tumor DNA-based screening tests, you want to make sure that you can detect cancer on both sides. To go back to visual screening methods like flexible sigmoidoscopy and colonoscopy, if you have a left sided primary you should be able to see it on colonoscopy and flexible sigmoidoscopy, but because flex sigmoidoscopy only really looks at 1/3 of the colon, flex sigmoidoscopy is definitely going to miss the other two thirds, particularly the right side of primaries, because you’re just not looking. But of course, with even with colonoscopy, sometimes you can miss the right side of primaries because either the prep is not very good or, you know, because it’s just harder to get there, and sometimes you can’t even get the scope all the way that far. So the right side is a little bit harder in terms of detecting cancer even with colonoscopy, but colonoscopy is still the best bet to find it.

Dr. Christopher Lieu 13:55
All right, I do want to talk about the first ever DNA test approved for use for screening, and that is a stool-based DNA test. So we talk about circulating tumor DNA, but here we’re actually talking about stool DNA. And what you’re looking at here are the performance metrics between the stool DNA test and fecal immunochemical test, which is basically looking for blood in the stool. You can see across stages the multitarget DNA test does seem better for early stage stage I and II cancer, and then performs about as well for stage III and IV. That question about left versus right is shown on the right side of this graph, and so proximal cancer would be the right side and distal cancer will be on the left side, and then you can kind of see that this test does perform better than than the FIT test. What’s interesting about this is that you can actually even detect pre-cancerous lesions with the stool DNA test. Obviously it’s not as effective in patients with polyps versus cancer. But you can tell that there’s a certain amount of pre-cancerous lesions that the stool DNA test is actually picking up. All right, and that gets us to circulating tumor DNA.

Manju George 15:11
Dr. Lieu? I have a question. So basically, they’re looking for cells from the polyps that are shed into the stool. Is that what they’re looking at?

Dr. Christopher Lieu 15:20
So they’re looking at DNA shed from the polyps into the stool. You imagine that over the course of time, these polyps have some genetic alterations. We know that there’s some early events even like KRAS and RAS and BRAF mutations are kind of earlier events in the development of cancer. But you can actually detect some altered DNA, even in polyps, and you certainly can detect it when there’s a full blown colorectal cancer. So it is interesting that in some of the altered DNA, you can see in some of these higher grade polyps, particularly there’s high grade dysplasia. They are shedding altered DNA that can be picked up by these tests, which is kind of cool, right?

Manju George 16:03
Okay, thank you.

Dr. Christopher Lieu 16:04
Absolutely. I know that you’ve had lectures from Dr. Cohen and Dr. Kopetz in regards to what gets leaked into the bloodstream. When you have a tumor that’s in place, sometimes tumors can shed actual tumor cells that you can pick up and even sequence. They release these things called exosomes into the bloodstream, but when tumors undergo cell lysis, or cell death, they do shed cell-free DNA into the bloodstream. Now the way I always describe this to my patients is that if you have somebody who’s pregnant and you draw their blood, obviously a majority of what you see in the mom’s blood is their own cell-free DNA. These are just cells, normal cells that are just turning over, and there’s release ofDNA into the bloodstream, which gets metabolized by your body fairly quickly. And so that represents a majority of the DNA that floats around in the bloodstream. But a portion of that would be fetal DNA. So you can actually sequence out the baby’s DNA, the DNA from the baby that’s being circulating around the mom, that also gets metabolized very, very quickly. Well, the same thing happens with tumors. So in our patients that have a tumor, a majority of the circulating tumor cell-free DNA in the body is that person’s normal DNA, but there’s a fraction of that that can be circulating tumor DNA, or CtDNA, which can then be sequenced and detected. And that’s really the basis of a lot of the technology that we’re looking at.

Dr. Christopher Lieu 17:39
And certainly, circulating DNA has its advantages. It’s stable – you can actually do mutational testing on it. There are established biomarkers, and it’s a short half life. Why is that important? It’s because a lot of times we get information from tissue, and that just represents one point in time. What’s circulating in the body is happening right at that moment.It gives you this real-time look of what’s happening in the body at that moment. And there’s the potential to do even further genomic characterization from the fragments of DNA that are released into the bloodstream. But of course, the disadvantages are the ones that are critically important, especially when we’re talking about screening for cancer. So not all tumors appear to shed detectable CtDNA. We worry, if a tumor is too small and is not releasing at least enough detectable circulating tumor DNA to capture in the blood, then you may, at that point, not be able to detect CtDNA, even though a patient does actually have cancer. The methodologies for analysis are really complex and expensive andthis idea that you have to filter out a lot of noise. And so part of this is that that noise can even be that as patients age, they develop these mutations that exist usually in their white cells, in their bloodstream, that are not harmful at all and are not precursors for cancer. They’re just these altered mutations that are benign. But we call this clonal hematopoiesis of indeterminate potential, or we call it CHIP for short. And that is that sometimes, as we age, we develop these mutations that exist in some of our cells that are completely benign and have nothing to do with cancer. Well, what if we detect those mutations and say, “Oh, you have cancer”. That would be obviously a real problem. So your take home point, only a fraction of cell-free DNA is circulating tumor DNA, but CtDNA may provide a real time look at what is happening in the body.

Dr. Christopher Lieu 19:33
And so there’s a couple of points as we kind of go into this idea of utilizing a test to detect cancer for the first time. One of the things that people ask is, “Well, why don’t we just use CEA?”. CEA is a blood test, and a protein that we look for in patients with colorectal cancer. And sometimes we can trend CEA to determine if a cancer is getting better or getting worse. But a CtDNA is better than CEA. What you’re looking at here is CtDNA versus CEA positivity in different stages of cancer. What I want to show you is that, particularly in earlier stage colorectal cancer, CtDNA definitely outperforms CEA. You can see that with CtDNA being on the left and CEA being on the right. You can see that CEA isnegative in a lot of patients that actually have cancer, whereas when you look at CtDNA for stage II and stage III colorectal cancer in particular, it’s almost never negative. Which means that when it’s positive, there’s definitely cancer there.

Dr. Christopher Lieu 20:41
I want to talk about two tests that are currently under investigation. One is colorectal cancer specific, and one is just looking for cancer, period. There are companies that are certainly developing both of these right now. So this is a multimodal circulating tumor DNA test looking at the primary detection of colorectal cancer. This is called a LUNAR-2 assay. Essentially what both of these tests are doing is they are looking at something called DNA methylation. And aberrant methylation signals in tumor, versus benign tissues, are different. Therefore, if you see this methylated DNA, you might be able to detect cancer earlier. And this is the test case: There were 434 cases, 271 controls, and this is the distribution by age in the controls and in colorectal cancer. Really what I want to show you is essentially this slide. What you’re seeing here is the overall sensitivity for this assay for patients with colorectal cancer or without colorectal cancer. You can tell that the overall sensitivity is unbelievably high: 91%. In the age cohort 45 to 84 which is traditionally the group that we’re looking at to detect colorectal cancer, it’s 90%. You’re seeing this high sensitivity across stages: stage I and II, stage III. Specificity is this idea that if you detect cancer and if the test is positive and you do have cancer, what is the accuracy there? And it’s 94%. So the key here is that again, across stages, it’s a really, really highly sensitive test. That’s what you want in any good screening test. Then this question of left sided versus right sided, it’s actually detecting cancers pretty well, maybe even slightly better on the right side versus the left side. And then transverse, there are not as many cases. There are only 17 cases of colorectal cancer, but it was 82% sensitive in that case. So a really, really interesting test, and I think this is really interesting early data. What they did was, – the company, Guardant – has a trial where they enrolled 12,750 patients to detect colorectal cancer, and we’re hoping to get data in the middle of this year. We’ll find out what the performance of this LUNAR-2 blood test is in the individuals that would normally be screened for colorectal cancer, and we’re going to see how good of a test this is. But can you imagine, drawing a blood test to screen for colorectal cancer, as opposed to potentially either putting in for a stool sample or undergoing a flexible sigmoidoscopy or a full on colonoscopy. So, very, very interesting, and we’ll see what the data is as they as they come out later this year.

Dr. Christopher Lieu 23:39
All right. So we talked about colorectal cancer. I just want to briefly touch on a multi-cancer early detection test, and this idea that can you utilize the same technology that we were just talking about, but look for all cancers. So imagine a blood test to be able to detect any cancer, and obviously, hopefully at an early stage. We had talked a little bit about this before, but this focus on DNA methylation. The idea is to have a low false positive rate, and we call that “high specificity”. And this idea that if you have a lot of coverage over these methylated regions, not only would you be able to detect cancer, but if different cancer sites have a unique methylation pattern, then you could at least tell somebody, “Well, you may have cancer. We have no idea where it’s coming from”. You might be able to point people towards, “Well, this fingerprint is more suggestive of lung cancer or pancreas cancer or colorectal cancer”. And that’s what this really complex figure basically shows you, is that you can draw somebody’s blood, look at the DNA methylation, and then what they’re really trying to figure out is that, is there a tissue specific methylation fingerprint where a specific methylation pattern might tell somebody, well, we really need to look for lung cancer or liver cancer or colorectal cancer. Because, you can imagine as a primary care provider, if you just get this test back that says, “Oh, we think you have cancer”. That’s not only incredibly anxiety inducing from the patient’s standpoint, it’s also incredibly anxiety inducing from the physician’s standpoint, because then, what do you do? Do you do a colonoscopy? Do you do a full body CT scan? So you can see some risk involved with these tests as well.

Dr. Christopher Lieu 25:29
This is a 15,000 participant study at 142 sites, and essentially what they had was a discovery group and a validation group. Essentially they wanted to see if the test could potentially work in a smaller group of patients, and then look at a bigger group of patients. These patients, some of them had cancer, some of them didn’t have cancer. What this test shows you is two take-home messages. Number one, the sensitivity is not great. It’s 51.5% which means in patients that had cancer, sometimes the test was positive, sometimes the test was negative. The other take home point is that it was a highly specific test, which means that in patients that didn’t have cancer, if the test was negative, they really didn’t have cancer. And there are very, very few false positives, in other words, where the test was positive, but they did not have cancer. So it meant that basically, the test was negative. There’s an incredibly high chance that they didn’t have cancer, and that’s obviously a good thing, but the sensitivity rates across diseases, range very, very differently. So you can clearly tell on the left side of this graph that this test is not a great test for prostate cancer. 11% sensitivity. That is definitely not ready for prime time.

Dr. Christopher Lieu 26:48
Well, what about colorectal cancer? Here the sensitivity is quite good, 82%. And then if you go into liver cancer or even carcinoma of unknown primary, there the sensitivity is 93 to 94% so it’s a big spread. So I would say the data is very promising towards the right side of this graph. Very not promising on the left side of this graph. And I think the main question that you have to ask is, well, will the technology get better? Can we get all of these sensitivity rates really, really high? So again, this is colorectal cancer sensitivity looking at stage I through stage IV. It’s clear that as you go higher in stage that the ability of this test to detect cancer goes up significantly. It always seems like these tests have a harder time with stage I, but the moment you get to stage II and III and IV, it gets actually quite good. I wanted to show you that detection of other GI malignancies. There’s really one take home message, and that is, for all these GI malignancies, it doesn’t do great for stage I, but as you get further into the stages, it does quite a good job of being able to pick up the detection of cancer. But again, the main question that you want to answer is, can this test save lives? We’ll say, additional studies are needed. I think you’re going to see this technology really change the way healthcare is delivered in the future. Right now the question is, is it ready for prime time? And I would say we don’t really know the answer to that quite yet. All right.

Manju George 28:19
Dr. Lieu, I had a question. So, Exact Sciences had a large trial. Is that more like a multi-cancer, or is it more like the Guardant Health?

Dr. Christopher Lieu 28:29
Yeah, so Colvera is really focused predominantly on CRC, although I know that they have data on other cancers as well. It’s interesting, because a lot of these tests that I’m showing you are casting this really, really wide net. Colvera is very interesting in the sense that they’re really looking at two genes. But they found that those two genes really do a great job of predicting for colorectal cancer. So, a little bit different, but dissimilar technology.

Manju George 28:54
Okay, thank you.

Dr. Christopher Lieu 28:55
Absolutely. I’ll just wrap up on this with the last five minutes, because, well, we talked about primary prevention of colorectal cancer. We talked about screening. Well, what about in patients that do have colorectal cancer? What happens to CtDNA in those patients, either postoperatively after surgery, but even during adjuvant chemotherapy? What happens to CtDNA? Does it go up? Does it go down? Does it become detectable? Does it become undetectable? We call that CtDNA kinetics. I just want to show you data from the Japanese group. This is their GALAXY study where they’re utilizing CtDNA, and it’s really interesting data. What this shows you is that postoperatively all the way to 12 weeks, if you’re negative and stay negative, you’re going to do great. That’s the black line. And what you’re looking at here is disease-free survival. Basically, nobody’s recurring, right? So that’s good. Interestingly, if you’re CtDNA positive post operatively, and then you turn negative, that’s almost as good as just being negative from the get-go. So that’s interesting. If you’re CtDNA positive postoperatively, you’re freaking out. – I’m worried, you’re worried. But if you turn negative, then your prognosis is quite good. If you’re negative and then turn positive, then there’s a pretty high rate of recurrence. And if you’re positive and stay positive, these are the patients that here, you’re looking at almost 70 to 80% of those patients recurring even within one year’s time.

Dr. Christopher Lieu 30:25
And I do want to show you that adjuvant chemotherapy can clear CtDNA. Interestingly, there is a 10% clearance rate by doing nothing and it makes you wonder what’s going on in those patients. Are those patients just clearing it due to their immune system? But interestingly, there is a significant rate of patients that even if they’re CtDNA positive, they receive adjuvant chemotherapy, they can clear it. We also know that if in patients that are CtDNA positive and they receive adjuvant chemotherapy, that they do better. And so that’s what you’re seeing in stage II, stage III and stage IV. That if there’s CtDNA postoperatively, and they receive chemotherapy, that their recurrence rates are significantly less. So the real question that everybody in this group wants to answer is, are the findings of this test, which is very, very cool, but is it actionable? Because that’s how we’re going to save lives.

Dr. Christopher Lieu 31:20
So what do we know so far? If CtDNA is positive, the recurrence risk is extremely high. That makes sense. If we detect tumor DNA in the bloodstream, it means cancer is there, and it means that at some point it’s going to show up on a CT scan. If CtDNA can be cleared, in other words, with adjuvant therapy, then disease-free survival is significantly improved, and we know that adjuvant chemotherapy can clear CtDNA. And we also know that if CtDNA is not detected, and it’s not detected over multiple time points, we also know that those patients are going to do incredibly well. This is the overall problem with stage III colorectal cancer, and that is that we’re treating 10 patients with with stage III colorectal cancer to save 2 to 3. I’m going to go through that. Why is that? In 10 patients that have stage III colorectal cancer, 5 of them are essentially cured with surgery. They never needed chemotherapy. In other words, they’re getting treatment even though they never needed treatment because they were cured. There are 2 or 3 that get treated with adjuvant chemotherapy who relapse anyway, which means that we didn’t help them with adjuvant chemotherapy. They were going to have recurrence whether we gave them chemotherapy or not. So we almost gave them chemotherapy needlessly. So essentially, we treat 10 patients to save 2 to 3, which means that we basically treat 7 to 8 patients needlessly with chemotherapy, either because they’re going to be cured or because they’re going to recur regardless.

Dr. Christopher Lieu 32:45
The idea is, maybe CT DNA can tell us who we don’t need to treat, and maybe we can tell with CtDNA who needs to be treated even more aggressively. I want to highlight this study, because this study is now open to enrollment and it’s going to be open up across the entirety of the United States. Essentially the way this trial is designed is that if you have stage III colon cancer and you have no CtDNA detected post operatively, you are then randomized to receive standard of care chemotherapy, which is what we normally do, or surveillance without chemotherapy, with serial CtDNA checks. If you’re negative CtDNA and stay negative, you never get chemotherapy. But if you’re negative, and then turn positive, at that point, you get chemotherapy. You get randomized to either receive standard of care chemotherapy or an escalation of chemotherapy, where we try a three-drug regimen versus a two-drug regimen. We do this because we’re worried that our patients have a poor prognosis when CtDNA is detected. Postoperatively, if you are CtDNA detected from the get-go, you undergo that randomization: either the standard of care chemo, or this triplet combination which represents an escalation of chemotherapy.

Dr. Christopher Lieu 34:00
And so the real question is, is CtDNA ready for prime time? I would say, in terms of identifying alterations in the bloodstream, that it is ready for prime time. But what we’re really trying to answer is, this bottom one. In terms of the detection of minimal residual disease, this presence of cancer, even though we can’t see it on a CT scan. The answer is possibly. Is it ready for prime time? It’s clear that CtDNA can detect cancer, but are the results actionable? And so the idea being, we know that this is an incredibly prognostic tool. It can tell us whether somebody’s going to recur or not, and we know that getting serial testing helps, but will it alter clinical practice? What happens if you get a positive result? Do you increase surveillance? We don’t know the answer to that. Will these tests save lives? So in other words, will a clinical trial like CIRCULATE-US end up showing good data in terms of well, can we use this test to determine who should and shouldn’t get chemotherapy? Can we use this test to determine who needs more chemotherapy? I’m hopeful that we’ll get the answer to that as time goes on.

Dr. Christopher Lieu 35:11
So I know that’s a lot of information in a short amount of time, but happy to – , I know Manju, you had to step aside for a little bit, but wanted to see if you guys had any questions? I see Julie has a question, can you talk a little bit little more about patient selection in CIRCULATE for stage II? Yep. So, I was trying to keep it a little bit simpler, but Julie’s asking a really, really great question, and that is the trial enrolls lower risk stage III, so if you don’t have a ton of lymph nodes involved. But there is this thing called high risk stage III, if the tumor is aggressively moving into other organs, or if a lot of lymph nodes are involved. There is also high risk stage II, where there are features of the tumor that are really concerning for the clinicians, and that’s usually related to how angry it looks under a microscope, or that tumor is actually invading into other organs. You can actually enroll into CIRCULATE if you get outside testing and that test is positive for CtDNA. You can actually enroll into the CtDNA-positive arm. We just want to give those patients the ability to have a chance of getting more aggressive chemotherapy. So if you’re high risk stage II colon cancer, or high risk stage III colon cancer, you don’t traditionally enroll into CIRCULATE, but if you have outside testing that you got as standard of care and you’re positive, then you can enroll. Annie’s asking, “The trial is only in this location in NRG?” Yes. So essentially my hope is that it’ll be open at more than 400 sites across the country. This is a collaborative effort between all the cooperative groups, which includes NRG, so this trial should, honestly, it should really be open within, my hope is 30 miles from every patient, but the reality of it is that it should be open in every state and in most, if not all, major cities.

Julie Clauer 37:13
So in terms of, you know, we have a lot of patients that come into COLONTOWN who would qualify for CIRCULATE-US, but they’re not necessarily looking at clinical trials at that point, because, they’re not high stage. They’re just recently diagnosed. Can you talk about what that conversation could be in terms of, how do they talk to their doctor, about, “Hey, I heard about this trial. What is it? Is it interesting?” Because the timing is, they might be post-surgery, but pre-adjuvant chemo, and so that’s good timing. So talk a little bit more about that, just because it seems like a quick turnaround has to happen, but it’s not necessarily people that are poised to have that quick conversation.

Dr. Christopher Lieu 37:58
So yeah, I think the timing of this is the most challenging part of the trial, and that is this idea that, if most people get seen by medical oncologists, usually a decent amount of weeks after their surgery. Capturing these patients early and getting CtDNA testing so it can inform which arm of this trial you go on is critically important. And so, I think where COLONTOWN and PALTOWN have been amazing is number one, it’s a resource. People are told they have colon cancer, and obviously, understandably, they’re freaking out. So I think the information that’s provided on COLONTOWN University is absolutely incredible. And then honestly, the earlier you can have the conversation, the better. So even before surgery, asking about it, “Is it available? Can I talk to somebody about it?” would be huge, because then everybody knows as soon as surgery is done, that they’re going to start thinking about the study, and they’ll know whether or not it’s even available at their site, or if there’s a practice closer, or within close proximity that they can enroll in. And so I think, honestly, COLONTOWN will find patients way before medical oncologists will. I think just getting the word out would be really cool, because I think, – but it’s a tough conversation, because people are just now getting introduced to this technology, and then they’re talking about clinical trials, and it’s a complex clinical trial. So having that information available and even people to talk to, I think, makes all the difference in the world for our patients but, can also help with a clinical trial accrual.

Julie Clauer 39:41
So let’s say it is available at their location. Would they connect then to the PI, or would they have CtDNA done before?

Dr. Christopher Lieu 39:54
Yeah, so I honestly would connect either through ClinicalTrials.gov, which would show the sites. Honestly, the easiest way to find clinical trials, and this is just in general, is to really ask the doctors in that area to see if, –because if they don’t have CIRCULATE open, I’m sure that they’ll actually know who does. But then also contacting the PI even like Dr. Dasari or myself, is always, I think, easy, because we’ll happily direct people to the right place.

Julie Clauer 40:26
Great, thanks.

Dr. Christopher Lieu 40:29
And then, can either a Signatera or Reveal test qualify for high risk stage II? It’ll need to be a Signatera test.

Julie Clauer 40:37
I have an unrelated question, but it drives me nuts. So now we have a lot of awesome tools that are using blood tests, like, you can get your biomarkers from a liquid biopsy, you have CtDNA to detect whether you have cancer, whether you have MRD, but it gets really confusing in terms of what to call these tests if you don’t call them by the brand name. So it’s like trying to explain to a patient like, “Oh, no that’s a liquid biopsy, but it’s a different liquid biopsy than the one…”. So is there an easy terminology of what to call these different tests? Because you say a CtDNA test, and some doctors still don’t necessarily differentiate between the different tests. So anything that can help on that end, because it gets super confusing.

Dr. Christopher Lieu 41:25
Absolutely, I think we’re all learning this new terminology, right? And I would say whenever you’re talking about: ‘is there cancer or not’, we should just call those MRD tests or minimal residual disease tests, that’s probably the easiest way. And if we’re looking for mutations in patients with stage IV cancer, we’re just basically looking for – we wouldn’t call those MRD tests or minimal residual disease tests, we would call them, I think maybe the easiest way to describe it is almost like a liquid biopsy to look for mutations. That’s essentially what you’re doing. And so I think the easiest way to kind of think about is, hey, if it’s trying to determine whether cancer is present or not, MRD is probably the way to go. And then the question, is this for rectal? Well, so CIRCULATE-US is only for colon cancer. Rectal cancer is a little bit tough, because a lot of times patients are getting a lot of therapy even before surgery. In fact, they’re getting almost all their adjuvant therapy before surgery. So this study is only for colon cancer, but these assays can be used for rectal cancer as well as colon cancer. And then Annie mentioned that for those over 70 with a high immunoscore. Yeah. The question is, is it only CtDNA? Could it be a combination of immunoscore and CtDNA? And I would love to see those collaborations in the future, because it may not just be “it’s one test to rule them all”. Maybe it’s a combination of different factors to help us make these determinations. But we’re starting with CtDNA, and then we’ll have to look how immunoscore may be added to this to help our decision making.

Julie Clauer 43:03
In terms of sensitivity. So we know this sensitivity is really high for for MRD tests, but there seems to be some things that tend to be more questionable, right? So lung mets, or maybe, the location of mets, if you’re stage IV. And I know we’re not necessarily talking about it in terms of stage IV, but a lot of patients are doing it or age or things like that. So is there any kind of good understanding of where, within colorectal cancer, how the sensitivity changes by either location of tumors or age or other facors?

Dr. Christopher Lieu 43:39
Yeah, we had talked about the age and the fact that sometimes patients have mutations that don’t have anything to do with cancer, so that can be a confounder that we have to be very careful about. But then, this idea that maybe we’re missing small lung metastases or peritoneal metastases, where they’re in the lining of the abdomen, I think that’s what keeps us up at night, right? And this idea that, are we going to miss patients that may benefit from chemotherapy? Are we just going to miss patients period that have cancer and we just can’t detect it? I think we mitigate some of that by having serial testing. Testing that’s done over the course of time. And so if patients are negative and they stay negative, that’s good. If they’re negative and they turn positive, that’s what we worry about. But I think that therein lies the risk. We want these tests to be perfect, but no test ever is. And so the question being, is it good enough? And that’s what we’re trying to answer. And then the testing is on site. I think for the study, they’ll get collected by the teams, and then they’ll be sent off, but oftentimes, these companies do offer at home blood draws.

Julie Clauer 43:42
It is very compelling, for patients from a trial perspective, and is in terms of cost. All those testing costs would be covered as part of the trial.

Dr. Christopher Lieu 45:00
That’s correct. Great question, Julie, that’s correct.

Manju George 45:04
This is about CHIP. So a test such as Signatera, you don’t have to worry about CHIP, right?

Dr. Christopher Lieu 45:11
Yeah, because it’s a personalized assay, and this idea of testing it, getting a personalized assay developed off of that really does help us with a sensitivity. It really does.

Manju George 45:26
Okay, thank you.

Dr. Christopher Lieu 45:28
Guys, thank you so much for taking the time. These are phenomenal questions and you guys are way more informed than even some of our practitioners. It is so fun to talk to you guys, and you guys are asking all the right questions, and really appreciate your interest in this, and hopefully patients will enroll, and they’ll find it interesting. The hope is that we’re going to change the way we treat stage III colon cancer. That is the hope. But at the least, at the very least, we’re going to learn a lot, and we’ll do better, and we’ll be better. So thank you guys. Really appreciate it.

Manju George 46:03
I want to say that we will have the CIRCULATE-US as a feature trial in COLONTOWN University, and our hope is that patients in COLONTOWN are, in general CRC caregivers and the patients in the public will be able to access it and find more information. The video of this talk will also be linked there, so we are hoping that this will be a great educational resource for everyone involved. Dr Lieu, thank you so much for your time, this is excellent.

Dr. Christopher Lieu 46:32
Thank you everybody. Have a wonderful day.

Manju George 46:35
Thanks everyone for attending. Take care.

Dr. Christopher Lieu 46:38
Bye bye.

Manju George 46:38
Bye

DocTalk
2022
Dr. Kopetz
KRAS

Dr. Scott Kopetz from MD Anderson discusses the latest KRAS-directed therapies for colorectal cancer with Paltown Scientific Director Dr. Manju George. Recorded in April 2022.

Table of contents

0:00 Introduction
1:46 What is adaptive resistance?
3:45 Lessons learned from BRAF inhibition in CRC
4:16 Targeting MAPK signaling & adaptive resistance
5:19 Pathways to resistance
7:33 KRAS mutations by tumor type
9:00 KRAS G12C inhibition
11:35 Sotorasib in CRC
12:18 Adagrasib in CRC
13:00 Adaptive resistance to KRAS G12C
23:00 How to combat adaptive resistance?
25:45 CodeBreak 101
27:00 Common mechanisms of resistance to G12C inhibitors
28:40 Summary so far
30:04 Combinations with KRAS G12C inhibitors
31:52 Beyond KRAS G12C
33:05 Clinical development of RAS inhibitors
35:19 KRAS G12D inhibitor- preclinical data
39:15 Other approaches
42:49 Conclusions
45:30 Q & A

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Dr. Kopetz
2022
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Immunotherapy in MSS Colorectal Cancer

Immunotherapy in MSS Colorectal Cancer

DocTalk
2022
Dr. Fakih
Immunotherapy
Liver
MSS
Stage IV
Trials

Dr. Marwan Fakih of the City of Hope Cancer Center takes a deep look at immunotherapy for MSS CRC in this Doc Talk, recorded in January 2022 with PALTOWN Scientific Director Dr. Manju George. Dr. Fakih discusses a number of recent clinical trials in this video conversation.

Table of contents:

1:38: Immunotherapy (IO) in MSS CRC—Broad overview: where are we currently with this?
3:02: What is MSI-H?
4:02: What is MMR?
6:35: dMMR Vs pMMR PD-L1 expression, how IO works
7:46: Why does IO not work in MSS CRC
9:25: KEYNOTE 177 results
10:31: Keytruda/Pembro or single agent IO in MSS CRC
12:17: IMblaze 370 trial Atezo+Cobi vs Atezo vs Stivarga in MSS CRC
13:35: CO.26 Double IO (CTLA4i+PD1i) vs best supportive care in MSS CRC
14:55: Liver mets & effect on IO-mice studies, what might be happening?
17:23: IO in mCRC patients: liver mets, a biomarker for lack of efficacy?
19:39: Immune modulatory effects of Stivarga
20:55: REGONIVO CRC-Japanese trial & similar combinations, results from GI22
28:10: CAMILLA CRC (Cabo+Durva) trial results
32:00: LEAP-005 trial (Lenva-pembro)
33:00: REGONIVO US study: why liver mets don’t seem to respond
38:10: New approaches for IO in CRC with liver mets
39:35: Summary
40:23: Other directions
42:50: Q & A Association of liver resection in the response to IO
45:00: Role of TMB in response to IO
48:22: Radiation therapy+IO in MSS CRC
50:46: Biomarkers for IO efficacy: TMB? CPS scoring? Others?
53:04: Role of gut microbiome?
57:21: IO in lymph node only metastases?
54:46: Treatment sequencing with IO?

Manju George 0:00
Hello everyone. I’m Dr Manju George. I’m the Scientific Director at PALTOWN Development Foundation, the nonprofit that supports COLONTOWN. Today we have with us Dr. Marwan Fakih. I’m sure that a lot of you already know him. He’s a professor of medical oncology and therapeutics research, a Judy and Bernard Briskin Distinguished Director of Clinical Research, Associate Director for Clinical Sciences, Medical Director of the Briskin Center for Clinical Research, Section Head of GI Medical Oncology, the City of Hope Comprehensive Cancer Center. We’re really excited to have you with us to talk to us about immunotherapy for MSS colorectal cancer.

Dr. Marwan Fakih 0:41
Thank you, Dr. George, and thank you for the invitation. Like many other physicians, we’ve all heard of COLONTOWN, and I have many patients actually, who participate in this forum, so it’s a pleasure to be here.

Dr. Marwan Fakih 1:01
I’m a medical oncologist, I treat colorectal cancer, and been doing so for the last 21 years. I’m very excited to see the field move forward. I know that we have a lot more work to do. Whatever progress we’ve made is good, but definitely not sufficient. So for those patients who are on the call, we feel you, we hear you, and I’m very hopeful that we will make more progress. So I’ve been asked today to talk about immunotherapy in microsatellite stable colorectal cancer. And this is an area that I certainly have a lot of interest in and I’ve seen some definite progress but I think it’s important that when we look at an area of research, to recognize where it’s working and also recognize where it’s not working. Defining a treatment is good, but it has to be the right treatment for the right patient. These treatments are not without side effects, and I think we have a lot more to learn, but I’m personally an advocate, and I think there are definitely patients who respond very well to immunotherapy with microsatellite stable colon cancer. I am personally treating many of those, and many of those have been on treatment for more than two years, but I’m also cognizant to the fact that not everybody responds. So when we start looking at immunotherapy, we have to ask ourselves, “what immunotherapy, and for whom”, and then try to understand how we can make it better. We all know that immunotherapy in colorectal cancer is approved for patients with microsatellite instability.

Dr. Marwan Fakih 3:09
What is micro satellite instability? I know that many of you have done a lot of your own research, are following the field of colorectal cancer very well, but, in a simplistic way, microsatellite instability – it means that there are errors in DNA within the tumor, and that the tumor cannot repair DNA damage, and that lack of ability to repair DNA damage is actually related to an error or a problem in the repair engine. And the repair engine here is what we call mismatch repair proteins, which simply are proteins that correct mismatches in the DNA. There’s two main reasons for mismatch repair protein loss. One is what we call Lynch syndrome, where one inherits a defective gene that is responsible for translation into one of those proteins: MLH1, MSH2, MSH6 and PMS2 are the four genes that we look for. And the other reason for mismatch repair deficiency or MSI-High, is silencing of those genes, which is more common in the elderly population, especially females, right sided colon cancer. And that’s really not a hereditary condition, but rather sporadic colon cancer, meaning colon cancer that we get without a hereditary predisposition. But both categories of patients who have this condition have the same issue, which is that they can’t repair the DNA damage, and therefore there is stacking of abnormal mutations in the genome of the tumor, which leads to a lot of abnormal proteins in the tumor per se, and now you suddenly have a tumor that has proteins that the body hasn’t seen before, and the body is able to recognize that tumor as, “Hey, you don’t belong here. You have proteins that are not part of my own normal makeup of protein and therefore I am going to unleash my immune system to attack this tumor”. And that’s why patients with mismatch repair abnormalities do a lot better when they have resected colon cancer than patients without mismatch repair abnormality.

Dr. Marwan Fakih 5:43
So if you look at patients with early stage disease, stage II and stage III who have MSI-High, they rarely relapse, and they have a better overall survival than patients who do not have MSI-High. And the main reason for that is that you have the immune system in the patients with MSI-High tumors, preventing metastases from happening, attacking the tumor before it develops micro metastatic disease, and therefore it gets a better overall survival. Indeed, if we look at the tumors from patients with mismatch repair deficient colon cancer, or otherwise known as microsatellite unstable or MSI-High – all is the same. You can see that these tumors have a lot of lymphocytes. These are CD8 positive cells. These brown dots are the lymphocytes at the tumor margin so it’s kind of preventing the tumor from expanding or attacking it where it is expanding. And so there are lots of what we call tumor infiltrating lymphocytes in the tumor, and the tumor is reacting back by trying to suppress these lymphocytes from killing it, and produces PD-L1. You can see the PD-L1 localizing at the sites of the CD8, and this PD-L1 is suppressing these lymphocytes. That’s simply why immunotherapy works so well, because when you give KEYTRUDA, you’re basically blocking PD-L1 from suppressing CD8s. Now these CD8s are happy, and they’re attacking the tumor and killing the cancer. And so either by using PD-L1 inhibitors, such as Atezolizumab or Nivolumab, or by using PD1 inhibitors where PD-L1 binds to, you can basically invigorate the immune response and stimulate these CD8 cells to attack the cancer.

Dr. Marwan Fakih 7:45
So why does immunotherapy work for MSI-High and why doesn’t it work for MSS very well? It is because you don’t have lymphocytes infiltrating the tumor in patients with mismatch repair proficient colorectal cancer, MSS patients. There’s not enough CD8s, and there’s not enough CD8s because the tumor is not hypermutated. The tumor doesn’t have a lot of antigens. Why it doesn’t have a lot of neoantigens or a lot of abnormal proteins, is because you don’t have that mismatch repair problem. So we’re looking at two different populations, and you have to think about these checkpoint inhibitors as unleashing an existing immune response, and that’s why they work in MSI-High, and why they don’t work in MSS is that there’s no immune response to unleash of significance in these tumors. But that’s the simple explanation as to the difference between MSI-High and MSS as far as to why we’re seeing differences in responses. Now, this is another way to look at the checkpoint inhibitors and differences between MSS and MSI-High. MSS is the blue and MSI-High is red, and you can see that CTLA-4 is higher in MSI-High tumors, PD-L1 is higher, LAG-3 is higher. All of these are checkpoint inhibitors. And you can see that in all compartments, especially in the invasive front of the tumor, the margin of the tumor. So there are inherent differences between these two tumors, MSI-High and MSS and that’s why in MSI- High tumors, we use pembrolizumab up front in the first line setting because it works even better than chemo, as we have seen from a very large study that compared patients with stage IV colon cancer who have MSI-High. Half of them received chemotherapy, and half of them received KEYTRUDA (pembrolizumab). And you can see that with KEYTRUDA, these patients who are without progression at three years, pretty much these are the cured patients. These patients rarely ever relapse afterwards. And I would say a lot of these patients may have something on their CT, but it could be just that tumor fibrosed, and you can’t tell that it’s gone, because it leaves a mark. We have many patients now who are MSI-High who are absolutely cured with immunotherapy for three years and never relapse. And so definitely a big difference in outcome, and we don’t want to miss those patients because they respond beautifully to immunotherapy.

Dr. Marwan Fakih 10:22
It’s not that KEYTRUDA has not been tested in MSS patients, patients without microsatellite instability. This is a study that said, “I’m going to look at MSS patients, I’m going to look at colorectal cancer patients. I’m going to only enroll patients who have a high PD-L1”. And PD-L1 is a biomarker of response to KEYTRUDA. In lung cancer it indicates that you have an immunosuppressive effect of the tumor against the lymphocytes, and the higher the PD-L1 is, the more likely the response in certain tumor types, such as non-small cell lung cancer. So in this colorectal cancer study, they screened 138 patients, and out of those, 138 patients, only 33 patients were PD-L1 positive. 10 had other exclusion criteria. They ended up treating 23 patients and only one patient had a response. The definition of response is shrinkage by more than half, by the way. When we use these terms, stable disease means either slight increase or slight decrease, but a partial response means major decrease, more than 50% of the tumor disappearing. As you can see, only one patient did very well on this study, and everybody else progressed, although for some it took almost about eight months before progression. But the only patient who had a good shrinkage or partial response actually was MSI-High, and all the MSS patients here did not have an objective response. So even when you’re enriching for PD-L1 positivity in MSS colorectal cancer patients it is not likely that a drug like KEYTRUDA or a drug like OPDIVO on its own is going to make a difference. We’ve been involved in this study as well.

Dr. Marwan Fakih 12:20
This study was published a while ago, looking at atezolizumab, which is a PD-L1 inhibitor, and patients who have gone through a couple of lines of therapy, first line and second line. In this study the comparison arm was Regorafenib, or STIVARGA, and 1/3 of the patients got Atezolizumab alone, so a PD-L1 inhibitor alone. 1/3 got cobimetinib plus atezolizumab. Cobimetinib is a MEK inhibitor, and at that point it was thought that that makes the immunotherapy work better based on a small phase 2 trial. But the bottom line is, in these patients who received atezolizumab alone, or atezolizumab plus a MEK inhibitor, there wasn’t really much of a difference compared to STIVARGA alone. So again, this large trial of almost 250+ patients failed to show that we gain much by using immunotherapy in patients with colorectal cancer, especially in microsatellite stable colon cancer. The majority of these patients in the study – I think, were 97% or so – were microsatellite stable. On the other hand, there was a glimmer of hope from a trial done in Canada called the CO.26 trial. And in this study, they used a CTLA-4 inhibitor, so another checkpoint inhibitor, another immunotherapy that takes off the brakes from the lymphocytes against the cancer, along with the PD-L1 inhibitor. So a KEYTRUDA-like drug called durvalumab, and that combination was compared to no treatment at all and even though there were no major shrinkages and there was no difference in the time for progression, there was an effect on the overall survival. The red line is the patients who got the double immunotherapy. The blue line is patients treated with best supportive care, and it prolonged survival by 30% in these patients, but it wasn’t really a big difference in terms of duration of how many months of addition, but it did add some, suggesting that even in this population of microsatellite stable colon cancer, there may be something to immunotherapy, but the signal is not very, very strong, and maybe adding CTLA-4 does make a difference as well as most of the studies so far have not looked at the combination of PD1, CTLA-4.

Dr. Marwan Fakih 14:56
Our group/myself had started looking at liver metastases and impact on response to immunotherapy, because we had many patients who would go on clinical trials receiving PD1 or PD-L1 targeting, who had MSS. What we would note is that some patients with lung metastases were having some shrinkage or prolonged stabilization, but everybody who has liver metastases, they tend to not do well at all on these studies. And I’ll show you some of the data that we generated, but some of the data that we published about four years ago after the REGONIVO data came from Japan also was substantiated by laboratory models. In this particular model, they treated mice by injecting colon cancer cell lines in their flank, and then they gave them immunotherapy with a PD-L1 inhibitor. And sure enough, the tumor in the flank shrunk. Now they got the same mice, the same tumor, and now they injected the tumor in the flank and the tumor in the liver, and let the tumor grow in the liver. And not only did the tumor in the liver not respond to PD-L1 therapy, but also the tumor in the flank of the mice did not respond to immunotherapy anymore, suggesting that when the colon cancer metastasizes to the liver, that that not only affects the response in the liver, but it may have a negative abscopal effect, a negative effect outside the liver on the response to immunotherapy. And there are many theories as to why that may be the case. Frankly, those theories come from mice models. They may not necessarily apply to humans fully. But one of the theories is that the tumors in the liver chew up the immune cells that are involved in attacking the cancer cells and therefore has a systemic impact on the overall response to immunotherapy.

Dr. Marwan Fakih 17:10
We looked at 95 patients who had microsatellite stable colon cancer, and those patients were treated with PD1 or PD-L1 therapy, and reported that data and in JAMA Network. What we did differently is we categorized patients according to their performance statuses. Are they: very weak/strong?; Do they have limitations in their physical activity? Is there any evidence of spread to the peritoneum? Any evidence of spread to the liver?; Any evidence of spread to the lung, lymph nodes, bone, brain? And then we also looked at tumor mutation burden in these tumors. And we looked at RAS mutation, BRAF mutation, APC and TP53. The thing that stood out the strongest here is that the liver was the biggest biomarker of resistance to immunotherapy. In this study, about 50-some patients with liver metastases were treated, and none of them had any major shrinkage. On the other hand, in the patients who did not have liver metastases, about 20% of those patients had major shrinkage, and you can see that the likelihood the impact on progression if patients had liver metastases – presence of liver mets, has a seven-fold increased risk of progression compared to non-liver metastases. We did see some other signs that are not very clear. The sidedness has a small impact on on on progression. The left did a little bit better than the right, so a higher chance of progression if they have right-sided tumor versus left-sided tumor. RAS mutation, there was slightly higher progression, like the progression of RAS mutation versus non-RAS mutation. I have to say, in other data sets that we have looked at we’re not as convinced on RAS, and that’s a story that needs to be unfolded some more. But APC mutation did not have a substantial impact. A lot of people report APC as a marker of resistance. – No. – You can have APC mutation with colon cancer, MSS, and still respond to therapy. So liver did come out as the biggest problem here, as far as response. And meanwhile, there had been some data suggesting that drugs that target what we call the vascular endothelial growth factor pathway, which is a pathway important in blood vessel formation that those inhibitors may substantiate or improve the response to immunotherapy. Particularly the drug STIVARGA, which is approved for refractory colon cancer, had been associated with decrease in macrophages or tumor-associated macrophages, especially the M2 phenotype, which associates with a poor outcome and switching it to the M1 phenotype, which are anti-cancer, that that may occur with STIVARGA, and that STIVARGA may also normalize the blood vessels, decrease the T-regs, the regulatory T-cells as well, which may also be important in reducing the immune resistance within the tumor microenvironment within the liver.

Dr. Marwan Fakih 20:43
I’m sure a lot of the folks on this forum had as much enthusiasm as I had about three years ago or more maybe, when this data from a Japanese group was reported at ASCO, I think it was three years plus now, looking at a small number of colon cancer patients, 24 patients, who had microsatellite stable colon cancer, I think, except one patient if I recollect right, and those patients were treated with STIVARGA (Regorafenib) plus Nivolumab (OPDIVO) and therefore the acronym “Rego” for Regorafenib; “Nivo” for Nivolumab. And the excitement was that these patients had progressed on standard of care, and when they were treated with this combination, almost half of those patients had not progressed at 7.9 months, or 8 months if we want to round it, and that approximately 1/3 of those patients had major response, – objective response, we call it. A majority had good disease control between stable disease and major shrinkage. And this data prompted many of us to consider offering this treatment on a compassionate basis, or rather than compassionate, the right term is “off-label”, even though this was not approved to offer this to patients with colorectal cancer. And to my surprise, when we were treating patients with this and we looked at our data in about 18 patients or so, initially we saw that 13 patients with liver mets, none of them responded, and that in the five patients without liver mets, maybe four of them had some minor shrinkages, not a major shrinkage, but were able to continue on treatment for a while and we reported that data.

Dr. Marwan Fakih 22:43
Before, we looked at the 95 patients. But this particular study from Japan has really triggered a plethora of trials looking at the same classes of drugs together, so a PD1 or PD-L1, plus what we call a “tyrosine kinase inhibitor”: pills that inhibit different enzymes and different proteins, including proteins that are important in the blood vessel activation process, what we call “vascular endothelial growth factor receptor inhibitors”. One such study is a study done in China. This is a tyrosine kinase inhibitor that is very similar to regorafenib, and this is a PD1 inhibitor, and 28 patients with microsatellite stability. Response rate was only 7%, but a lot of patients had stabilization and a good disease control so that’s not meaningless when you control the cancer in your patients more than six months. And so there are some signals, but not as strong as what’s been shown in the Japanese trial. This is a study that looked at STIVARGA plus pembrolizumab that was reported this meeting by a colleague of mine. Very discouraging is the fact that none of 73 patients had major shrinkages here. But when looking at the 16 patients who didn’t have any liver metastases, at least half of those patients were having ongoing benefit beyond the four months mark, while most of the patients had progressed at two months with liver metastases. That shows what we call the “progression-free survival curve”, the time to patients progressing. So those are the 16 patients in blue. And you can see that there are some patients who have more prolonged benefit, even at the one year, but that’s a small number of patients. Only two of the 16 probably were still deriving a benefit. So who are these two, and why and how can we identify them, is the big question. Who are those getting benefit beyond six months, right? Because, yes, liver metastases is a marker of resistance, but it doesn’t mean that everybody without liver metastases is going to benefit. Some will benefit more than others, and it does appear that those without liver metastases have a better survival. There are other studies we can go over and over, again. That’s another study of STIVARGA, plus another PD1 inhibitor and metastatic cancer. Again, microsatellite stable, and you can see, again, a big difference in response rates: patients without liver metastases – major shrinkage, more than 50% shrinkage, and 30% of patients stable disease, 20% here, major shrinkage with liver mets is only in 8% of patients. So again, showing a difference in time to progression in non-liver is better than liver. And this is a study presented… this meeting looking at bevacizumab, which is again a vascular endothelial growth factor inhibitor, plus KEYTRUDA (pembrolizumab), and they added what we call a MEK inhibitor, binimetinib to it. And here you see that about 1/3 of the patients had some form of shrinkage. And the patients who had major, major shrinkage – more than 50% shrinkage, are about 13% of patients. But a fair number of patients between mild increase and mild decrease. This is what we call stable disease. (That’s the yellow.) Again suggesting that there’s a signal here, but not too strong. And how can we identify those folks who benefit the most from this?

Dr. Marwan Fakih 26:38
That’s another study presented at this meeting, a couple of days ago, with a PD1 inhibitor, plus, again, an angiogenesis inhibitor that is novel because it blocks two angiogenesis pathways, angiotensin 2 and VEGF. There’s more shrinkages than growth here and I think the exciting thing is, definitely there are patients who continue to benefit beyond the eight months mark. But the bottom line is, all these studies are not telling us: who are the patients with liver mets and who are the patients without liver mets? They’re not really reporting yet the characteristics of those patients. I do believe that it’s less likely that patients who are having great response here are liver mets patients, and it’s important for you to know that you’re going to have a lot of variations and responses and benefits dependent on what type of patients are going on the study. If it’s a patient who has only lung mets, that’s a patient who probably is going to be more likely to respond. But a study that uses the same regimen and enrolls 90% of the patients with liver metastases, the results of that study are going to be dismal. And so it is very hard to extrapolate from these 20, 30 patient trials into: “What is a better regimen for a patient?”. You may hear a little bit more in your forum about this study. So cabozantinib is a compound by a drug company called Exelixis Inc., and which is a drug that is approved for kidney cancer and liver cancer. They have a couple of reports this meeting on cabozantinib, plus a PD-L1 inhibitor. This is durvalumab, which is the PD-L1 inhibitor and plus cabozantinib. This is called the CAMILLA trial, and they looked at colorectal cancer here, 29 patients is reported as efficacy. And then they say, well, eight patients out of 29 had major shrinkage, 27.6% but in six out of the eight that response was sustainable, meaning on the next CT, the were still benefiting versus two out of the eight, the next CT that were progressing and you can see the median progression-free survival is 3.8, they don’t report on the characteristic by liver or non liver, but they do show that there is slightly better outcome for the RAS wild-type versus the RAS mutant. Again, something that we have seen on our multivariate analysis from a year ago. So the question is, should this be evaluated further in RAS wild-type? The problem is, they didn’t do the analysis here based on where the tumor spread. Could it be that the patients without RAS mutation were more more enriched in patients without liver mets here, and that’s why you’re seeing that signal? We don’t know. The other thing about this study is that they actually enrolled 36 patients, and seven patients actually didn’t reach the first CT scan, so they did not include them in the analysis. So the reality is that this study shows similar outcome as all the other studies in that the final confirmed responses, if we include the full sample of 36 patients, is 16.6%. So again, there are patients who benefit. This is very exciting. If you follow the 25 months mark, there are some patients at two years who are still benefiting. So who are they? And how do we identify them and offer them these strategies, and how do we make sure they don’t get diluted, and in the patient population sample who are not benefiting? And more importantly, how can we exclude patients who don’t benefit so that they can find other strategies to look into. Interestingly, this meeting from two days ago, looked at cabozantinib plus atezolizumab. Atezolizumab is not much different than durvalumab that it’s a PD-L1 inhibitor. And here again, they looked at 31 patients. The difference here is that the objective response rate is actually quite a bit lower than the previously presented study here. Only 3 out of 31 patients had major shrinkage. But then they report that most of these 3 were in the patients without RAS mutation. So again, something that needs to be explored further. Does RAS wild-type tumor, no RAS mutation, enrich for better likelihood of response? Could it be that patients without liver metastases and without RAS mutation could be the best patient population to look into – I think the challenge is, all of these are small studies, and you can’t do this kind of deep analysis on a small sample size, and I wish we could pull all these efforts from different investigators to answer that question, and it would require that all the sponsors agree to do so, which may not happen.

Dr. Marwan Fakih 32:03
Many of you have heard about the LEAP trial. This is KEYTRUDA plus lenvatinib, again, same concept, the tyrosine kinase inhibitor that at least partly targets VEGFR plus KEYTRUDA. And this study reported a 22% major shrinkage, and at six months, almost 1/3 of the patients had not progressed. This regimen actually moved on to a randomized phase 3 trial that is ongoing, so we will know soon. The good thing about that study is that they are stratifying by presence or absence of liver metastases so we’ll have a better idea as to the outcome in patients without liver mets. On the phase 2 study, which I am showing you here, the company did not report the outcome by liver and non-liver metastases. So finally, this is a study we reported last year on regorafenib, Nivolumab in microsatellite stable colorectal cancer, we enrolled 70 patients, 23 without liver metastases. You can see the response rate here. The major shrinkage is about one in five patients, but the stable disease is another 1/3 of the patients. Half of those patients still progressed by three and a half months. The liver metastases did not respond. What we reported at this meeting is that we know partly why liver meds don’t respond. If we look at biopsies from liver metastases versus no liver metastases, the liver metastases have less CD8 cells. These are lymphocytes that attack the tumor, and when we enrich further for granzyme B positivity, which is the substance that lymphocytes release when activated against the cancer. Again, we don’t see much of that in the liver. We see more of it in patients without liver mets and tumor biopsies that are not liver. The immune system is more robust in these non-liver metastases, which results in a higher regulatory T-cells in those tumors. You don’t see as much in the liver, and you see also more macrophages outside the liver. So basically, there’s more of an immune activation in tumors that spread outside the liver than in the liver. I don’t think it’s the same between lung, and peritoneum, and bone, and abdominal wall, and lymph node. I think there probably are differences. I think at the end of the day, the question is, which sites of disease may benefit the most: is there a biomarker of site of metastases, number of metastases, size of metastases, molecular biomarker? What type of mutations the tumor has, is there a special formula that we need to know about, that we need to come up with? I’m sure we’re not going to come up with the perfect one, but there are a lot of efforts being made to try to identify at least some form of biomarker that helps us further. So this is the same study we conducted. Now, you can see that patients without liver metastases: this is a good thing. You can see you have 1-2-3-4 patients out of 23 who had not progressed at the 40 week mark. And frankly, we’ve got two patients who’ve hit the two year mark without progression in our institute on this study. And so that’s not something you will achieve with STIVARGA alone. How much of this is from OPDIVO versus OPDIVO plus STIVARGA remains to be seen, but there’s probably some synergy between these two, but I don’t think it’s sufficient for the majority of patients versus liver- the majority had progressed by the 24 week mark. Very few patients continue beyond, and most of those eventually did progress. And you see the tumors. None of these tumors had sustained shrinkage below the 30% decline in tumor in the target lesions versus the non-liver mets, you have quite a few blue squares that go in the “PR” partial response category. So this is work we’ve done in our institute. When we stain the tumors of liver and we look at what we call the core of the tumor, you can see that the core of the tumor has very few lymphocytes that get into it versus lung, a lot of lymphocytes get into it. (That’s the blue here, is the lymphocytes) and so part of the problem with liver metastases is that the immune cells don’t get into it to attack and that’s been a challenge, frankly. I don’t think anybody has the definitive answer today, although a lot of efforts are being made to answer that or to overcome it, whether it’s viruses or other type of drugs. Finally, I want to say that the CTLA-4 question is not really done yet. This is a study that looked at a novel CTLA-4 inhibitor, plus a PD1 inhibitor in patients with colorectal cancer. Here at the upper right corner they enroll 20 patients. This is without regorafinib, this is just the CTLA-4, PD1, no TKI, no tyrosine kinase inhibitor, just the checkpoint inhibitors. And four out of the 20 patients here had major responses. And you can see a lot of these, some of these are quite durable. And again, they did not report in the poster if these were non-liver mets or not but I think that means something to me. Probably we do need a CTLA-4 inhibitor. And the question is, do we need the three drugs together or not? And so this is actually what we had proposed to SWOG. First of all, we’re pretty certain liver mets don’t respond to regoraphenib-nivolumab, so we think those patients should not be treated with this combination. And also, we have some data that peritoneal metastases are little bit more resistant and may not benefit that much from that combination. And so we’ve proposed a study looking at STIVARGA plus OPDIVO, REGONIVO compared with regorafenib, ipilimumab and nivolumab so, CTLA-4, PD1 plus regorafenib, we have already completed a study with REGONIVO IPI in our center. That data has not been reported yet, so I can’t go over it today but we think there’s enough to compare these two to see if there is a winner, and perhaps that can move forward to be compared to a standard of care in the future. I’m hoping that this will move forward. It’s too early yet, but that’s one way of approaching colorectal cancer with a microsatellite stability to recognize the patients who are more likely to benefit from a strategy and then explore it further, and then narrow down more the biomarkers so that you can identify even better who the potential super responders are. So what I summarize today is that microsatellite stable colorectal cancer is not all one disease, and especially with immunotherapy, it’s different than chemo. The site of metastases matters. And liver metastases are different than lung. They have biological differences in lymphocytic infiltration, antigen presenting cells, B cells, etc, that we are reporting on, and that the lung metastases have more active immune microenvironment that may contribute to the response to immunotherapy.

Dr. Marwan Fakih 40:17
So where do we go from here? I think there are a lot of studies across the nation and across the globe trying to look beyond checkpoint inhibitors, beyond STIVARGA and tyrosine kinase inhibitors. There’s a lot of studies looking at what we call bispecific antibodies, which typically target tumor-specific antigen and CD3. There are cellular therapeutics going on, including tumor infiltrating lymphocyte infusions, but you have to harvest the tumor here, grow the lymphocytes infiltrating the tumor. It’s a long process, and then grow these lymphocytes into the billions and then re-inject them in the patient and hope that they infiltrate the tumor and attack it. There’s some data that that is effective in non-small cell lung cancer and melanoma, and there are some efforts in colorectal cancer. There’s no data yet if that is effective or not, but that’s what those studies are doing. There are studies called neoTCR, where you basically take a biopsy, identify cancer specific antigens, and then clone receptors to those antigens, and then engineer the lymphocytes of that patient to express those receptors and then re-infuse those lymphocytes. There are CAR T in early development. CAR T in solids have been much harder than CAR T in liquid tumors, and because these engineered T-cells have more difficulty infiltrating within the solid tumor. But certainly it is an area of interest and should be evaluated. But where CAR T is going to be, we still don’t know. There are some studies looking at combinations of neoantigens and vaccines plus checkpoint inhibitors. Certainly there are other studies that have integrated immuno-checkpoint inhibitors, like nivo plus FOLFOX early on, and those studies should be maturing soon. Whether one should also engage with CTLA-4, PD1 plus chemo early on, is another question. But those are other directions. So I hope this is a little helpful, and I think we can open it up for discussion.

Manju George 42:48
Okay, thank you, Dr Fakih, that was awesome. I have one question, and then we will look at the chat and look through all the questions. So in the mouse model that you mentioned when they had the tumor also implanted in the liver, in addition to the flank tumor, the animal did not respond to immunotherapy. Did they do an experiment where they then remove the liver tumor and then try to see if the animal was again sensitive to –

Dr. Marwan Fakih 43:10
–They did not. But we have clinical data that shows that with regonivo and others, that hepatectomy patients will respond. So there are data that our group/myself have generated that show that if you have a hepatectomy, and now the patient, six months later, has lung-only metastases, that those patients could respond, and some of them for a very long period of time. Whether it is as robust as patients with never liver metastases our data shows a little bit less robust, maybe, but some surprisingly, very protracted benefits. Once you don’t have active disease it’s a little bit different story. It’s important to note that all of these are associations that we are describing. So the question becomes, is an association, a cause-effect? Is it or not? Is it the biology of the cancer that leads to liver metastases that makes it more immune resistant? If that is the case, you wouldn’t expect that the surgery would fix that problem, right? Or is it also possible that the biology that is favorable enough that a patient can undergo liver surgery means that they are also a little bit more immune sensitive. It’s possible, but association is important enough in your patient selection, right? Even if you cannot prove a cause effect, if you have an association of lack of response, at least it helps you on how you define your patient population is to benefit from a specific strategy.

Manju George 44:43
Okay, thank you. So we will go through the questions. Annie has a question, “Can you comment on the KISIMA-01, combo approach with the vaccine, where Dr. Kopetz has indicated there has been response in liver mets?”.

Dr. Marwan Fakih 45:02
No, I can’t comment on that. I don’t have additional information.

Manju George 45:06
Okay, then other than liver mets and RAS status is tumor burden a factor determining efficacy of IO and MSS?

Dr. Marwan Fakih 45:17
Yes and no. If, for example, and I didn’t present that data, I think we reported the first case of Pol E mutation responding to immunotherapy. So about 0.5% of patients will have Pol E mutations, which is polymerase E, which is important. Those patients are MSS, but they have what we call an ultra mutated colorectal cancer. Their tumor mutation burden is more than 200. They respond as well as MSI-High, if not better. Those are one in 200 patients. You don’t want to miss them. You identify them by the super high TMB, and they definitely should get immunotherapy, even though there’s no indication for immunotherapy for those patients, yet (-official indication). Then you have what we call intermediate TMB. They’re not MSI high, but their tumor mutation burden is 14, 12, 16. I think some of these patients, may respond somewhat to immunotherapy. I don’t think they respond as well as the MSI high. They usually are more stable disease or less durable responses. There’s been case reports of such cases responding to pembrolizumab. It’s important to note that the keynote 158, that we reported that led to the approval of pembrolizumab in the TMB of more than 10. Actually, that study did not include colorectal cancer patients, so it’s hard to extrapolate as to the benefit, but even in that particular study, there was a correlation between the level of TMB and response, and even though it’s not in the paper. Merck, the sponsor of that trial, had reported that if you look at those patients who had a TMB of 10 to 15, the objective response rate, the major shrinkage rate, was less than 15%. The overall population was 29% but if you look at the 10 to 15, they didn’t do that well. And therefore immunotherapy in patients who have a TMB of more than 10, but less than 20 should not be first line and should not be second line, in my opinion, because the benefit is not clear, but they should not be excluded from from getting KEYTRUDA. In the MSS patients that we looked at in our center, we didn’t see a correlation between TMB in response to regonivo or other PD1 inhibitors. And we have many patients who had an objective response or durable, stable disease with a TMB of one and two. So those patients that you see that have the tail of the curve with ongoing benefits were not intermediate TMB, you know. So, the bottom line, yes, there are patients with very low TMB that respond to immunotherapy, but not liver mets.

Manju George 48:06
The second part of the question is, is there any evidence that in low burden or low tumor burden settings radiation treatment previous or concomitant to IO could increase IO efficacy? Can it make the tumors more immunogenic?

Dr. Marwan Fakih 48:22
I personally, I doubt. I think the data has been extremely thin. We had done a study of Y90 followed by a PD1 and CTLA-4 inhibitor. Unfortunately, we had to close the study because we had nine patients, and none of them responded, whether in the liver or outside the liver, to the immunotherapy. I think there’s been some reports about SBRT plus immunotherapy. Those data have been extremely mixed, and the benefit was slim, and it’s not really clear if it’s attributed to the SBRT or not, so I don’t think so. I am aware that the recent study, and I think everybody should take that with a grain of salt, that the REGONIVO that was reported at this GI ASCO has said the patients with prior radiation did better, but there’s two reasons to give prior radiation. One is rectal cancer, which tends to have more lung mets. So when you say prior radiation is… they had chemo radiation for their primary rectal cancer before surgery, and then they develop probably lung mets. So it’s enriching lung mets. The second is SBRT, right? And who gets SBRT? -The patients who don’t have diffuse disease, the patients who have only few metastases. And who are the patients who have only few metastases? -Those who have a robust immune response against their cancer. So here, the prior radiation therapy is likely enriching a patient population that would have responded to immunotherapy whether they got radiation or not, by selecting patients who have a better immunoscore. So a lot more to be learned. But I think the radiation concept had been tested for a very long time now, and the data should be still evaluated in a research setting, but I don’t think clinically there’s any reason to believe that we should be radiating to induce a response at this point. I think we need to evaluate it further.

Manju George 50:29
Okay, so the next part of the question, I think it’s very important to address that, how should, when patients are considering immunotherapy – you just mentioned TMB. What are the other ways to find the PD1, PD-L1, CPS scoring or TPS scoring? What do you comment about that?

Dr. Marwan Fakih 50:45
I think it’s important to note that not all tumors are the same, and I think we have to really look at the data within colon cancer. So far, the PD1 story has not panned out that much in colorectal cancer and we’ve had patients with a CPS score of 20, 30 with liver mets that we got excited about with them on immunotherapy, and we don’t see a response. And so I don’t think that we have a biomarker today of a response to immunotherapy in somebody with a low TMB, with the exception of saying that liver is a biomarker of high level of resistance, and frankly, everything else is still under investigation. I wish I would say otherwise, but there’s no definitive answer yet, and there’s a lot of conflicting data from different sets of studies.

Manju George 50:45
Okay, thank you. So maybe some kind of composite score where they look at the location of the mets, maybe CPS, maybe TMB, or all of that together?

Dr. Marwan Fakih 51:50
Yeah. I mean, eventually that would be the hope, right? It’s coming up with a formula that takes into consideration the host, the tumor, and the clinical presentation. So a molecular score, right? Patient score, it could be ECOG as well. We’ve seen ECOG 2’s don’t do as well with immunotherapy than ECOG zero likely, and site of metastatic disease. And also from my personal experience, somebody who has 1000 lung mets what we call “miliary disease” in the lungs, we don’t see them respond to immunotherapy, and partly because probably the tumor has escaped/there’s no immune system to prevent it from exploding in a diffuse process. Versus somebody with well defined 15 spots in the liver may respond to immunotherapy. So you cannot come up with such a score unless you have prospectively collected data sets that are very large, treated in a homogeneous manner, and the data is collected prospectively on all these variables. To my knowledge, that data set is not there.

Manju George 53:01
Okay, thank you. So another question is about the microbiome. Do you have any thoughts on whether the diet, gut microbiome – Does it have any effect in MSS CRC?

Speaker 1 53:13
I don’t have any data myself. I think the microbiome story is still evolving on some of the data with fecal transplantation had been intriguing in couple cases with melanoma. I think the disheartening thing is that that data came out three, four years ago and you would expect that somebody could have validated it already. There’s been so many trials that have included capsules that have different bacteria, etc, to try to answer that question. And I hope it’s true. I think it needs to be validated in probably non-small cell lung cancer and melanoma first. But today I don’t have any special diet that I prescribe to my patients. I’m not against them trying. I’m very open about that, but the evidence is not there.

Manju George 54:12
Okay, there’s one question about efficacy of IO and MSS patients with isolated lymph node mets, the rationale being that lymph nodes have a high concentration of the immune cells.

Dr. Marwan Fakih 54:21
They do very well. In our experience, lymph-only metastasis, not all of them respond. But I think if you ask me today, based on my observation and what we have seen, the two sites that benefit the most are lung and lymph node.

Speaker 1 54:39
Okay. And then there was this other question about sequencing. Dr. Barzi had reported that subsequent treatment with TAS-102, the responses were higher after people were on radiation. What do you think about it?

Dr. Marwan Fakih 54:54
I think one has to be very careful and anecdotal evidence from subgroup analysis, from studies. It seems to me that if you give immunotherapy, you change the course of the disease after immunotherapy. It’s not necessarily making TAS-102 work better. You’ve seen the data with the Canadian trial. There was no difference in progression, but the curve separated for overall survival. So even when patients do progress, we do see that not all the tumors necessarily progress after IO and so you’re dealing with a little bit different biology after immunotherapy. It doesn’t mean that because you gave immunotherapy, it’s going to make the chemotherapy… – It could be that those patients, even without TAS-102, may have had a more indolent course. So those are only hypothesis-generating questions and need to be validated. Of course, I would rather use a regimen of IO that has a 30% chance of keeping 1/3 of patients without progression at eight months than using Lonsurf. And hey, if Lonsurf works better afterwards, that’s great, but we need more work on biomarkers.

Manju George 56:07
Okay, so basically, what you’re saying is that – there is this talk in COLONTOWN too – that if you get immunotherapy, and then people who have gone back on chemo, they are responding better. And what you’re saying is that that might be because the immunotherapy affected the progression without actually responding to chemo, right?

Dr. Marwan Fakih 56:25
The disease may become a little bit more indolent in some patients. There are a lot of patients who, prior to IO, when they go and study you have 20, 30, tumors progressing. They have stable disease, and then only five tumors are growing, and the other 15 are still regressed, but they meet the guidelines of progressive disease, and they come off study and and now their immune system has been conditioned to attack those 15 tumors, but the other five have escape mechanisms. And even when they have escape mechanisms, they may not be growing at the same pace that they did before going on IO. It doesn’t mean that every patient that gets IO will have that benefit. That’s very important to note. You know, there’s even some thoughts of hyperprogressors with IO, where the disease is progressing more quickly. I haven’t seen liver metastases change course that much after IO for example.

Manju George 57:28
Looks like there are no more questions. Thank you, Dr Fakih for that very interesting and informative talk. Thank you all for attending. The video of the talk will be available soon at the Lecture Hall in COLONTOWN University.

DocTalk
2022
Dr. Fakih
Immunotherapy
Liver
MSS
Stage IV
Trials

Dr. Marwan Fakih of the City of Hope Cancer Center takes a deep look at immunotherapy for MSS CRC in this Doc Talk, recorded in January 2022 with PALTOWN Scientific Director Dr. Manju George. Dr. Fakih discusses a number of recent clinical trials in this video conversation.

Table of contents:

1:38: Immunotherapy (IO) in MSS CRC—Broad overview: where are we currently with this?
3:02: What is MSI-H?
4:02: What is MMR?
6:35: dMMR Vs pMMR PD-L1 expression, how IO works
7:46: Why does IO not work in MSS CRC
9:25: KEYNOTE 177 results
10:31: Keytruda/Pembro or single agent IO in MSS CRC
12:17: IMblaze 370 trial Atezo+Cobi vs Atezo vs Stivarga in MSS CRC
13:35: CO.26 Double IO (CTLA4i+PD1i) vs best supportive care in MSS CRC
14:55: Liver mets & effect on IO-mice studies, what might be happening?
17:23: IO in mCRC patients: liver mets, a biomarker for lack of efficacy?
19:39: Immune modulatory effects of Stivarga
20:55: REGONIVO CRC-Japanese trial & similar combinations, results from GI22
28:10: CAMILLA CRC (Cabo+Durva) trial results
32:00: LEAP-005 trial (Lenva-pembro)
33:00: REGONIVO US study: why liver mets don’t seem to respond
38:10: New approaches for IO in CRC with liver mets
39:35: Summary
40:23: Other directions
42:50: Q & A Association of liver resection in the response to IO
45:00: Role of TMB in response to IO
48:22: Radiation therapy+IO in MSS CRC
50:46: Biomarkers for IO efficacy: TMB? CPS scoring? Others?
53:04: Role of gut microbiome?
57:21: IO in lymph node only metastases?
54:46: Treatment sequencing with IO?

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HERKULES-3 trial for BRAF and RAS

HERKULES-3 trial for BRAF and RAS

DocTalk
2022
Dr. Lee
BRAF
KRAS
MSS
Stage IV
Trials

Dr. Michael Lee of MD Anderson discusses the HERKULES-3 clinical trial for BRAF and RAS-mutated GI cancers. Recorded in December, 2021.

Manju George  0:00 
Hi, everyone. I’m Dr. Manju George, the Scientific Director of Paltown. Today we have with us Dr. Michael Lee. He’s an assistant professor at MD Anderson. And he finished his MD from Duke University. And he’s board certified in internal medicine, hematology and oncology. Dr. Lee, I’m really excited and happy to have you here with us. Please take it away.

Dr. Michael Lee  0:24 
Thank you very much. Can I just confirm you’re seeing my slides and slide screen view?

Manju George  0:30 
Yes, I think yeah, yes.

Dr. Michael Lee  0:32 
There we go. All right. So I’m very pleased to be here. Thank you so much for inviting me to talk about this exciting new study, that we and many other centers are getting underway, looking at novel targeted therapy combinations, particularly focused on this new class of drugs called ERK inhibitors, in certain molecularly defined subclasses of colorectal cancer. This is the HERKULES 3 study. So just as a way of background, cancer cells in general, or cells in general, are very finely tuned regarding when they proliferate and multiply. Typically, when a cell multiplies, it only does so in response to when the environment is right. And usually in that situation, there will be molecules called growth factors released around the cells and these bind to receptors on the surface of the cell. In particular, in colorectal cancer, something called the epidermal growth factor receptor, or EGFR is a very important growth factor. Now typically, when this binding occurs, this triggers kind of the cascade of proteins being activated into an active state, and kind of propagating the signal through one protein through another through another, until it eventually leads to a number of cellular changes that actually cause the cell to multiply, you can think of these intermediate steps as a series of molecular switches. In particular, this MAP kinase pathway, so to speak, which is downstream of this EGFR receptor is a very important kind of modulator of cell multiplication. Normally, this process is very tightly regulated, as I said, in a normal cell. However, in the process of colorectal cancers going from a normal colon cell to a cancer cell, typically, these cells acquire abnormal activating mutations in one of these molecular switches. And we know that a significant proportions of patients with colorectal cancer actually have activating mutations, in one of these key genes, that eventually leads to this kind of pro growth switch being turned on all the time, inappropriately.

Dr. Michael Lee  2:41 
So we know about 45 to 50% of patients have a mutation in a gene called KRAS or NRAS, which causes constant activation of these growth pathways. Another 5 to 10% of patients have activating mutation in a gene called BRAF, with the particular mutation in BRAF called the V600E mutation most common among the BRAF mutations. These are very clearly driver mutations driving the biology of these cancers. And while we’re starting to develop new therapies, kind of targeting these very clear potential vulnerabilities of these cells, we need more novel, more effective therapies for these ranges of mutations.Clearly, the cells are being driven by abnormal signaling through these kinds of constantly turned on genes. And if we can find more effective ways to switch off these genes, or kind of block the downstream signaling that is a consequence.and this is a potentially very powerful strategy. ERK is one of the key downstream kind of effectors –downstream of activated RAS or BRAF. ERK is one of the last kind of switches that then goes on to directly activate a number of these kind of transcription factors that cause the cell to go on to multiply, and so on and so forth. So it’s one of the last common nodes in this pathway that we could target. And kind of because it’s further downstream, there’s a lot of preclinical and laboratory data showing that targeting ERK maybe a particularly potent strategy, even more so than targeting some of these upstream components. And in fact while they’re not currently ERK inhibitors that are FDA approved, there are several novel ERK inhibitors that are being developed, and one that’s particularly exciting is being studied in the HERKULES 3 study. This is the ERAS-007 compound. This is an oral pill based treatment, that’s a selective inhibiting ERK and it’s been active in the laboratory. So without going into too many nitty gritties actually, shown here are on the left hand panel are a number of mouse models of KRAS or BRAF, mutated colorectal, or pancreatic, or other cancers. And you can see here the red line on the bottom actually shows the activity of the ERK inhibitor, which was previously called a different name. And you can see that kind of when you looked at it compared to other kinds of earlier ERK inhibitors, or other classes of drugs targeting upstream like at MEK or BRAF, that the ERK inhibitor, at least as a single agent for a limited period of time in these mouse models seem to have the most promising level of activity. On the right here, you can see specifically in a range of colorectal cancers, that the ERK inhibitor was active in the majority of the mouse models that were studied. And in particular, here, the shaded kind of  maroon or blue bar show KRAS or BRAF mutated mouse models where you can particularly see benefit.

Dr. Michael Lee  6:00 
Now, with all that being said as much as  we’ve studied single agent or inhibitors and the early phase studies looking at single agent drugs, we know that from long experience with kind of inhibitors of this pathway, that you have better activity for a longer duration of time, if you target in combinations of therapies. Without going into too much detail, generally in the past when we tried targeting this path of the single agent, for example, MEK inhibitors or BRAF inhibitors, there’s been a lot of kind of adaptation within the cancer cell, that kind of reactivates upstream signaling, and it can kind of bypass the level of drug inhibition. As a consequence, we’ve learned that we -and studies in the lab have also shown- that we have better outcomes, if you treat with combinations of therapies, we really think the best chance of having more activity that’s clinically significant for our patients, is using combinations of ERK inhibitors with other rationally targeted drugs. So one combination that’s being studied in the HERKULES-3  study in KRAS and NRAS mutated patients, which again, about 45 to 50%, of colorectal cancers, is combining this ERK inhibitor with a compound of drugs called the cyclin dependent kinase 4/6 inhibitor CDK4/6 . The reason this is rational is that one of the other key pathways that is activated when you have activation of the signaling pathway, it leads to activation of CDK 4/6 –which is very important for helping the cell multiply its DNA and ultimately divide. The cell cannot multiply and divide without actually going through the cell cycle process to replicate its DNA. So if you can block that process, the thought is that if you’re blocking it at 2 different levels, both kind of at the ERK inhibitor level plus at the cell cycle pathway level, that this would be more effective. Andactually, our laboratory has shown that impairing that kinase pathway in combination CDK 4/6 inhibitors was synergistic -was particularly effective- in a range of KRAS mutated models, both in cells in the laboratory and also in mouse models. And consequently that’s combining ERK inhibitors -which again, as we think would be a more potent strategy with the CDK 4/6 inhibitors- we’re hopeful will be even more likely to be effective. Palbociclib  is the drug that’s being studied in combination with the ERAS-007 compound. And this is a CDK 4/6 inhibitor that is actually currently standardly used in some other cancer types, like breast cancer,  is being studied in clinical trials in a number of other cancer types as well, typically in combination with other kind of targeted drugs. And so that’s one rational combination that we’re looking to study. In the BRAF mutated patients, this study will be looking to combine ERK inhibitors with other targeted therapies, targeting BRAF. In particular, as we’ve kind of learned in the last couple of years, the current standard of care for patients with BRAF mutated Colorectal cancer is to treat with a combination of drugs called encorafenib and it is a BRAF inhibitor directly impairing BRAF. And again, kind of talking about this multi level inhibition strategy, combining it with a drug targeting upstream at the EGFR level, called cetuximab. So the combination of encorafenib and cetuximab is currently FDA approved for BRAFV600E mutated colorectal cancer.

Dr. Michael Lee  9:40 
And this is based on the positive results of a large phase III study the Beacon CRC study, which did kind of represent an important advance in our management of these patients with BRAF mutated cancer. While this was absolutely an important step, we also know that there’s more improvement to go. We know from the Beacon CRC study that the response rate among patients was about 20%, which means only about one in five patients were having a significant shrinkage of their tumors, the remainder of the patients are having stable disease or even growth, despite this being our kind of active, a combination, targeted therapy approach. We know that the median duration of time that patients did not progress through the study was about 4 months, 4.3 months, and the median survival for the patients receiving this combination was 9.3 months. Now, this was actually a significant improvement compared to the prior standard treatment. But I think we all acknowledge that we want to improve on these numbers, there’s more we need to do for these patients. And that’s motivated kind of new strategies to look at how can we build on this ground to further improve outcomes here. There has been a range of laboratory studies that actually shows that another level of inhibition, hopefully more potent inhibition, would better allay the resistance that can develop when you’re treating with just the BRAF inhibitor plus the EGFR antibody. For example, we’ve seen that you can see emergence of small sub clones of mutated cells with other kinds of resistance mutations elsewhere in this pathway, which renders resistance to just the encorafenib and cetuximab . And as a consequence, there’s additional preclinical data showing that adding an ERK inhibitor, like ERAS-007, to the BRAF inhibitor and the EGFR antibody, may well be more effective in treating or preventing the onset of resistance. And that has motivated another arm of the study looking at encorafenib and cetuximab plus ERAS-007.

Dr. Michael Lee  11:44 
Now you may be asking, what do we know about the tolerability and side effects ERAS-007. So this is a drug that was previously studied in a single agent, prior clinical trial. So they looked at just the tolerability of ERAS-007 alone. I will note that in that single arm study, while this was a single drug given –not even a combination, there were some patients with a range of BRAF or other RAS mutated cancers that actually did have significant shrinkage of their tumors. Now granted, none of the tumors that shrink was meant to be colorectal cancer. But I think this does provide an important proof of concept that this ERK inhibitor approach can be quite potent in the right patient with the right kind of mutational profile, further motivating this, the HERKULES 3 study. The side effects from this study were as expected, and generally included side effects we would have expected with this class of drugs we have learned to manage pretty well. And they include things like nausea, diarrhea, rash, and eye side effects, which do require kind of being vigilant for any new changes in vision or other concerning eye side effects. And the study does require ongoing eye exams just for safety through the course of the study. With that being said, these are side effects that are pretty common to this class of MAP kinase inhibitors. And so these are not unexpected per se, and certainly things that we would aim to be able to manage with supportive care.

Dr. Michael Lee  13:18 
So that’s motivated the HERKULES 3 study. So this is a study that has two different arms based on the mutational profile of the patients. This study at present is currently up, enrolling patients only who have either a KRAS or NRAS activating mutation –again, about 45 to 50% of patients, or patients who have a BRAF V600E mutation, about 5 to 10% of patients. Unfortunately, if your cancer does not harbor one of those mutations at this point, you would not be a candidate for this study, just based on the principle that we’re trying to kind of find the best personalized approaches based on the underlying mutational profile. There are other trial options. Aside from HERKULES 3 for patients who don’t have a mutation in any of these genes. Patients who have a mutation in KRAS or NRAS as I mentioned, they will be studying the combination of the ERK inhibitor ERAS-007 with the CDK4/6 inhibitor, palbociclib. For patients who have a BRAF V600E mutation study will look at the combination of the ERK inhibitor ERAS-007 with an otherwise standard approach of encorafenib and cetuximab.

Dr. Michael Lee  14:36 
It is important to make sure that patients who are interested in this study know what the key eligibility criteria are when at the point in their disease, it is really important for you to be evaluated for this study. All clinical trials have particular time points –or are kind of they’re designed around particular points in a patient’s journey with typically stage four colorectal cancer, at which they should be considered for the study. And if you’re not quite at the right point in your journey, the trial would not be the right fit for you. So in particular, the HERKULES 3 study is looking at patients who have had some prior standard chemotherapy regimen. So for the most part, this specific study is not for patients who have had no prior therapy. But usually they will have gotten a standard prior chemotherapy based regimen. It also requires that they haven’t been given drugs that are usually given in patients who are more refractory to standard chemo therapies, drugs like regorafenib or tipiracil/trifluridine — these are oral drugs that are FDA approved, are usually given after kind of prior lines of IV based chemotherapeutic regimens. And so, if you’ve gotten one of those treatments before, this wouldn’t be a good fit. So you really should come evaluated for this study, before your oncologist is talking about putting you on regorafenib or tipiracil/trifluridine, because if we start that you won’t be eligible for this study anymore. It also requires the patients who have not had prior RAS, MEK, ERK inhibitors, these are not currently standardfor patients. So I wouldn’t expect you to have gotten this unless you were on a prior clinical trial. And while the criteria are evolving, it’s preferred that patients with the BRAF V600E mutation have not previously received encorafenib and cetuximab. So ideally, if your oncologist is talking about putting you on that combination, you would kind of quickly get into a center which has the study open to try to get onto this study, if you’re interested.

Dr. Michael Lee  16:45 
I think a lot of the patients are probably familiar with clinical trials.gov. But you can get more information for this study, look up the sites that are currently enrolling on the study, because it’s several sites, not just MD Anderson. So you can go to clinical trials.gov and type in a keyword like HERKULES 3 or this specific identifier number. This was just kind of the header. But if you scroll down, you’ll see more extensive inclusion and exclusion criteria, the sites that are currently enrolling, contact information for the study. So I would encourage anyone who’s interested to go to this site for more information. Again, this is a very exciting study, it only recently got underway. So we do think that there will be a lot of slots in the upcoming months for patients to go on the study. There are a number of sites that are active and continuing to be activated across the country. So looking to kind of where your closest site is, we’re always happy to see folks here at MD Anderson. But I’m very excited about the study. I think it’s very promising and I  I’m happy to answer any questions from anyone.

Manju George  17:57 
Yeah Dr. Lee, thank you very much. This was very informative. There are a couple of questions in the chat. So maybe we can go through that first. So this question is about prior BRAF and MAPK pathway treatments, are you okay, if people wait for a little bit? Or you said ideally, you don’t want any prior BRAF or —

Dr. Michael Lee  18:19 
Yeah, so it’s a great question. I think in general, patients try to determine what’s the best timing for coming into being evaluated for a clinical trial. It can be hard, because the reality is that logistically, there’s always a little bit of lead time that’s required to get in a new study, especially if you have to travel and figure out kind of life issues with that. And the reality is, if you’re kind of actively progressing, sometimes patients may have more significant symptoms that are building. What we don’t want is for a patient to wait, not get any active therapy before they know that they’ve been off of therapy for a couple of months and then start having worsening symptoms or other issues. I’d encourage patients in general, if you’re interested in the study, you know that you have a potential activating mutation in one of these key genes, to get an opinion at one of the sites that has the study. While you’re in the middle of your first line therapy, you may be able to get a kind of with a planned restaging scan. That way you can get plugged in well in advance, you talked about the study, you have an updated sense of the actual slot availability. Particularly in earlier phase, the earliest portion of the study, I will tell you we do have to be a little bit slow and methodical in how we enroll patients, just because we were looking very cautiously for safety of these new combinations. And so we don’t want to enroll a ton of patients all at once and find out there was a significant toxicity and we have to adjust the dose. So there are kind of slots that come and go particularly in the early phase of the study. So it is helpful to get plugged in and really get an updated sense of what are the study options — really other study options other than HERKULES 3. While this is a very promising study, there may be other study options that may be right for you. So rather than waiting until you’re progressing, and then risking a long wait time to try to get into the center, I think it’s good to try to get in kind of earlier, when you have a little bit more breathing room to figure out what the options are, so that when the time comes, you can get in quickly.

Manju George  20:21 
Yeah. Okay. So what you’re saying is that, so is it true that when a person starts, say, for example, FOLFOXIRI, and do they have to wait through like eight cycles or till progression to start thinking about this trial? Or should they initially  start thinking about it and get talking about it?

Dr. Michael Lee  20:42 
Well, I encourage patients in general to think about trial options, even from the beginning. So if  know you’re very motivated to go for trials, you understand. I mean, I always advise all my patients, there’s always kinds of downsides, particularly having to travel  farther than normal to get on a study –it is important to be aware of logistically what’s involved. With all that being said, if you know you’re interested in a trial, I think it always behooves you to get plugged in to a center with a large number of trials earlier in your course. When you’re getting standard FOLFOXIRI based therapy,  or even a chemotherapy doublet, if that’s whatever standard therapy you’re getting. If you’re having a really amazing response to therapy, I don’t think anyone would tell you to stop what’s working. And we would hope that that response would last for a long time. But of course, we also understand that at some point, that response may run its course, and we want to be prepared and have this plan ready to go at that time. Usually, that requires restaging every two to three months, we typically will do it every two months at our center to keep an eye on things. And so if you already know you’re interested in the study, many patients will actually get their restaging scans done with us, for example, so that we are immediately aware of when we need to switch gears.

Manju George  22:02 
Yeah. I had a question about the side effects of ERAS-007. You talked about the ocular side effects, what particularly are you seeing or what is known?

Speaker 1  22:13 
Well, these classes of side effects in general can be associated with a retinopathy, which is a retinal inflammation, or, specifically, if you recognize it, and you hold the drug, it does get better. And it may manifests in things like blurred vision or flashers or floaters. The study is building in regular eye exams, but you should also be aware, and kind of letting us know if you’re having any of those side effects. This is a class of side effects that generally we’ve seen with other kinds of MAP kinase inhibitors, even other nodes of that pathway. So for example, this is a common side effect we see with MEK inhibitors as well. So it’s not unexpected, but it is something we need to be aware of. And of course, when you’re giving drugs in new combinations, we have to be aware of that maybe a different side effect profile, again, kind of part of the reason in the early phases study, we proceed with due diligence and caution to make sure we’re maximizing patient safety.

Manju George  23:13 
Okay. So the other question was you mentioned a couple of doses, right for thyroid cancer and for the other cancers, 180 milligrams and 250. So what is the dosing? Are you also dose escalating during this initial part of the study?

Speaker 1  23:27 
The initial part of the study does have a dose escalation. Now the initial that’s kind of part of the slot, the slow and steady kind of slot determination, there is an ultimate dose expansion that’s planned. But we are planning a priori for the potential for needing to modulate the doses based on the toxicities we’re seeing –the unique novel combinations. So there will be ongoing tweaking of those doses.

Manju George  23:49 
Okay. And then about this ERK inhibitor, this is ERK1 and 2 inhibitor combined, right, blocking both? –And how does it compare to say the other ones available? Like ulixertinib or the BVD drug? –What is the difference?

Dr. Michael Lee  24:06 
So, I mean, every drug pharmacologically has different kinds of affinity for binding for the receptor and different kind of selectivity. Generally, the more selective the drug is for its intended target, and the less it hits off target, we would hope for better toxicity profiles, we do also see differences in the pharmacokinetics, which is kind of how long the drug persists. And that not only affects dosing, but the idea is that it can affect the optimal effectiveness level of the drug. This is a little bit subjective. But there are folks who will even say that this is more promising, I think you had seen in those preclinical studies that responses did tend to look better than then some of the predecessor ERK inhibitor –the prior ERK inhibitors. So we’re very hopeful that this will be even more effective than kind of prior drugs in the class.

Manju George  25:07 
Okay, I think there’s a question about what information do you have on palbociclib? In other cancers, what is the toxicity or efficacy, what have you seen?

Speaker 1  25:16 
Sure. So we have a pretty good handle on the expected side effects of palbociclib — at least kind of as a single drug. As I mentioned, it is approved with kind of estrogen directed hormonal therapies in combination in a range of estrogen receptor positive breast cancers. In that context we typically will see the biggest potential side effects with palbociclib typically is your blood counts. So it can cause low red blood cells or white blood cells or platelets. So that’s a known side effect we would have to follow, it actually doesn’t usually cause too bad of like febrile neutropenia, which is what we usually worry about with, say, chemotherapy and low blood counts. But that being said, we obviously do have to monitor and be very wary of potential infection and keep an eye on your counts. It can be other side effects like fatigue, like, rarely lung toxicity, or pneumonitis. Rarely, things like mouth sores. These are things we would obviously pay attention to. And obviously, their risk in combination will be more potentially there. Palbociclibn isn’t really given as a single agent, really, in any disease type, it hasn’t shown much activity, it tends to probably work best in combination, when there’s another targeted drug that’s already partially impairing cell cycle pathways, and then you further hit the cell cycle pathway. So tends to synergize better with other targeted drugs.

Manju George  26:37 
Yeah, I think there’s another question about the combination of the ERK inhibitor with KRAS-G12C inhibitors, do you know anything about it?

Speaker 1  26:49 
That would obviously be very exciting. There are a range of trials that are ongoing, obviously, specifically for the G12C patients. If you hypothetically had a KRAS-G12C  inhibitor, you could go on this study in the KRAS arm. With that being said, there are a wealth of studies that are specifically looking at direct KRAS-G12C inhibitors, as we’re all aware of. And it’s actually there’s an increasing number of compounds and an increasing number of combination approaches. And frankly, that would be a really good option. And something that’d be more unique to you if you had a KRAS-G12C mutation. So while you certainly could consider the study, and I would consider it, I would also look very hard into KRAS-G12C  inhibitor based combinations, because, there is a rationale to look at G12C plus other inhibitors of the EGFR MAP kinase pathway that is being studied in colorectal cancer. The exact best strategy remains to be seen, but most of the studies we have we’ve enrolled a number of patients on on other G12C  inhibitor trials, and they’re looking at an ever increasing number of potential new combinations to look to see, is there a signal of being more active while remaining tolerable compared to just single agent? So there’s a lot more options if you do have a G12C  mutation.

Manju George  28:13 
Yeah, and the other one question here is about EGFR inhibitors. So prior EGFR inhibitors don’t affect being on the trial at all right?

Speaker 1  28:24 
Well, if you have a KRAS, or NRAS mutation, you should not have gotten a prior EGFR antibody. So it would be a moot point. For the BRAF arm, it’s more relevant about if you’ve had prior BRAF in general, I wouldn’t expect you to be getting an EGFR antibody alone. But even if you hypothetically did, it will really depend on whether the trials at that phase of whether it’s enrolling patients with prior BRAF and or EGFR antibody therapy or not. But I would say if you have a BRAF mutation, even if you’re getting standard of care, it really should be in combination with another targeted agent, like the BRAF.

Manju George  29:07 
Okay. Okay. And then so the exclusion or  you prefer to have people who don’t have prior BRAF inhibitor exposure, right?

Speaker 1  29:20 
The study actually, the reason I phrase it that way is actually different phases of the study, it may allow or may specifically prohibit prior therapy. So generally, it will be safer if you haven’t had prior therapy, because at some point, the study will reach a phase where if you’ve had prior therapy it will actually probably be an exclusion criterion for this study.

Manju George  29:42 
Okay, so that means that for right now, prior BRAF inhibition is not an exclusion but it could be later. Yes, okay. Okay. And then we have one question from a patient she’s currently on FOLFOXIRI plus Avastin. And then she’s asked she’s got an HAI pump and to get to the liver resection and she’s asking, this would be the best time to think about this trial, right? For her?

Speaker 1  30:07 
I would think about it for sure, I think the biggest question for you specifically is going to be do you in fact, get to the point of a liver resection happening. Because if you have, what it would mean is that your liver metastases have responded very well, and that you’re actually having your shot at surgery. So, if you actually do have surgery and have all visible, known tumors removed with no evidence of radiographic disease remaining, then frankly, wouldn’t really be a candidate for this study. But that’d be great. So I would think about it just in case it doesn’t happen. But obviously, the hope would be that you would get to resection.

Manju George  30:46 
Okay. How can a BRAF V600 patient decide between Beacon doublet and this trial and which is more likely to help?

Dr. Michael Lee  30:57 
Well, Beacon is your standard of care doublet, right? That’s always available to you, as a standard of care with your local oncologist. I think but knowing what we know, about expected response rate, progression free survival and wanting to continue to push things forward, improve outcomes, I do think there’s an important role for novel therapies, looking at trying to see if the addition of the ERK inhibitor will build on the Beacon kind of backbone. So, ultimately, I think, if you’re willing to go on a trial and kind of have the logistical bandwidth to go on a study, I would highly encourage you to at least look into it. I think if for other reasons lifestyle, quality of life, it just doesn’t make sense, that’s totally understandable. And the Beacon regimen is going to be totally reasonable to get as your standard of care and is obviously the best standard care approach you could take.

Manju George  32:05 
The next question is about washouts. So if somebody is on chemo, how long do they have to wait till they get on the trial?

Speaker 1  32:13 
I believe it’s three weeks,  let me confirm it. It would. It would be in the clinical trials. I believe it’s three weeks though.

Manju George  32:24 
Okay. So not too much of a wait time. Yes. Yeah. Okay. Any other questions? When you showed the figure with the mouse models, you had some wild type animals in there, too. Right?

Dr. Michael Lee  32:43 
In the mouse models, there were wild type as well. Yes.

Manju George  32:47 
So it’s responding to people who don’t have the cancers which don’t have mutations in the BRAF and KRAF too?

Speaker 1  32:58 
So at least from the mouse data, it did look like that was the case now. Certainly, that the potential future area of investigation, because we obviously know that all patients with a range of kind of mutation profiles, we want to push things forward and have new trial options. So, but I think the study was designed with this priority for now, because we know there’s a particular need for patients with these mutations. I think I saw a question about what is the known toxicity profile. The study has started enrolling, but it’s actually quite early in its course, there haven’t been any major unexpected toxicity so far. But this is with a very small handful of patients. And certainly hasn’t been, like, reported at a meeting or anything, just because it’s still so small. I can assure you there are very regular safety calls ongoing to make sure all investigators in the study are staying abreast of any updated safety kind of in real time, which we do standardly for any new combination of drugs, and that’s certainly happening with this as well.

Steve Schwarze  34:01 
Manju, can I jump in? Sorry. Yeah, just I mean, obviously, we know something or like we have some data about CDK 4/6 for KRAS patients. Do we have any sort of evidence about what that would do for BRAF patients?

Speaker 1  34:25 
The CDK 4/6? Yeah. It’s a great question. We are increasingly looking, we’ve been looking at CDK 4/6 in a range of mouse models, actually. And while there certainly is kind of some promising preclinical data, I think. It certainly would be another realm of investigation for us to want to look into. There are a lot of really promising BRAF trials right now actually, that are trying to build on Beacon so really the question has been a matter of what is the most promising way to go? So CDK 4/6, certainly there’s a lot of interest in it. I will tell you at our center, my colleague, Van Morris, who I’m sure you all are very familiar with, has probably talked to you about some other emerging data about kind of the Beacon regimen plus immune checkpoint inhibitor therapy, and that he’ll actually be discussing those outcomes at the upcoming GI ASCO meeting. With the early data, and, there’s ongoing discussions about that becoming a larger, kind of much larger study. So I think we’re very excited about that data, in particular for BRAF patients.

Manju George  35:44 
Okay. Again, going back to the mouse data, so you had the HCT 119 cell lines right? In that figure, so is that like a subcutaneous model? Or do you have you checked in like a PDX model or something?

Speaker 1  35:59 
So it’s looked both kind of traditional cell line models, right. But on the right side of that figure was actually a range of colorectal PDX , is specifically patient derived xenografts. So it was looking both at kind of traditional cell line models plus PDXs.

Manju George  36:18 
What else? This is very useful. Thank you so much for your time. And we’ll probably give like one or two minutes, if anybody has any other questions.

Speaker 1  36:29 
I think someone had asked about efficacy even in the last few months. I wish I could tell you something more concrete. But right now, it’s still extremely early in the course of the study. We’re still even kind of at a point of getting dosing or firming up the dosing and the tolerability. So it’s very hard to say right now anything broadly with just a handful of patients.

Steve Schwarze  36:58 
Can I ask one, Manju? That dosing question is really important. I mean, so I was on a Beacon doublet, on the trial arm,  like four years ago, and then over the past year, I did it again with ulixertinib, through their expanded access program, and like I ended up getting eight months, I got twice as long on this combo with ERK inhibitor –I got four months on the trial, even though I’m much farther out. But it was a real challenge to try to juggle those doses, because we really didn’t know how much and I had a lot of toxicities related to it. So, yeah, I don’t really have a question. It’s just more of an n of 1 example, that it was figuring out what those right dosage was gonna be.

Speaker 1  37:52 
And I think that’s really important, because it’s exactly what we’re getting at. And I will say that targeted therapies, some patients think, oh, targeted therapies are not going to have any side effects like cytotoxic chemotherapy. And that’s, of course, not the case. It’s a different side effect profile, right? It’s more not like the really bad toxicity that gets better. It’s more like we have to learn how to live with these toxicities over a long time. So like a moderate toxicity that just never goes away, is quite bothersome as well, and perhaps arguably more so than a more significant toxicity that goes away in a couple of days. Right? And so part of the study is looking very carefully at what is the best dosing schedule along with dosing there are. That’s all kind of being pre specified, and still active discussion, and that’s kind of a key point of the early phase of the study. So we know what is the best strategy to go to before we kind of go into a larger expansion phase where the slots aren’t going to be so limited, we will have a better handle so that other clinicians, the investigators on the study, have a better sense instead of feeling like they’re having to go it alone to figure out the dosing, right?  which may have been your n of 1 experience.

Manju George  39:05 
Yeah, I think there’s a question. He’s asking, do you have a sense of how quickly you expect to see results or not? So are you going to have like interim results when you have the safety part done before you go into a dose expansion?

Speaker 1  39:21 
Yes, and no, I mean, so, of course there will be ongoing evaluation of the results, but it’s always very tricky when you have only like a handful of patients to make a firm conclusion about the efficacy of the study. Even the Beacon regimen, which as we all recognize was a major advance, had a response rate of about 20%. So hypothetically, I mean, I know actually, the earlier patients actually had a really high response rate, but hypothetically, if you’d had a treatment that had a one in five response rate and your first five patients you didn’t happen to see anyone have a response, you might prematurely say, “Oh, that’s not active” — and that wouldn’t really be accurate. So you do have to be really careful about that. We obviously do want to get the results as quickly as you can, but we also need to recognize that we need to get a large enough sample to know really what the true efficacy is.

Manju George  40:20 
Yeah. Okay. I have a question. So, in Dr. Corcoran’s trial, where he had the Spartalizumab with the MEK inhibitor and the BRAF inhibitor, he was using CtDNA to see whether the BRAF levels go down, and that would be an early indicator of effficacy, right? Are you planning to do something like that? What exploratory endpoints are you looking at?

Speaker 1  40:42 
Sure I mean, there are a range of –any early phase study has a lot of endpoints like, additional correlative studies, a lot of them are pharmacokinetic studies where they’re really looking to see what is the dosing level obtained by the drug and like, what is the level of the drug in your body at that time point that standard. It’s pretty cumbersome, honestly, for the patient to have, but that standard. CtDNA is built into practically every study at this point, I will tell you, it’s probably not like an immediate readout or necessarily going to be used to determine if it’s working or not–continue or stop. From that perspective, we’ll still be using the tried and true kind of radiographic imaging based endpoints. But, pharmacodynamics, and pharmacokinetics are a key point of what happens in these early studies. We’re very grateful that patients are so willing to take those steps, we can truly know was the drug working, was it doing what we intended it to do, because we really need patients to be willing to get extra blood draws or even biopsies and things as needed. So we’re very thankful for patients to be willing to do that.

Manju George  42:03 
Okay, thank you for that. Yeah, I think we covered all the questions. And this has been very useful. So what I’ll do is that I’ll have the video available in Colontown University as well as Colontown. And if you want, if you’re interested in having your patients watch it, or somebody who’s interested in the trial watching it, I’ll be happy to share a link so that you can have them watch it.

Dr. Michael Lee  42:31 
Yeah, that would be great. Thank you so much.

Manju George  42:34 
Yeah. Okay. Thank you very much for your time.

Dr. Michael Lee  42:37 
Thank you, everyone.

Steve Schwarze  42:38 
Thank you. Bye bye.

DocTalk
2021
Dr. Lee
BRAF
KRAS
MSS
Stage IV
Trials

Dr. Michael Lee of MD Anderson discusses the HERKULES-3 clinical trial for BRAF and RAS-mutated GI cancers. Recorded in December, 2021.

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New treatment strategies for MSS CRC

New treatment strategies for MSS CRC

DocTalk
2021
Dr. Parikh
ctDNA
MSS

Dr. Aparna Parikh  of Mass General discusses “Strategies for Making Cold Tumors Hot.” “Cold” tumors do not respond to immunotherapy. This DocTalk was recorded in the fall of 2021 with PALTOWN Scientific Director Dr. Manju George.

Dr. George  0:00
Hello everyone. I’m Dr Manju George, the Scientific Director at PALTOWN Development Foundation, the nonprofit that supports Colontown. We are very happy to have Dr Aparna Parikh with us, and she’s going to talk about colorectal cancer strategies to make cold tumors hot. And just a little brief introduction about Dr Parikh. She completed her MD from the Indiana University School of Medicine, residency from Mass General, and fellowship at UCSF. She’s board certified in internal medicine as well as medical oncology, and she has a lot of nice papers, the most recent one is in Nature Cancer on radiation therapy and immunotherapy. And we are really excited to have you here with us. Take it away.

Dr. Parikh 0:13
Great. Thank you so much, Manju for inviting me. I want to just thank Manju tremendously for her incredible collaboration with a lot of our work that we’re working on kind of pan- stages of colorectal cancer, and I’ve gotten to know her through our Stand Up to Cancer Colon Dream Team and her advocacy and voice in our adjuvant study. So, you know, there’s lots of different areas where I sort of thought we could talk about today, but in light of our recent paper and some work that our disease group is working on, I wanted to share some of the strategies that we’re looking at in the metastatic setting to make some of these cold tumors hot, in colon cancer, but as well as other GI cancers. But I’m hoping today that we will leave ample time for discussion, and I know Manju had asked me to just briefly also comment on the status of our stage III CtDNA trial, as well as the study that our group is doing, this being led by Ryan Corcoran in the BRAF setting. So I will go through this deck, and we’ll have some questions, and then I’ll give some brief updates, and then we can close with a Q&A which I think would be very much welcome to me as well.

Dr. Parikh  2:06  
So I do apologize if some of you attended AACR, because this is somewhat of a repetition of the talk that I gave there, but I hope we’ll be able to spend a little bit more time in terms of our next steps from these first generation of trials in the setting. So here are my disclosures, and as part of this, I do need to mention that I am discussing Investigational Use of ipi and nivo as well as 3TC in colorectal cancer.

Dr. Parikh  2:39  
So this is a slide that won’t be new at all for this audience, but it’s one of my favorite slides, just in showing the gains that we have had from the 80s. But you know, except for biomarkers, subtypes, really, since 2014 with the pivotal 80405, first line study for the RAS wild type patients haven’t really seen a slope increase where we need it to be, in terms of where we are in 2021 and arriving on 2022 soon. I think it’s always helpful to put in context where our median OSs are for the latest non-biomarker, selected drugs such as rego and lonsurf, where rego was FDA approved first in 2012 and subsequently lonsurf in 2015…

Dr. Parikh  3:33  
Dr. Parikh: …where we see median OS is still less than two months. And except for these biomarkers, which I’m not diminishing the role of these biomarkers, because in summation, these biomarkers do add up. And a lot of exciting work obviously happening in the BRAFV600E and other activating non V600E alterations, The tremendous gains that we’ve seen in MSI disease over the last several years, the HER2, and the trastuzumab deruxtecan data, as well as several other small molecule inhibitors and TKIs for the HER2 setting, and then rapidly evolving G12C, plus, you know, D, V and others in that space too. So not diminishing the importance of predictive biomarkers and the great strides we’re making in those particular settings, but I think it’s really humbling to look at the rego and lonsurf data and put that in context of where we need to go.

Dr. Parikh  4:41  
Personally, if we’re sort of having a DocTalk, I don’t even really use rego, I do use lonsurf, if we don’t have a good trial option because we do see patients, with no great biomarker of who those patients are. But do have patients that do derive benefit for quite some period of time, but in now, kind of seven years sort of being an attending, just with Rego, haven’t seen anything. And as you all know, toxicity is tough. But I do use lonsurf.

Dr. Parikh  5:13  
So this, again, for this audience, isn’t going to be news to any of you, but I think it just goes to show that the PD-1 story in colon cancer has actually been around for some time, as far back as 2010 where we have tried to use PD-1 therapy without efficacy. So if you look at sort of summary of the numerators and denominators, very humbling numerators with a non trivial number in the denominator in terms of MSS patients that were treated with checkpoint inhibition. I think just for time, I’m going to skip over the MSI data, because you guys all know the keynote 177 data, but again, noting which many of us are paying close attention to, including approaches such as using CtDNA in the setting to try to really understand who these patients are that are dropping off early. So when you look at the keynote 177 data, the thing that I always like to point out is in the pembro group that you had a 30% non response rate. And so even for these patients, even though we have made tremendous headway with the MSI patients in pembro, nivo, nivo/ ipi, what are the biomarkers that are predicting lack of response here? And can tools such as CtDNA be used as a guide to predict who those non responders are going to be and potentially salvage an opportunity to switch to chemo sooner rather than later for those patients?

Dr. Parikh  7:01  
So this cancer immunotherapy cycle is, again, not a figure that’s new to the field, and was kind of a figure that initially came out of Ira Mellman and colleagues, but really shows us at the cellular level, what the problem is with these cold tumors and the various checkpoints and opportunities we have to try to engage tumoral responses. So some of the things that we’re going to be talking about too, is not only where we’re looking at removing the brakes of the checkpoint inhibitors, but I think a lot of interest in the TGF beta, the CMS4 colon cancers too, and how we can really help with infiltration into tumors, both enhancing the chemotherapy response, but protect potentially, other signaling pathways such as TGF beta to try to hinder TGF beta signaling and allow for immune trafficking, but also efficacy of chemotherapy. And then what we’re trying to do with some of our approaches here, are there ways for us to kind of stimulate antigen presentation and basically stimulate an in-situ vaccine response to try to get these tumors from here over to the left to the right side of this diagram.

Dr. Parikh 8:32  
So we at MGH have a very radiation heavy group, kind of a phenomenal group of radoncs, led by Ted Hong, who is the NRG chair. And because of that, we entirely recognize that, not only in colon cancer, but rectal cancer, pancreatic cancer, we’re a very radiation bias  sort of group. And do a lot of trials and work, to try to exploit radiation as a tool. And some of this work actually came from the Penn group initially, and the men and colleagues now several years ago, that showed that using radiation and dual checkpoint inhibition may actually activate non-redundant immune mechanisms. We’ve seen several other studies in other tumor types, such as lung cancer, GU cancers as well, showing that low dose radiotherapy may actually help your tumor presentation and prevent the resistance to immunotherapy that is happening. It is very controversial what the right dose of radiation is and whether one time radiation is sufficient or not. I actually think that you may need to give subsequent doses to create that T cell repertoire and  then maintain that T cell response over time, and maybe a one time or a couple dose of radiation isn’t going to be sufficient. But if you look here, with the Minn paper, here, with the preclinical data, looking at the control in the gray here, but combining the control with RT and CTLA4 and RT again responses here in the preclinical colon cell lines. So based on some of that work, and they used sort of an 8 gray times three fractionation schedule, and that’s what we ended up ultimately taking into the clinic.

Dr. Parikh  10:39  
So it’s complex, I think it’s one of these things that we’re really trying to understand what is happening. But we do know that it does seem that radiation is helping promote T cell infiltration, antigen presentation and shaping your T cell repertoire. We see that the responses that are happening to radiation seems to be happening in an interferon dependent manner, so really activating the innate immune response and not just sort of adaptive immunity. There is some evidence, preclinically, that there is actually through the kind of cellular processes and turn around that are happening with the low dose radiation, we’re not exhausting your T cells or burning them out, that you are releasing tumor specific antigens, and with those tumor specific antigens, mounting a direct T cell response to that. And we know actually that RT activates dendritic cells as well. And one of our lab collaborators who works in Nir Hacohen’s labs, Arnav Mehta, is really trying to look at some strategies using TLR9 and others to right now in pancreatic cancer, is where he has funding to try to look at dendritic cell activation with kind of TLR anti- agonist and RT. We know that anti CTLA4 promotes the expansion of T cells, inhibits TREGs and effectively increasing your CD8/ TREG ratio, and that PDL-1 blockade may actually reverse your T cell exhaustion and help mitigate that depression in your CD8 to TREG ratio further. Again, the idea being that we’re trying to get an oligoclonal T cell response here, even though we are going to be getting polyclonal responses. Really, the idea here is, is there a way to figure out a way to get that oligoclonal T cell expansion and response, and then help subsequently, with your T cell infiltration. And can we use these combination approaches to really kind of harness what radiation is able to do? 

Dr. Parikh  12:53  
So, given this, we embarked on a trial. It was a single institution trial funded by BMS, with correlatives supported by Stand Up to Cancer for the colon component. It was a trial that combined colon cancer, pancreatic cancer, as well as MSI disease. We haven’t completed the MSI cohort yet, but did complete the MSS, CRC and pancreatic cohorts. And what we did here is we gave Nivo and IPI at cycle one, day one. And then cycle two, six weeks later, we gave Nivo and IPI again, and we gave 8 gray X 3 to a single lesion that was radiated.

Dr. Parikh  13:44  
And what’s important to note here is that the lesion we radiated was not the lesion that was measured. We are pulling the data to look at the radiated lesion response, but currently what we reported and what the end point of study was to look at response outside of the radiated field. And then we continued Nivo and IPI after that initial 8 gray X 3 to a single lesion beyond that initial treatment. So here were the consort diagrams for both cohorts. For colon, we had 40 patients.

Dr. Parikh  14:24  
I do think it’s important to note from both cohorts we had around a 30% drop off from the start of Ipi+ Nivo to radiation. And so I’ll show you the data for both the all-comer population here, sort of the Intent To Treat, but actually what we call the modified Intent To Treat. So the response of people that actually went on to receive radiation. And what you can see the reasons for discontinuation, toxicity was a few, I think, keeping in mind that when we started to study in like 2016, 2017, IPI and Nivo were still relatively new to the GI space, so we were sort of figuring out how to manage the colitis and others, where we have made a lot of headway in the recent years  within the GI community, how to handle those side effects. But we were still learning how to safely give these drugs at that time. We had nine other patients that had PD (progressive disease). This is a heavily pre treated patient population, so unfortunately, by the time you register the patient and actually start treatment, we had nine patients that dropped off, and ultimately weren’t able to get to radiation.

Dr. Parikh  15:43  
So when you look at the per protocol analysis, these were people that actually ended up getting radiation, so not the all-comer, we see a disease control rate of nearly 40% and an objective response rate of 15%. And what I want to call attention to is the duration of responses in the patients that were deriving benefit. So if you look here at the CRs (complete response) and PRs (partial response) as well as the stable disease patients, and we didn’t put this figure in the paper, but we actually did map out the previous lines of therapy for these patients and how long they were on their last previous line. And I think what was notable to us was that for a number of these patients, the duration of treatment is exceeding a year.

Dr. Parikh  16:35  
And we don’t think that was just sort of biologically selecting patients, because again, when we looked at the previous line of therapy for those patients, it wasn’t quite nearly a year by any means. There was only one patient that had lung only Mets. She wasn’t a PR patient, but she was a stable disease patient, and so sort of lower volume lung only disease that her biology was clearly favorable. But besides her, we don’t think that this was sort of a fluke in terms of biologically selecting favorable patients.

Dr. Parikh  17:15  
All right. So here is just one example of the out of field responses. So this was a patient that I shared with Ted, and we did not pre-specify in the protocol what needed to be radiated. So Ted Hong or his colleague Jen Woo, would sort of pick if there was a lesion that was needed for symptom control or palliation, often would pick that region or another region that was amenable to biopsy, because we had to do a lot of correlatives here. And here what you can see for this particular patient, he radiated the liver. And what you can see here is a really nice response in the lung metastases. So these are the same cuts, and you see improvement, here of this lesion and actually disappearing of some of the other lung nodules that we saw.

Dr. Parikh  18:09  
When we look at the Kaplan Meier curves, just for, I put the PDAC (pancreatic ductal adenocarcinoma) just for reference here, but when you look at the PFS and OS for the patients that actually went on to benefit or not, 5.2 versus 2.4 months, and then the OS 20.9 months versus 7.7 months for patients that were not deriving benefit.

Dr. Parikh  18:36  
One of the questions–this actually we hadn’t done initially– because we sort of assumed it was fine, just based on this and then the reviewers actually asked us to go back and look at TMB, which we did, and not surprisingly, these were all low TMB patients, so TMB albeit controversial, and colorectal cancer was certainly not the reason that was driving this change. We had 41 samples, or we had paired germline and DNA, 17 patients that were actually analyzable with the radiation. There was really no change in TMB before, during after treatment. Profiling is what you would sort of expect–KRAS, P53, APC alterations. We did note, interestingly, some change in sort of DNA damage response genes, but again, numbers are really small, so hard to really draw a lot of conclusions around kind of any DDR signatures as well. But what was interesting is, you know, when we started to look at what was coming out, and sort of the bulk RNA Seq, and one of the other kind of changes that we were seeing is David Ting, who did a lot of the correlative work for this, was noticing that in the responders, they seem to be enriched in these, again, interferon signature response genes. So signifying again, that we’re something is happening with kind of the innate immune system, and perhaps that these patients that were going on to respond were somehow primed to respond to this approach. And what we’re really trying to figure out is, is there a way for us to figure out how can we make more patients sort of primed for this approach? And are there any ways? And I’ll show you what some of those ways are to try to exploit this vulnerability for patients.  We saw some change in antigen presentation, as well as kind of T cell recruitment signatures before and after radiation. And then we saw this differential expression of these non coding RNA repeats and all the biopsies from the responders to non responders, particularly one repeat, which is called HERV-K. And I’ll tell you a little bit about what these repeats are and in the subsequent slide or two.

Dr. Parikh  21:12  
So like I mentioned, HERV-K was one thing that came out, but also LINE-1, which is another repeat. And they’re actually kind of ISH (in-situ hybridization) assays that are easy to do to ascertain HERV-K and LINE-1 status. And again, we saw this, and what we have learned in other cancers, actually urothelial cancer, there was a great paper that I put in reference here, and I can make sure Manju has these slides, that basically showed that HERV-K was associated with response to urothelial cancer, and HERV-K sssociation, or HERV-K is actually been associated with NK (natural Killer) activation. So maybe there’s something with these non coding repeat elements that are actually the ones that are driving these tumors to be primed for responding. Our hypothesis is, and what we’re trying to really understand is, is there a way to exploit these repeats further?

Dr. Parikh  22:09  
So what we saw was that this strategy of CTLA-4 and PD-1 did show some activity in a subset of patients. I’ll show you the schema for our trial that we will have our last patient on this week and have finished this next MSS trial to kind of confirm the signals, and with this next trial, we tried to mitigate some of that toxicity fallout.  But also Nir Hercohen and others have done work that’s showing that perhaps  PD-1 blockade prior to the antigen priming, may paradoxically lead to T cell exhaustion. So independent of toxicity if we expose to the checkpoint inhibition early. can we help with the responses and obviously the ongoing biomarker work that we’re doing.

Dr. Parikh  23:13  
So this was the study that is 30 patients, and patient 30 will come on this week, where we did the exact same thing, 8 gray X 3 (RT), but moved Nivo and ipi up to cycle one day one. And then actually are only continuing with four cycles of IPI, just based on other tumor types, the data that maybe you don’t need the IPI long term.

Dr. Parikh  23:41  
So we’re seeing, it’s too early, we haven’t yet looked at the data. I’m treating a lot of these patients, and so we are seeing some benefit. I don’t think it’s going to be where we would like to be in terms of 40% response rates, but I do think I mean, I know we’re seeing some patients benefiting, and we’ll see what those numbers look like. And now we’re really trying to figure out what our path forward is here, and are there better ways to get more to respond? Or will BMS support a larger study with this approach? Because, as you all know, if you’re in that 20% of patients that you’re driving benefit for a while that’s real and meaningful, and it’s our job now to kind of figure out with biopharma how to support this.

Dr. Parikh  24:34  
So we’re doing a lot of  correlative work with this too. We’re looking at ctDNA. We’re doing single cell RNA sequencing. And the way I like to sort of think about some of these immuno oncology correlatives is it’s the single cell approach is to really understand what is in the tumor so, what is the composition of, NK, CD8s, dendritic cells. And then what’s important is not only in understanding what, but using some of these multiplex approaches to understand where are these different cellular components located, to try to understand what’s what, to try to help us understand what’s happening.

Dr. Parikh  25:15  
So then going back to the repeats. So this was something that also actually came from David Tings lab, and when he was in the cancer center director Daniel Havers lab, as a postdoc, long time ago now, and they started to identify, as well, some other groups these, what it’s being called as the repeatome, and it’s an unexplored facet of the genome. Which, when I first met with, the backstory is, I showed up at MGH, almost six years ago too, and David Ting and I met, and he was like, Hey, we found this stuff. It’s constituting 50% up to 70% of the genome, and we don’t think it’s just junk. And he showed me some data that he had in colon cancer, and we started to put our heads together kind of digging through the data and the repeat landscape. And was there a way for us to try to think about how to harness these repeats, which, interestingly, these repeats we see in embryogenesis, and you see really high levels of these. And then it seems to be pretty quiescent until expression, again, in cancer pathogenesis, but also in aging and autoimmune disease. So there’s something going on. And I think  from a very simplistic standpoint, it makes a lot of sense, like, why would something be there? And it must have some purpose. And if they’re suppressed, they don’t cause problems. But if they are not suppressed, it can lead to problems such as epithelial malignancies.

Dr. Parikh  27:05  
And so this is just to show you that these repeats have actually been around for some time and act like endogenous retroviruses and actually have their own reverse transcriptase (RT). But only in the last few years, are we seeing this, not only in GI cancers, but a lot of other malignancies, in terms of the role of these and how they may actually stimulate immune responses. We know that they represent in the genome, like viruses, they have an RT (reverse transcriptase) so different things like methylation can actually help derepress them. And then you can have this RT that we think helps them reintegrate and expand into the genome.

Dr. Parikh  27:55  
And this is sort of a nice diagram of the RNA to the RNA/DNA. And rdDNA constructs there, and how they eventually are reintegrated and expanded. And can we use something like an RTI (Reverse Transcriptase Inhibitor) to prevent this reintegration and then expansion? This was a Nature Genetics paper, a couple years ago that looked at these repeats and several different malignancies. And Interestingly, esophageal cancer is one of the higher ones, but you see here, colon cancer is another cancer where these repeats seem to be differentially expressed. And like I mentioned, is that we think that these RNA repeats are actually triggering an innate immune response. And with these repeats, we see a lot of these inflammatory cytokines go up. And what you can see here with HSET- 2, which is one of these repeats, you can see a difference here between  TNF, IL-6, expression, IL-12. So seems to be something happening with these and interferon responses.

Dr. Parikh  29:11  
This was a JCI paper. David Ting was a collaborator on this, as well as from Bersani and colleagues a few years ago, looking at these NRTIs. So using 3TC, for example, and to inhibit these tumor spheres of  p53 mutant colon cancer. I won’t go into some of the details of how TP 53 is repressing these repeats, but we do think that actually, these repeats tend to be linked to TP 53 expression. So if you see here, this is LINE-1 in the green. And if you look at TP53 Colon cancer versus wild type colon cancers, the TP53 mutant seem to be enriched in these repeats as well.

Dr. Parikh  29:55  
So David Tang sort of treated some mouse xenografts with 3TC, and you can look here in pretty standard colon cancer xenografts, here in cell lines, looking at what’s happening in TP 53, mutant tumors, as well as wild type tumors. In HCT 116, cell line versus the xenograft what is happening with 3TC and tumor growth here? So showing some activity of this in the mutant patients, but not in wild type.

Dr. Parikh  30:37  
So this led us to write a small grant that was funded by a foundation. You can imagine, it’s really hard to get these funded because biopharma, there’s not a clear R and D sort of path for these. So we tried lots of different avenues, and ultimately, a foundation, the Gateway Foundation, funded this trial, and it was a small study with 3TC alone. And we didn’t really think that 3TC alone was going to, I think we know even going forward, that we’re going to need to look at combination approaches, but we wanted to make this sort of a biomarker driven trial and see that with 3TC alone and doing biopsies, are we actually hitting the target here and engaging these repeats. And so we did the trial. We started initially at the HIV dosing, which is our hepatitis dosing too, which is 300 milligrams daily, and we ended up going up to 1200 milligrams daily. And this was actually based on the initial HIV data, where there were no DLTs at the 1200 but given the efficacy they saw in the  viral space, around 300 that’s what ultimately was approved.

Dr. Parikh  31:56  
And so we had nine patients that were enrolled at 300 and then we went up to 23 more patients with the higher dosing. Really no significant side effects, some fatigue. Hard to sort out was that cancer versus drug, and we had eight out of 32 patients that had disease control and one out of 32 patients that had a mixed response, that one person the mixed response did not meet RECIST criteria for response, but had a really nice CEA  decline, and then had some tumors that were actually regressing, and then others that were growing, but the CEA overall was coming down. So that’s this patient here with the CEA response, and you can see a little bit of CEA response there, and some stability, at least here.

Dr. Parikh  32:47  
And when we looked at the patients that were deriving benefits, again, what we saw was that in the responders versus non responders, the same thing this LINE1 protein which is another, it’s a another one of the proteins that is expressed or formed by these repeats, sort of the LINE-1 leads to LINE-1 protein. And we looked at line one status, and again, looks like differentially expressed in patients that were benefiting versus not. So that study is we are under revisions right now for publication and trying to figure out our path forward with both of these approaches. And I hope we can all continue to work together as a community, because these are hard studies for biopharma to support. But  we’re looking at other options to try to get some of these concepts through, and our priority options for even when we get patients that are interested in supporting trials and things too. So we’re looking at options with 3TC and RT, based on the initial data that I showed you from our RT study. If you use epigenetic drugs and preclinical data, you may be able to get these repeats expressed. They seem to be linked to DNA damage and DNA damage response and as a kind of repair mechanism for double stranded DNA breaks. And so we have brokered some pre clinical contracts with David Ting to look at some of the DNA damage drugs out there, but are really working hard to try to figure out how to exploit these and get patients access to some of these combination strategies.

Dr. Parikh  34:49  
So with that, I think I went a little bit over what I wanted to with the 30 minutes, but wanted to share with you all some of the things that we are working on and where we are headed. So maybe I’ll pause for questions, and I can give you kind of brief non slide updates on the BRAF study as well as the CtDNA studies. Does that sound okay?

Dr George:
Yeah, that sounds good. This is really exciting. Thank you. Dr Parikh, so we have some general questions, so maybe we can go through them quickly, what is the rationale and risk benefit for triplet chemo, like FOLFOXIRI,  in the first line versus sequential doublets?

Dr. Parikh
Yeah. So I think there is a lot of institutional bias around this. And in general, I think taking a step back, of triplet versus doublet as well as I think maintenance versus holidays is a big discussion that I think a lot of people sort of split our hairs around in trying to understand. I do think when you can give FOLFOXIRI safely, I do think that there is, it’s truly synergistic, right? It’s not just additive. And so I do think that there is a survival benefit. And I sort of believe the TRIBE 2 and studies that for patients, and we’ve seen this with pancreatic cancer and others. And, in cholangio, there was a study that just looking at FOLFIRINOX and Gem/Cis, and didn’t show that FOLFIRINOX was better than Gem/Cis. So it’s not always just more is better. But for colon cancer, I think we do have compelling data to say that  in the right patient who we can get through FOLFOXIRI and in experienced hands with dose adjustments and things, you can get people through FOLFOXIRI probably with survival benefit. So I, I’m biased. We’re a pro FOLFIRINOX group, FOLFOXIRI group, have been for years, and so I do believe that there is a survival benefit, but I’m also, I don’t think, not surprisingly, treatment holidays lead to a detriment in PFS, but overall survival benefits are the same. And so I’m a firm believer in quality of life discussions with the patient and what their goals are, and don’t think that with the right patients you’re going to lose survival by both, doing maintenance. But I’m also a believer in good induction.

Dr. George  37:26  
I mean, what would you think, would you give it to a younger patient? I know that many of the  BRAF V 600E mutant patients, they get FOLFOXIRI in the beginning, right? So do you use some criteria to decide who are the patients that you will give FOLFOXIRI up front?

Dr. Parikh
Even older patients that have good performance status, I feel like performance status is in the eyes of the beholder, but we have given FOLFOXIRI or FOLFIRINOX to octogenarians of pancreatic cancer, and have gotten them through. So I’m not shy about it and recognizing that we may have to dose adjust and things along the way, but I think performance status to me more than age.

Dr. George  38:09  
Okay, And then the next question is about re challenging with say, FOLFOX or FOLFIRI for a patient later, like two or three years after they have had those. What do you think about that as part of a statement strategy? So it’s something that you follow? 

Dr. Parikh
Very much. So I think we have good enough benefit if  I think if data that have neuropathy and things are okay, that you can  regain response, particularly to the platinum. So even with FOLFOXIRI, I should mention, I’m not pushing through necessarily six months of FOLFOXIRI, sort of doing four months, get a response, then ,I tend to be pro-FOLFIRI, just because of the neuropathy issue and trying to save the platinum for later. So FOLFIRI Bev or anti EGFR, depending on sidedness and mutational status, and then, giving a holiday at some point in time, and then reintroducing later

Dr. George 39:12  
Okay. And then the next question is about, what are some of the conditions under which you decide to stop the chemo? And then consider local or regional treatments.

Dr. Parikh  39:25  
Yeah, so this is a good question, and it gets debated all the time, because as you may know, that, for example, liver directed therapy hasn’t been survival advantages there. But we are a site that I said for limited disease, depending on locations, particularly if a patient needs a break from chemotherapy, whether it’s toxicity or just fatigue, or is that a good response for some time, and we have shown that we’re not going to get behind. Have certainly used, sbrt to a dominant liver lesion. And as long as we think we have a good handle of lung, we do ablation for small volume liver lung Mets, for example. So it’s really about following the biology and making sure that the systemic disease isn’t going to get ahead of you. And if you feel like you have that window to stay on top of the systemic disease, but you can treat a dominant liver meth that may cause problems imminently, and prevent that from causing problems, in discussion with the patient, sort of understanding that we haven’t [had a lot of trial data] yet. There’s an NRG trial that’s looking at oligomet treatment and radiation and things, but I think we’re all starting to get a sense that oligomet sort of treatment was probably kind of beneficial. So our group, again, recognizing the biases of not a lot of survival data yet to support these, but in the right patients aren’t shy about like organ specific disease control approaches.

Dr. George
Okay, thank you very much for that. There’s one question about trials, but maybe we’ll go to that later. There are some questions in chat. So any insight on overcoming resistance to G12C inhibitors, or ideas on sequencing? Is there any news on if switching to a new G12C inhibitor after failing another one will work?

Dr Parikh
Yeah, I don’t think another G12C inhibitor in of itself, is going to work. I think we are seeing the differences between the G12C inhibitors and which ones are better versus others. But I think the kind of dual, triple pathway blockade approach with looking at better, I think there are better ERK inhibitors that are coming. ERAS is a company that I think has a really exciting ERK inhibitor. I think we’re still looking at some of the SHP2combination approaches. So I think it’s going to be combination strategies, because as far as we know, Dr. Corcorans Lab is doing a lot of work in this, but a lot of the resistance alterations that we’re seeing, and then what they saw in the New England Journal lung cancer paper, aren’t necessarily resistance alterations that are going to be able to be overcome with just another G12C inhibitor. So it’s sort of combination or downstream approaches too.

Dr George
Okay. The next question is, how do experts use CtDNA or NGS testing to know when to re challenge targeted treatments –like CETUX, Ras treatment, BRAF inhibitor, etc? Is it an estimate of how many months between treatment is needed for optimal possible results?

Dr Parikh
It’s a great, great question. And you’ll see people like Len Salz argue from CHRONOS that it’s only a 20% response rate. And the reEGFR inhibitor  challenge of person is really like cost effective and useful? So, I don’t think we really know. I think we do kind of have a timeline of what we would expect, the kind of resistant clones half life of a few months in terms of decaying and six to eight months seems to be that window. What I tend to do at the time of RE, when people are going on either holidays or something else, is I just get, kind of every two months  ctDNA test and see what is happening to those resistance clones.  And, I think what’s so challenging with even just up front  ctDNA testing, is does a small KRAS clone at 0.1%, does that actually portend resistance or not? And the dogma now is  of course, I guess KRAS is a resistance alteration and has detriment to anti EGFR therapy. But if you see that a RAS wild type tumor, and then you see this small clone, is that really clonal? Not clonal? Should you not give that patient anti EGFR therapy,  when you have a limited toolbox of things to try?  Same thing with HER2. I had a patient that had a RAS mutation, but I didn’t have a lot of things to try, but was really and I had a HER2 at 25 to one. Am I going to believe that small CtDNA result and not give them HER2 directed therapy? It’s hard not to, right, when you have an amplification that sort of at 25 to one. So that patient benefited. But again, the purists  would say, KRAS alteration came up, and that’s a known resistance mechanism. Those patients aren’t getting benefit. But you’re not necessarily looking at the fact that, again, that for that particular patient, you had a amplification, it was like at 25 to one, and clearly your driver event here, and that KRS was probably just a sub clone that overall, wasn’t going to hinder benefits. So ctDNA is a great tool, and I’m obviously biased, but it is a tool,and you have to sort of think about what you have in your tool box to care for the patient individually. And luckily for colon cancer, sometimes you have a little bit of time to try one or two things before people fall off.  Unfortunately, you know where you may not. That’s not always the case. And sometimes you just have to make your best clinical judgment, but I think we use it as a tool, but not as the end all be all

Dr George
Like with with clinical judgment, right?

Dr Parikh
Yes, right.

Dr George
So I had two questions about your talk. So the HERV K that repeat element as well as the LINE-1. So are you seeing that before treatment itself, you could look at the tumor and see if there is over expression or not?

Dr Parikh
Yeah, yeah. David Ting did a really great look. He hasn’t published this yet, or we haven’t, but actually, when you look at we did a cohort of just neoadjuvant rectal cancer patients that did not go on to have a clinical complete response. And what he showed was that the patients that were what was left were these HERV K elements. So it’s almost seemed to be a biomarker of non response to just the chemo, too. And so what we’re trying to figure out, can we make these repeats engaged more to try to therapeutically, use them to push these tumors over to response.

Dr George
Yeah. And I was also curious to see that, like with the mutation, with the TP53 mutation, you’re seeing more LINE-1 expression and things like that, right? So, I mean, I would think that ideally, if they, if some of the testing companies, CtDNA, or the tumor testing companies, would also look at these elements that would be kind of nice to see for your trial itself, to select patients who you’d get a better response, right?

Dr.Parikh
Yeah. So we are actually working with some colleagues, actually at the Brigham to look at a LINE-1 blood assay as well, and then we’re trying to validate that with the tumor to sort of figure out. But as you can imagine, biopharma is like, what are these? What do we do with them? And David Ting and I are pitching this constantly, like, hey, we have an ISH, we have an assay. We can sort of, but it’s really hard for them to currently get it, but I think we’re getting there.

Dr George
Okay, thank you for that. So there is a patient with a pole mutation. It is like a S314A, missense variant and the TMB 7.4. So she’s asking, if there is, it will have an effect in choosing immunotherapy, like with the low TMB with pole? What do you think?

Dr Parikh
Yeah, so probably not. Unfortunately, I think I would have to look up this particular polE variant. It may just be a kind of a VUS. But you know, the typically, the PolE ones that we’re seeing response are like hundreds of TMB.

Dr George
Okay, thank you for that. I think that we can go for the updates, and then there is one BRAF-related question, so we can look at that. So you’re going to start with your CtDNA trial, right, first?

Dr Parikh 48:17
Yeah. So the CtDNA trial has had lots of challenges, but we’re not giving up on it yet. Some of the challenges came with being a trial that, just by nature, the Stand Up to Cancer team was only a northeast heavy team, and I don’t think when the team came together it was based on the correlative expertise and clinical expertise, but not necessarily like a cooperative group study. So it was a small number of sites that could activate the study and then COVID hit. And because it was a stage III trial, a lot of our institutions weren’t allowing stage III trials to continue on, because they were trying to improve cure, not necessarily metastatic, where they didn’t seem that there were other options. So we had a really big delay, and we so we’ve had around 40 ish patients at MGH, and it was only the last couple months that MSK and Hopkins and Cornell all came on board. So I think we’ll see now a rapid increase there. But we’re behind, but I think the  Stand Up to Cancer, even though the team is over, is still really committed to the question, and they’re not pulling funding from it, so we’re continuing. And, I think Manju, I had mentioned to you, and there was a lot of controversy around rectal. We were getting close to adding rectal, but people were very concerned that if we added rectal, we would get a lot of challenges about the meaningfulness of the data if we didn’t stratify it. And actually we ran the stats to stratify for rectal, it was going to be.. it’s already a 400 to 500 patient study to try to find 80 patients that are CtDNA positive after treatment and to give you a sense of that, almost 40 ish or so patients we have, it’s good we don’t want to be seeing positive results. We’re not seeing a lot of positive patients, which is good, but it’s not yet enough to sort of show that we’re able to, I don’t have it yet. I can’t tell you yet if we’re seeing a signal of clearance or not, with a small number, but committed to continuing the study. 

Dr. Parikh  50:27  
And then I think, mainly the updates from it that may not be yet, even on the clinical trials.gov was the HER2 edition, which I know I have mentioned to you. We have the cohorts that are just the MSS, getting FOLFIRI if they’re CtDNA positive versus randomized to a little bit more stringent surveillance than you would get under the NCCN guidelines. And then we have a Nivo arm for the MSI positive, HER2 arm for the HER2 amplified positive, and then the BRAF arm for the BRAF positive patients.

Dr. George 51:22  
I think that we are showcasing some of the trials in the COLONTOWN University website. So I think this might be a good trial to showcase. So maybe I’ll reach out to you after the call. So and then about Dr Cocorans trial?

Dr Parikh
Yeah. So no updates since ESMO, we haven’t looked,  so that’s the last update, but we had an expansion that already filled that BMS gave us for additional patients, so we’re looking through all of that now. Still have MSI BRAF spots open, but the BRAF MSS is finished accrual, and so now we’re looking at all their data. I think we’re hoping to repackage it, maybe for GI ESMO.

Dr. George  52:14  
Okay, July, then?  And then this is this question, some BRAF V600E patients in other countries are trying to replicate Dr. Corcoran’s and Dr Morris’s trial: checkpoint inhibitor + BRAF. Prior BRAF or IO, how has it affected the results? I think that he was allowing prior IO, and then, and now you’re not accepting it now…

Dr Parikh
We’re not Yeah, because it actually seemed the patients that were benefiting first were the untreated BRAF patients. So there were a few patients that had prior BRAF therapy that seemed to be benefiting, but it seems like the patients that were deriving the most benefit were not treated patients.

Dr George
Okay, okay, yeah. And then I think we’ve covered those questions. I was really interested in seeing that the 3TC results. I mean, are you planning trials? How can we help?

Dr Parikh
We are pitching it to a bunch of different people. So  we have five or six different schemas with different combinations, with radiation, checkpoint inhibition, with epigenetic drugs. Epigenetic space has been really tough for solid tumors, right? And so the companies that have guatacytabine, AZTEC, and ASA, given the challenges they’ve had, in solid tumors in the past haven’t been too key on a development path for solid tumors. So we’re trying, we’re looking at, potentially, there may be some opportunities just to do, like, via cooperative group, or Stand Up to Cancer, for example, like just in like a neoadjuvant FOLFIRINOX setting for rectal, sort of a proof of concept with 3TC and radiation. But we’re trying. we’re like, looking, we had some concepts brewing with ATM and ATM/ATR inhibitors, plus 3TC and IO, but biopharma is tough.

Dr. George 54:18  
Yeah. So again, in that also, are you seeing the LINE-1 expression in the TP 53 mutant? Like, I mean, actually, with patient selection, you should be able to get patients and I mean feasibility wise, it will be a great study, right?

Dr Parikh
Like, yeah. So I’m hoping, what’ll happen is once, if we can get these revisions out, it’s at a pretty high profile journal right now with kind of some major revisions. And so I’m hoping if that paper comes out in combination with this IPI and  NIVO study, people will kind of believe the story a little bit more, and then we have the tools, like we know how to select for these patients. So we’re not giving up.

Dr George 55:05  
Okay, I think the last question is about promising trials for all wild type MS patients. I mean, for  your patients, what are some of the things that you look for?

Dr. Parikh  55:16  
Yeah, we’re trying to look at some opening some new ADCs that are coming in the Phase I world. I’mnot gonna lie, I’m not too keen. We’re opening them because I think they’re good options to have. But some of the VEGF IO trials, I think we’ll just have to see where these Pembro lenvatinib Rego Nivo approaches. It’s interesting. You wonder if there are certain patients, liver metastases, patients where that may be more beneficial. And so it’s a little bit hand wavy now, but given kind of the responses we’re seeing with the TKI, VEGF combos in HCC, is there something about like liver mets or primary to see if that would allow those patients to benefit more. So very much looking at combination studies. But I think ADCs are another  area that we’re kind of paying attention to, in terms of companies that may have ADC for MSS disease. I think the other challenge with the MSS, which I don’t quite understand why biopharma hasn’t quite adopted is, sort of really looking at subsets of patients, right? We know, there was a TGF beta trial that ended up not showing.. the company ended up not deciding to put in colon cancer as an expansion cohort. But they didn’t select the right patients, right, that are kind of high stromal driven patients. And so I think, as we’re having conversations, trying to really encourage them to think about what the biomarkers are, and if it’s not CMS, is it things like this that can help us select patients.

Dr George
Yeah, it makes sense. So are you looking at the two ADCs, like the HER3 and the TROP2 those ones?

Dr Parikh
Okay, yeah, the TROP2. I think there are some, they’re looking at it potentially in the adjuvant setting too, using CtDNA too. So,yes. So exactly the HER3 and the TROP2.

Dr George
Okay, And then in your talk, you mentioned that you’re not a fan of stivarga, regorafenib- you choose lonsurf. Are you seeing that kind of a difference? Because the trials, they say they’re kind of comparable, but is there a larger number of patients that respond to lonsurf versus Stivarga?

Dr Parikh
I think so. I think I’ve seen true responses with lonsurf, and these are platinum refractory, 5FU refractory patients, Stivarga I’ve had very, very limited actual some disease control. But I’ve again, I just haven’t seen, I’ve seen maybe one true response. And getting getting to dosing at 160 is also really tough.

Dr George
Yes, yes, okay, it’s two o’clock. Thank you so much, this was amazing. The recording will be posted in COLONTOWN University. And thank you so much for your time and all the information. Thank you all for attending.

Dr. Parikh 58:19  
Bye, take care.

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2021
Dr. Parikh
ctDNA
MSS

Dr. Aparna Parikh  of Mass General discusses “Strategies for Making Cold Tumors Hot.” “Cold” tumors do not respond to immunotherapy. This DocTalk was recorded in the fall of 2021 with PALTOWN Scientific Director Dr. Manju George.

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Circulating tumor DNA: a new frontier in colorectal cancer

Circulating tumor DNA: a new frontier in colorectal cancer

DocTalk
2021
Dr. Cohen
ctDNA

Dr. Stacey Cohen of the Fred Hutchinson Cancer Research Center discusses circulating tumor DNA in this DocTalk, recorded for COLONTOWN in September, 2021. 

Manju George 0:00
Today, as part of Doc talks, we have Dr Stacey Cohen with us. She’s an associate professor at the University of Washington and an associate professor at the Fred Hutch Cancer Research Center, and she’ll be telling us all about circulating tumor DNA and its role in colorectal cancer. Thank you so much for doing this.

Dr. Stacey Cohen 0:19
Thank you. It’s a wonderful opportunity to get to speak with you, and I’m happy to talk today about circulating tumor DNA, which I’m calling a new frontier in colorectal cancer. Here are my disclosures.

Dr. Stacey Cohen 0:34
So we’re going to go over CtDNA, what is it? How do you detect it? Thinking about it as a marker of molecular residual disease, and then finally, it’s use in active cancer. So first taking a step back and what is CtDNA? So if we go at a really basic, basic level, inside every cell, there’s DNA gets converted to RNA, and then proteins, and from there, we can use those as potential, what we call biomarkers, or ways to try to sample what’s going on- that’s all within the cell. And then, if you take a single cell, and it’s a cancer cell, and it replicates and makes a tumor, then we’ve got a ball of cells there. So if we’re actually trying to sample or biopsy something, we could do our classic tissue biopsy, and then we have,a needle being put in, or a surgical biopsy, where we’re taking a piece of that ball of tumor. Or we could use blood based markers. So this could be something like CEA, which is a protein that’s made by the cells. Or the so called liquid biopsy, looking for circulating tumor DNA. And so this is a newer concept, because there you’re actually looking for the DNA of the cancer cells themselves in the blood. So in everybody, we have cell free DNA that can be detected, even in healthy individuals at low levels. And when it was first done as a screening tool, it was applied to prenatal screening- look for abnormalities in the numbers of chromosomes. So as an example, it could be used in a pregnant woman to look for trisomy 21 which is the hallmark chromosomal change of Down syndrome. But we now apply it in cancer to look for circulating tumor DNA, or CtDNA, which is the idea of looking in the blood for the mutations that we would expect to see in cancer, specifically.

Dr. Stacey Cohen 2:19
The reason why this could be very interesting is it gives us a real time sample of cancer activity. So it has a half life, or how long it’s around in the blood of less than two hours. So it changes very rapidly. And we know that there are some things that are good about it and some things that are limitations. So it is higher at higher levels of cancer. So we disay it’s cancer burden dependent. And there are ways that you could get potential false positives. So when we think about looking at CtDNA, there’s a lot of different ways that we can do it, but because it’s relatively easy to obtain, we can actually check this more than once. So we could do this early on.

Dr. Stacey Cohen 2:59
So this is kind of a timeline diagram here. So we could use it for the detection of cancer in the first place, hoping for screening or earlier diagnosis. We could think about it after a cancer is found, for molecular profiling or prognostication, to have an estimate of how someone might do with cancer. After surgery or definitive management, we could think about for detection of residual disease. If someone’s on longer term therapy, we could use it to monitor response to treatment. And then finally, we could do something looking for what’s called clonal evolution, or looking at the profile of different mutations in the DNA, and see how that changes over time, to try to see if that will help us better understand how to treat a patient.

Dr. Stacey Cohen 3:45
So when we think about methods for detection, there’s various different ways of doing this. There’s our basic PCR based approach, where you pick specific targets and it has fairly good sensitivity. Meaning that you don’t need very much of it to find it. And then we’ve got our fancier technology, next generation sequencing, where compared to the one target of PCR, we might look at over 1000 targets in this situation, and has much better sensitivity, though there is a range depending on the assay. Or you could do an even broader look, what they call whole genome or whole exome, where you look across the whole area, as opposed to specific area., And then you look at it with a little bit less sensitive approach. Within this we can also think about ways of detecting it that’s either what they call tumor naive so you’re checking the same sample or the same assay for every single person. Or tumor informed where you’re actually taking someone’s specific tumor sample and trying to find specific markers from the tumor sample that are also present in the blood. And with the data that we have so far, there seems to be some correlation between an individual’s tumor and finding it in the blood that might be a little bit more sensitive for molecular residual disease detection. Though, as I’ll talk about, as the assays get better, then that might not necessarily be the case.

Dr. Stacey Cohen 5:07
So this is not necessarily information that every patient needs to know, but I put this up here to say that there are pitfalls and limitations of CtDNA, just as there are with everything in medicine, and if something either isn’t collected correctly, or the person that’s ordering the test doesn’t know how to interpret it correctly, we can’t really use the information as readily. So again, important concepts are that it needs to be collected in the right types of tubes. This is not just a regular blood test. You have to know that you’re going in to order it. That the more cancer that there is, then the easier it is to detect it. And if you’re looking for really rare mutations, but you don’t have the type of test that’s looking for that, then you’re not going to find what you’re looking for.

Dr. Stacey Cohen 5:52
So as an example, this graph is supposed to show how different amounts of cancer in the body can actually affect the ability to detect CtDNA. So this person on the left here has a low amount of cancer, and so and then this person on the right has a higher amount of cancer, and you’ll see, in terms of the colors, they have more genetic variability. So if you’re doing blood samples, when you have lower amount of cancer, might be harder to detect the cancer at all. But as you get more amount of cancer, it’s easier to pick it up, and then you also get a greater variety of genetic mutations in your sample. So one way to overcome this is to take multiple blood tubes, and you’ll see that commonly, if you have CtDNA detected, or if you’re getting that drawn, that you’ll have two blood tubes, as opposed to our standard one blood tube because they’re trying to look for these rare mutations.

Dr. Stacey Cohen 6:45
So to kind of summarize the section of what is it? CtDNA is an emerging technology. It can be very useful as the so called liquid biopsy, as long as you recognize the limitations of this type of test and the particular platform or company that you’re using. The detection is based on the amount of tumor in the body, and tumor informed panels may be more sensitive, especially for molecular residual disease. Though, again, as the tumor naive platforms get better, they’re probably going to be more head to head. Next, we’ll think about this as a marker of molecular residual disease. So this is the idea of MRD, which either could stand for molecular residual disease or minimal residual disease. It’s been published in both ways. And this was done quite a bit in heme malignancy, so blood based cancers, with the idea that you’re looking in the blood to sort of see if everything is gone. And so the idea in a solid tumor is that we typically use scans to try to determine if the cancer is there or not, but what we’re actually looking for is with MRD, is trying to find an even smaller volume of disease sooner than you would be able to pick it up on scans or other clinical measures. And the idea here is that CtDNA might be that biomarker that helps us evaluate for MRD and might be able to pick up recurrences faster than CEA or other blood tests. The problem is, is that most of our analyzes so far have been retrospective or observational, which is a bit limited.

Dr. Stacey Cohen 8:15
So let’s think about how do you figure out if a biomarker is a good biomarker or not? The two terms that we’ll use to describe types of biomarkers, one is prognostic and one is predictive. So prognostic means, does it help us better understand overall survival. And predictive means, does it help us better understand treatment selection so that’s specific acute action. When we look at different patient samples in a retrospective series, so this might be, let’s say, a clinical trial, where they happen to check some blood samples along the way. It had nothing to do with the trial, but they looked back to see if they could find a biomarker for how people did. It could suggest a potential role, but there could be other causes going on, and it could be the result of chance, because it wasn’t really part of the trial. specifically. When we collect things in a prospective or forward moving way or in an observational way, this is better. But you need to have a certain number of events or occurrences of something that you’re interested in to be able to statistically say that something is different between groups. So again, in an observational study, that’s better, but we still don’t have a clear answer. So the best way to figure out that a biomarker is the right thing to do to make decisions on, is that it’s prospectively collected, and you’re actively making decisions in the study based on that biomarker. So for example here, let’s say we had a CEA, and we said, if someone had a high CEA, we were going to start a new chemotherapy regimen. If that was built into the study, and that was true, that that seemed to help people, that would be the best option for that test to become a new standard of care. So with circulating tumor DNA, we have some retrospective studies, we have some observational studies. But we’re still working on these prospective type studies.

Dr. Stacey Cohen 10:05
So why do biomarkers matter? Because again, we’re trying to help at time point zero decide how we should treat patients to try to get the best outcomes. So this is an example of a Kaplan Meier curve, and so at the top, at time point zero here we have 100% of people alive, and in this case, recurrence free. And if we look at the axes down here, we’re looking at time. So if we just take the black line in the middle in this supposed patient population, this is how all patients did. But we know some people are going to do better than that, and some people are going to do worse. So the question is, if we had CtDNA was a good biomarker. If CtDNA was negative, could we actually give them and we knew that those patients did better, could we give them less intense therapy? Or alternatively, if patients are CtDNA positive and are more likely to recur, could we actually increase or escalate their therapy to try to make it more intense and see if we can impact those outcomes.

Dr. Stacey Cohen 11:05
So now I’ll start to talk about some of the data where we’ve actually looked at CtDNA and see how it would impact survival. So first we’re going to start with prognostic markers, so looking at overall survival. This was done within the IDEA France study, which was one of the three versus six month trials. This one done in Europe, looking at adjuvant FOLFOX or CAPOX and stage III colon cancer. So they had over 2000 patients in the study, but about 1000 had Ct DNA that was sampled prior to the initiation of chemotherapy. There was a slightly higher risk population compared to the total sample. They looked at two methylated markers by PCR. So remember, PCR is kind of, in some ways, our most limited way of looking at CtDNA. And this was a tumor naive approach. So everybody got the same two markers. They showed that 14% of patients were CtDNA positive after surgery, and that the disease free survival was worse for patients who were CtDNA positive, as opposed to patients who were CtDNA negative. When they looked at three versus six months, this was significant within the three months population. And when they looked at low risk versus high risk, this was significant within the high risk population. So when compared to that example curve, where the curves could either go high or low with CtDNA, they did separate out the two groups, but maybe not as profoundly so as the cartoon showed. So this platform here is low cost. It’s very reproducible. It’d be easy for someone else to run this test. But the how useful this is, checking these two methylated markers is less clear because we didn’t see as profound differences.

Dr. Stacey Cohen 12:51
Next, I’m going to show some data from the Australian group, which has published a lot about CtDNA. And they were looking also at how does clearing CtDNA and checking it over time, how does that affect prognosis? So this is 96 consecutive stage three colon cancer patients who had surgery and then they were planned to have six months of adjuvant chemotherapy. CtDNA was collected after surgery and then again after chemotherapy. And in this particular one, they looked at 15 commonly mutated genes and picked one from the tumor to track in the blood. So it was a tumor informed approach. The majority of patients, but not all of them got an oxaliplatin based therapy. In this test, 21% were positive after surgery, and that decreased to 17% after chemotherapy. But where I think this is most interesting is when you look at patients over time. 25% recurred overall, and the majority of these were in CtDNA positive patients. And again, the majority of CtDNA positive patients did have a recurrence, which typically happened about two months difference from what you would see with imaging. So looking here, we see a more polarized difference between patients who were CtDNA positive versus CtDNA negative, but it was even more polarizing when you looked after chemotherapy in terms of survival being much worse in patients who were still CtDNA positive versus patients who were negative. So when we look at this over time, this is where I think it becomes interesting. So if someone was positive after surgery and they stayed positive despite chemotherapy, the survival was quite poor. But if they were positive after surgery and then cleared their CtDNA and became negative, their survival was much better. Similarly, patients who were negative after surgery did the best, especially if they stayed negative, but if they were negative after surgery and then their ctDNA turned positive, their survival is much worse. So this shows that this is a biomarker which is helpful, not just at a single time point, but also over time, and helping us understand prognosis for patients.

Dr. Stacey Cohen 15:01
So how does this compare to CEA? Because we have another blood marker. Do we really need something better? In this particular situation, the CtDNA outperforms the CEA. And so we can see here, patients who had the CEA elevated did worse in purple versus the patients who are negative and in green for normal. But I think the interesting part is when you compare both CEA and CtDNA. So there were six patients that had high CEA and also who were CtDNA positive, and five of them recurred, so almost all of them. But when you looked at the discordant ones, there were six patients who were high CEA, but negative CtDNA, and only oneof them recurred, suggesting that the CEA was not the best predictor, and CtDNA may be better. If we compare it to when we would have seen it on scans, this is two different studies, this is sort of a funny curve, but you read it from the bottom, so time to detection of relapse. Here’s zero time point down here at the bottom. And in the blue dots we have CtDNA, and in the yellow dots we have radiographic. And if it’s pointed up towards the left, it means that it took a longer time to see it on scans. And a median of 8.7 months in both trials actually. In a separate panel where they did a tumor naive panel, the lead time was 11.5 months, suggesting that those tumor informed approach may be better.

Dr. Stacey Cohen 16:37
So of course, though, we don’t just live in a bubble, and we want to say, is there something that we could actively do to try to help patients clear their CtDNA? So then we look at, does giving chemotherapy actually help us do that? So in this study, we have 130 colorectal cancer patients, and 89% were positive before surgery, and 11% were positive after surgery. And when we look at that after surgery time point, the majority of patients who were CtDNA negative did much better than patients who were positive. If we look at how chemotherapy influenced that, approximately 70% remained positive despite chemotherapy, so only 30% were able to clear their CtDNA. But if they did, and they got grouped in this upper group, they tended to do better. So this particular tumor informed panel seems to help us make some decisions. But again, downsides of this type of panel is that it’s expensive, it’s proprietary, so you send it off to the company. We don’t really know which specific gene they’re testing. It requires tissue, but it could be highly informative and give us much more interesting information and helpful information than we might have had with some of the more rudimentary approaches from before. But the more that these panels improve, the better options we have.

Dr. Stacey Cohen 18:07
So this is very recently published data. 84 patients of colorectal cancer undergoing curative intent treatment, all stages and you can see there’s a variety of stages here. 45% in neoadjuvant, 54% had adjuvant therapy. So there’s a variety of treatment patterns. 24% were positive for their CtDNA, and when we look at recurrences, so 36% recurred. It was much more common in the CtDNA positive folks than CtDNA negative. And the sensitivity while low with that original panel, when they added epigenetics or methylated markers, then we could improve the sensitivity. In comparing that with CEA, as you can see here, it really wasn’t as helpful with CEA alone. So again, in this sort of newer version of a tumor naive panel, again, expensive and proprietary, but has the potential to be highly informative and have rare false negatives. So some folks have said, we should be doing this type of platform for most patients, because you don’t have to wait for the tumor sample and have enough tumor to biopsy, and it takes a little longer to get that first result if you’re using a tumor informed panel. But I will say that in looking at the trial itself, they still had quite a few patients that had some either sample quality issue or limited sample issue where they couldn’t run the test. So in neither the tumor informed or tumor naive is there a sure thing to do. So we leave it right now is that we have a couple of different options that we could do.

Dr. Stacey Cohen 19:47
So could we actually change our treatment plan based on the CtDNA? So again, this is going back to the Australian group. So this is stage II colon cancer, and patients had surgery. And they got adjuvant chemotherapy, as was recommended by their physician. But recall that many people in stage II, and probably most people in stage II, did not get chemotherapy. As expected, it wasn’t as common to have CtDNA positivity, but 9% had it after surgery, and it did reduce in patients who had chemotherapy. So if we look at their CtDNA status again, patients who were negative did much better than patients who were positive. And if we look at clinical risk factors, so like T stage and other surgical features, patients who were considered to be low clinical risk did better than they were high risk, but maybe not as profoundly separated. Where it’s interesting is if you take this low risk group and you say, is there any way to figure out, just becauseyou’re T3N0 does not mean you’re never going to respond, its just less likely. So if we look at that low risk group and break it down, patients who are low risk and CtDNA negative did really well, but patients who are low risk but actually had CtDNA detected, they did much worse. So this suggests that maybe we could actually figure out which of these stage II patients we should give chemotherapy to, if we were able to separate out, not just by CtDNA, but also by looking at our clinical risk factors and combining the two together.

Dr. Stacey Cohen 21:21
I want to point out that a lot of what I’ve showed has been colon cancer, but we do have very similar data in rectal cancer, just not as much of it. So this is an example of one of these studies where we have, now radiation included, and we’ll see that from diagnosis to the end of radiation to after surgery, we see a decrease in the detection of CtDNA. And if we get all the way to that point and someone’s after surgery, again, someone who’s CtDNA undetectable or negative at that point has much better outcomes than someone who has positive CtDNA. This particular study did not include TNT or total neoadjuvant therapy, where we’d be giving chemotherapy in the neoadjuvant setting or before surgery, but it remains interesting and good to know that these patterns exist in rectal cancer as well.

Dr. Stacey Cohen 22:09
Now when we’re able to be aggressive in stage IV, of course, we can sometimes take these patients through surgery as well. And then we would want to know if what we’re doing in earlier stage disease also applies to stage IV. So this is some data that I presented last year, which is a so called “real world” approach, where this was clinically ordered CtDNA. So again, observational data, without being within a clinical trial. But what we could see again is that for patients who had pre surgical testing, that CtDNA was commonly detected. And it was found still after surgery in about half of the patients. If they got chemotherapy, it was suppressed, but again in the surveillance time, so after the chemotherapy was done, we still saw CtDNA positivity in about 50% of patients, which goes along with the expected relapse rate. I haven’t mentioned it too much, but we can also quantitate the CtDNA or give kind of a number to that positivity. And as we would expect after surgery, the numbers would go down, and then when we’re starting to pick up on that CtDNA in the surveillance setting, it’s going to be a lower number, because we’re looking out for recurrences in a faster timeframe.

Dr. Stacey Cohen 23:24
This is a bigger study with that same assay. So again, looking at metastatic patients in Europe undergoing curative intent treatment. And they had their CtDNA checked at some defined time points, and a portion of them had adjuvant therapy. Again, about half of patients had CtDNA detected after surgery, and what they were able to show again is that recurrence was higher in the CtDNA positive folks, 98% versus 37 of negative.So again, just because your CTD negative does not mean that the recurrence is zero, but it does suggest that it’s a much lower risk. If we look at a single time point after surgery, we see that there is good separation of the curves, and CtDNA negative patients do better than patients who are positive. And if we follow with multiple subsequent time points, then we can really tell that better over time. And I put some of the information here. So before we were talking about a lead time from imaging of 8, 9, 11, months, because these patients were being imaged a lot more often being stage IV, the lead time was 3 months, but still preceded what we would expect for radiographic occurrence. So to summarize this section on MRD, ctDNA positivity at the end of treatment is associated with worse outcomes. Detection of CtDNA during surveillance is highly associated with recurrence and may precede what we would see on imaging by several months, but we still need prospective data to use CtDNA to adapt therapy recommendations.

Manju George 25:04
Dr Cohen, can I ask a question? This is excellent. Lots of great information. So my first question was about the rectal cancer trial, where you said that they were doing radiation and then using CtDNA to show that after every step, the CtDNA levels were coming down, right? My question was did they mention in the study,what is a good time after radiation therapy to do CtDNA testing?

Dr. Stacey Cohen 25:32
Yeah, I think it remains a good question. I don’t think we fully know the answer. So after surgery, we typically say two to four weeks would sort of be the ideal time to check that. And there’s been other studies trying to find that key time point. It’s a little harder after radiation, because you don’t just take the tumor out of the body and then the blood can clear. Here, there’s a process of cell death that can last six eight weeks, so I don’t think we truly know, except to say that very few people are willing to wait that full six to eight weeks to find out just on a blood test, what’s going on. So I would think checking it around the four to six week mark might make the most sense. But in reality, we could be checking it sooner. I think we just don’t have the data for different time frames to understand when the best time is.

Manju George 26:20
Okay, thank you. And then my other question would be about what you just showed the stage IV treated to Ned, so the right side graph said that 37% recurred even when they were CtDNA negative. So was that like one time testing?

Dr. Stacey Cohen 26:40
They did a couple of time points, but again, it was still kind of an observational study. So we don’t know if that would really exactly mirror what’s currently done in clinical practice, but they did have a few time points that were checked there.

Manju George 26:58
Okay, so in relation to that, is it true that, like, for example, with early stage they say that the the highest chance of references in the first 18 to 24 months after the end of treatment. Does that hold good for this group, stage IV treated to NED?.

Dr. Stacey Cohen 27:13
Yeah. So I mean, many of the CtDNA studies are only checking it for two years after the time of surgery, regardless of any chemotherapy or anything else that’s given with the idea that if by the end of that two year time frame, you’re still negative, you also have this lead time, hoping that that would be farther than what you would see on imaging. And so two years should be sufficient, because the majority of recurrences do happen in that early time frame, and probably happen even faster for stage IV.

Manju George 27:43
Okay, thank you very much. Yeah. Does anyone else have questions? Or can we go forward? Yeah, I think so.

Dr. Stacey Cohen 27:53
Great. Thank you. I just wanted to throw up here a couple of studies, because of again, it’s really important that as we learn about CtDNA, that we’re supporting the efforts to learn more. So we really can make this part of practice, if that’s the right thing. And so I just included a couple examples of studies. There’s not a lot out there, but there’s a couple of examples, so we can both think about de escalating or escalating therapy. But the ones I show here are largely looking at, can we give different or more intense chemotherapy for patients who are CtDNA positive? And I expect that this is something that is going to be very well studied in the future, moving forward.

Dr. Stacey Cohen 28:35
So lastly, I’ll talk about the use of CtDNA in active cancer patients. So we already talked a little bit about a tissue biopsy versus a liquid biopsy. So the liquid biopsy is certainly less invasive, has less cell content, and there are pluses and minuses with it, but it is relatively easy to obtain. Does it actually matter, though? So this is an example of of why we could still use it. So this is an example of metastatic colorectal cancer patients who are receiving first or second line therapy. 77% had detectable ctDNA at baseline. Now this is lower than some of the other studies, and again, it also refers to what type of panel you use. And I think a bigger take home point is that it really matters which panel in which study, because we can’t necessarily say that we learn from one study to the next. And then, you get one company and then the other company, because each one sort of has to be replicated on its own. But within sort of the general concepts they seem to be the same. So what they showed is that higher levels of CtDNA were associated with worse survival. Which sort of goes along with what we’ll see with CEA, so maybe not that different. We can use it to detect commonly altered mutations. So KRAS, BRAF, these are key molecular markers that we need to know about every metastatic colorectal cancer patient. In this particular study, all had detectable CtDNA, and it had very good accuracy when we compared tissue to the blood based assay, so showing that these were reliable ways of checking it. But a more interesting thing that we’re starting to think about is, could we use this more longitudinally? Could we do this over time, to try to think about re exposure and whether or not that’s working? So as an example of this, this is the CHRONOS study that was just presented at ASCO this year. Patients who had prior EGFR therapy, not right before, but at least two lines before. So think of it, maybe someone who had it in first line, then they added different therapy in second line, and now you’re trying to decide what to do for third line. They used digital droplet PCR, so again, our more basic method, on cell free DNA to look for resistance mutations. And if patients seem to still be RAS RAF wild types, suggesting that they might respond to EGFR therapy, they were offered to go on this re challenge study where they received EGFR inhibitor again. And the response rate was 30%, they said they expected a response rate if we hadn’t done this test of 20%, so maybe it was a little bit better. And disease control rate of 63% with a progression free survival of four months. But what it concerns me a little bit is sort of what we see here over time. So this spider plot, what it’s showing is how patients did over the course of the study. So for lines that bend up, those are patients that are progressing. And in red, we have patients who cross the threshold where they’re going to call it progressive disease. In gray, you have the patients who have stable disease, and then in green, patients who actually hada response. And so you can see here that there is a group of patients that seem to respond, or actually have at least 30% tumor shrinkage. But those responses don’t seem to last very long, so almost as soon as they go down the lines go back up, suggesting that those responses were not durable or not maintained. So it means that, yes, we can potentially re expose patients to older therapies, but it still always begs the question of, did it work and is it worth it? And I think that’s something we’re still trying to figure out.

Dr. Stacey Cohen 32:19
One nice thing about CtDNA is we can use it to detect rare fusions. And this is important because sometimes there are targetable mutations and therapies like NTRK. And might work better than than tissue in certain examples. So for NTRK, specifically, if we look at it here, they were able to detect it at a slightly higher frequency as compared to tissue. But again, if we look at the scale here, these are incredibly rare. And notably, there was a lead time or difference of 24 months, (two years), between when the tissue was collected and when the CtDNA was collected. So if you think that someone’s mutation profile may be changing over time, going back to the old tissue and trying to find a mutation may be less helpful. But of these, the only one really approved for colorectal cancer is NTRK and they’re very similar. So I’m not sure that we necessarily need to all go out and get retested, but I think it’s just important to know that this could work quite well.

Dr. Stacey Cohen 33:21
Microsatellite instability is a lot harder because it’s not one specific genetic marker, but you’re looking at this pattern of change in the tumor. And so when we look at CtDNA versus standard methods, it seems to work pretty consistently. When we compare it to PCR and NGS, there are some discordant cases. So these are the ones in blue here where the CtDNA was positive, but the tissue was negative. And it probably has to do with the fact that IHC can sometimes be a little bit buggy, but in general, it was very well concordant, which are these dark gray and red bars that you’re seeing here. Again, we can use this over time. So this is an example of monitoring CtDNA while someone’s on therapy. So these patients were getting PD-1 therapy. And so this was from not just colorectal cancer, but other cancers as well, as long as they were MSI and getting this PD-1 therapy. And when we look at progression free survival, we see some differences.Looking at the tumor mutation burden in the plasma, patients who started out high did better than patients who were lower. And interestingly, you would expect all these patients were MSI by tissue, and so that’s how they got enrolled on the study. But what this was showing is that if we actually looked at the tumor mutation burden by the cell free DNA, that was probably a better marker for tissue response than looking at old tumor tissue for MSI analysis. So maybe it’s because it’s real time. Maybe it’s because there’s some variety what they call that mosaicism, where there’s different patterns of mutations in different parts of the tumor. And that kind of gets equilibrated out when you take a blood based test, but it’s interesting and thought provoking. Again, we right now don’t do this in trials. We don’t know if this is really the right or wrong thing to do, but it is interesting that maybe this could be something we would start doing.

Dr. Stacey Cohen 35:18
So finally, to summarize, so non invasive, liquid biopsy can be helpful to assess the cancer profile, or if a tumor biopsy can’t be obtained, then we could definitely use that to do molecular markers. Some platforms, but not all are validated for MSI or tumor mutation burden. And so these are things that, of course, if we were checking that we’d want to know in advance if our panel could do that. And importantly, if we take these tests over time or serial biopsies, we can sometimes watch how someone does, either from resistance or success, but the problem is we don’t know how to apply this to the clinic. And there remains issues regarding cost and reimbursement. So where are we at today? With CtDNA, these tests can be ordered by your physician. We can debate tumor informed versus tumor naive type panels, and there are good options and bad options for both, and there’s pros and cons of each strategy depending on the platform. So it would be deciding with your physician which they’re comfortable with and what you’re kind of looking for. The problem is it’s not yet clear how treatment decisions should be changed based on CtDNA results for minimal residual disease. So at this point, I consider it as another leg to stand on. We have our clinical factors, we have our imaging, CEA, and now we have a fourth leg to that stool, which is CtDNA, but by no means is it the be all and end all. It’s also not currently part of the NCCN or national guidelines, and I highlighted some of what they put here, which is that we right now don’t have that predictive data. We don’t know how we should use the CtDNA results to absolutely change therapy, and so because of that, we don’t yet recommend this for every patient, but the NCCN encourages enrollment in clinical trials, because we think that at some point this may be really useful information. And with that, I’ll say thank you for listening.

Manju George 37:09
Yeah, thank you so much. This was great. I have a couple of questions. So your slide on NTRK fusions. You thought that both the tissue and CtDNA were kind of similar, right? So do you suggest, then that for people who are interested, it’s best instead of having a new biopsy or tissue biopsy, it might be just better for them to do a blood test, right?

Dr. Stacey Cohen 37:34
Yeah, I think it would be fine to do a blood based biopsy rather than going to the old tissue if, it was that or get a new Bnew tissue biopsy, it might be very reasonable just to do the liquid biopsy instead.

Manju George 37:49
Okay, my other question was, like, I was kind of interested in what you said about that figure for MSI high, where you had that blue box, where there was some discordance between tissue IHC and CtDNA. So from your personal experience, do you think that the CtDNA test is better than the IHC? Does IHC have more false results? Is that what you meant?

Dr. Stacey Cohen 38:14
Right. So IHC, even though it’s one of the most common ways that we look for MSI in the tumor, it does have some errors, because we can’t always tell, it can show artificial loss of expression at the wrong times. And so my institution, for example, pretty much only runs next generation sequencing because we think that it gives the highest quality result. And so this would be next generation sequencing on the tissue. And I would say that versus the liquid biopsy are probably pretty similar. But it’s a more complex test to do NGS, more expensive, and so depending on institution and resources, IHC is still done routinely, but there sometimes is some interpretation that’s needed for it.

Manju George 39:07
Okay, my last question was about CtDNA for MRD. What you mentioned was the NCCN guidelines and all about escalation or de escalation of therapy. What is your opinion about using it for surveillance post treatment?

Dr. Stacey Cohen 39:24
Right. So I think that different providers have their different biases about whether or not they think that this is potentially a useful platform. Clearly, I have some bias thinking that it could. But I also remain cautious, because I’ve had patients say, start chemotherapy in the adjuvant setting, let’s say for low risk stage III, and say, okay, my CtDNA came back negative, can I stop? And I’m not yet comfortable making that determination. So I say it just gives us more confidence in maybe what we’re planning to do anyway. So if we were thinking, okay, you have a high risk stage II, and you really wanted to stop at three months, because we think that the differences in survival are only a couple of percent there. Maybe that CtDNA would give us some confidence, if it was negative, to stop early, and if it’s positive, maybe that would give us some motivation to say, let’s really try and clear it with the six months and see if that helps. So I think that it can kind of add to what you’re going to do anyway, which is why I think of it as another leg to stand on, as opposed to the only thing that’s determining how we treat patients.

Manju George 40:36
So but what about like, two years after adjuvan therapy? Would you recommend that among all the other tools, like, forexample, a patient who’s CEA is not useful. If it was like one or less than one, what in your mind would be the value of using a CtDNA test for surveillance?

Dr. Stacey Cohen 40:55
So I like to use it for my patients. Again, not everybody does, but I have been checking it on a lot of my patients. However, if someone was already a year two years out, I probably wouldn’t start checking it now, because I think in terms of timelines, the majority of the recurrences do happen earlier on, so I don’t know how much benefit we would getin starting to do surveillance testing at this point. But if someone was newly in the last few months, had had their surgery, then I think would be reasonable to ask your provider about if this was a test that would be useful.

Manju George 41:32
Okay, okay. I think we have one question in chat. Yeah. So he said the heather, do you want to read your question?

Heather 41:44
Yeah, sure. Thanks. So unfortunately, we just haven’t been able to get any traction with getting my husband’s care provider to even really have a conversation with us around potentially ordering a CT DNA test and the unfortunate thing is, his scans, nor his CEA level have given us any insight, and so I feel like this could be potentially beneficial. And when I had the conversation, I said, I don’t necessarily want to do this for you to drive treatment considerations off of but I think informationally, it may potentially give us a heads up. And I mean, they just shot us down quickly and wouldn’t even… So I mean, is there something I could say differently, or a way I could phrase the question or go about it to maybe get them to entertain the idea?

Dr. Stacey Cohen 42:34
Yeah, I think it’s really hard. Because, again, I think to some degree, like anything new, there’s kind of believers and non believers, and it might just be that the physician that you’re currently working with just doesn’t feel that it’s going to be reliable, or doesn’t think that we will know how to interpret the information well enough. And I mean, there’s a good lesson in medicine, which is, don’t order a test that you don’t know how to act on, right? So, but at the same time, I think that you named some really important features, which is when if we’re standing on those four legs, and we can’t stand on the CEA one, and the imaging is a little iffy, then it’s a lot harder to do surveillance reliably. And so, I feel like I might, not knowing the full story, I might be comfortable ordering in that situation, but a colleague might not. And so maybe one thing to do is just to consider a second opinion of someone at an academic institution nearby, or if you’re at an academic institution, a different one, and see if just a different provider might be more open to it, because I’m not sure you’re going to be able to change someone’s mind, because, again, the should part is not there. But I can tell you, anecdotally, I’ve had number of patients where the regular scans were unrevealing, the CtDNA went positive or high. And then we did a different type of scan, like an MRI or a PET scan, because of their unique situation, and we did detect a recurrence. So I have had situations where I do feel that the CtDNA helped me, and often it was in patients where the CEA was unrevealing, because not everyone makes CEA, so we don’t always have that as an option.

Manju George 44:20
Thank you. Thank you. Yeah. And what we have done in COLONTOWN is that since people started using Signatera, we have a Google Doc, or a Google sheet where any person who has ever had CtDNA testing would write the name of theirdoctor and this cancer center where they got the test. So our idea was that, when you have a new patient coming in and who’s interested in Signatera, we would say, hey, take a look at the list. If you have a doctor in your institution, somebody else who has ordered the test, the simple thing would be to tell your oncologist. Could he or she talk to that person ? Maybe that would change their mind. Or if you see the list and then see that they’re not the only person in that whole state using it, but there are a couple of people who have used it, maybe that would make them want to learn more. And kind of be helpful for the patient. The other question that I had is, like, recently, we have seen some plasma TMB tests that people are getting, and then the values are, like, 30 or 40 or something like that, when compared to, like tissue TMB, where the FDA approval for pembro, for example, is at beyond 10, right? And then there is some confusion, because, I think that there was maybe one paper or something which said that a plasma TMB of 18, maybe or 28 I don’t, can’t remember it right now, that was somehow similar to a tissue TMB of 10. I mean, I see these kinds of comments where people are confused about how to interpret it, and especially when they see the numbers, they’re like, Oh, should we be doing immunotherapy now that we have the number?

Dr. Stacey Cohen 46:08
Right. And I mean, I would say, even with tissue, we think that people are unlikely to respond at 10. With colorectal probably need 12 or higher so, and maybe even 15. So even though the FDA might make these blanket statements within an individual cancer, it might not be exactly correct, so I have to look at the specific test. But again, I think this goes back to that issue that even though we think of CtDNA as one concept and tissue is another concept, each individual person running the test may report out or analyze the data differently, such that we can’t always apply it across different ways of looking. And so we’d have to look and see like, kind of what their scale is in that particular plasma assay for how they call higher or lower, and then try to kind of equilibrate that down to what we would do for standard tissue based testing. Yeah, but yes, it’s incredibly confusing. Yeah, which is why I think a lot of doctors are not ready to order it, and that’s okay, because, again, if you don’t know how to interpret the results, as many providers do not, then it makes sense to not order the test that you might not feel comfortable with. But I think that this is a technology that is not going away anytime soon.

Manju George 47:24
Okay, thank you so much. This was great, and I’m hoping that I can edit it and post it in CTU so you can take a look and you’re welcome to share it with your patients, or you know however you want to use it.

Dr. Stacey Cohen 47:35
Okay, sounds great. Okay. Thank you. Bye, everybody. Thank you.

Manju George 47:38
Thank you! Bye. Thank you all for attending.

DocTalk
2021
Dr. Cohen
ctDNA

Dr. Stacey Cohen of the Fred Hutchinson Cancer Research Center discusses circulating tumor DNA in this DocTalk, recorded for COLONTOWN in September, 2021. 

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Tackling targeted therapy refractory BRAF V600E mCRC

Tackling targeted therapy refractory BRAF V600E mCRC

DocTalk
2021
Dr. Kopetz
BRAF

Dr. Kopetz of MD Anderson discusses options for therapy refractory BRAF V600E metastatic colorectal cancer in this Doc Talk, recorded for COLONTOWN in August, 2021.

This is an automatically generated transcript.

Dr. Scott Kopetz 0:00
So thank you all for coming together and spending a little bit of time to talk about how we’re tackling targeted therapy refractory to BRAF, decent center D, metastatic colorectal cancer. I am Scott Kopetz faculty at MD Anderson. I had a few slides just to kind of set the stage and where we are. And then we’ll dive into some discussion on, on, some of the efforts ongoing, just to set the stage a bit, I think this group knows well that BRAF has been a bit of an enigma for colorectal cancer, in the sense that that treatments that have worked well in melanoma did not work well in in colorectal cancer, even though the same drug, same mutation, and so this really kind of sets the stage for a lot of how we are thinking about a kind of a treatment refractory colorectal cancer. What are the key findings? And I have just a few science slides here to show but some of the key findings is that really we have in colorectal cancer, we had a hard time really fully inhibiting that pathway. So when we give a drug, what we can see is that in melanoma, you get really nice inhibition of the pathway. And so what we can see in western blots is where there’s a dark, dark line that’s an expression of a protein. And so this is signaling through this key pathway that we’ll come back to in melanoma, really single dose of the drug, and you get this complete inhibition, you know, whiteness here on this area, but in colorectal cancer, on the top, what’s seen is that you get very transient inhibition, and then the signaling starts to restore. And so this is kind of the science that’s the fundamental behind the issue in colorectal cancer, which is one of kind of adaptive resistance. And so adaptive resistance is, I describe this as really kind of the homeostatic regulation. So networks have a way of wanting to go back to where they were. And so, you know, when you have a really complex system, think about, you know, a the power grid, right? Someone can, can drive into a power pole, knock it down, the lights blink, and the power is back. You know, before you’ve had, you know, a chance to even acknowledge that the lights were temporarily out because the network has a lot of redundancies and other pathways, and is the networks restored. And so the same thing happens in biologic systems. And so cancer has a set point, like a thermostat of where it wants these, these pathways to be, and when you try to perturb it, what the system does is it is it adapts and rewires to try to restore that signal. And so what we’ll be talking about is really this concept of adaptive resistance, homeostatic regulation. So what does that look like? Well, it means that this is our signaling cascade, where we have growth factors that come in, and these are a series of cascading proteins that signal one into the other. And they do these in a way to try to coalesce a number of different signals. So we have this as a very linear process here, but there are multiple growth factor receptors. We’ll come back to that, that all kind of feed down into this growth signaling pathway here. And there’s also amplification steps that occur. So each step down, the signal gets amplified, other inputs get interrogated. So the end results is, you have ERK, which is the factor that really goes in the nucleus and that starts to change the program of the cell. So what happens is, when you give up the BRAF, the here, green is activation, blue is is, is quiet or inactivation. We give a BRAF inhibitor. You get a transient inhibition downstream signaling. What happens is you see all these arrows going up. These are some of the adaptive feedback mechanisms. And what happens is this, these negative regulators then get inhibited as well. So you’re inhibiting a negative regulator. What happens now is then you get upstream activation. And so this is where we see EGFR now, all of a sudden become important. Signaling drives this, and it drives through KRAS and then BRAF is a family of RAF. There’s ARAF BRAF CRAF, right. And within our cell, we’ve got one mutated copy of BRAF and a colorectal tumor. But then there’s a wild type BRAF that’s there as well, right? So they have two copies of everything that get passed along in most cancers. And so what happens is that it can use the existing normal signal signaling, kind of signal around the BRAF, and then restore the pathway homeostatic response. And this is how the tumor so the key finding was that when you inhibit EGFR as one of the kind of key feedback mechanisms, now you block BRAF, you block what pops up, and then your signaling can be inhibited. And so that’s the was the rationale between a lot of studies and just highlighting the one that led to FDA approval, the BEACON study, of course, where we’re looking at the doublet of a BRAF and an EGFR inhibitor versus control. And that was what ultimately the FDA approved as a current standard of care. Now there was another arm, bimimetinib, and that was the MEK inhibitor. And so the idea here was, well, maybe we just need to hit a little bit further downstream with the MEK inhibitor, and that’s going to even any leakage that we had, maybe that’s going to blunt it even further, right? And so that was the hope. Now we know, unfortunately, that this hypothesis didn’t pan out, and that when we looked at the overall survival, we saw clear improvements with the BRAF and EGFR, but the MEK turned out didn’t do anything, right and and you know, part of that is, you know, the balance of toxicities and efficacy, and that’s despite the fact that what we see is, we saw higher response rate, and I won’t show you the data, but you know, we saw that the tumor shrink down more. They just didn’t stay down quite as long, or they stayed down just as long, I should say, is the BRAF and EGFR alone, so that added toxicity didn’t really provide any benefit for patients long term. So, you know, this is where the field has been. And really kind of thinking about, how do we inhibit this, and how do we improve upon it? And what I want to highlight, because this is certainly an area of interest to this group, is how do we really understand signaling at progression and clinical approaches to modulate resistance, and so that really kind of sets the stage. Now we’ve known for many years, and this is now almost worked far as maybe 10 years ago, that at the time of resistance to some of these inhibitors, you get number of different things that can occur, EGFR amplification, KRAS amplification here, and there’s a number of these different things that have been seen circulating tumor DNA has provided a lot of insights into terms of KRAS and NRAS mutations that also appear. One of the key features that we see is that all of these are converging onto what we call a MAP kinase pathway reactivation. So this is intriguing, because in other settings and other tumor types, you may have resistance that develops to a treatment, but it may be four or five very different pathways that may get turned back on right. maybe this pathway over here got turned on in one patient, a different pathway in another patient. But what we can tell, and I think we’ve now seen enough to say that this is probably the vast majority of patients. Then the tumor starts to progress on treatment. It’s still very dependent on this exact same pathway, the matpatus pathway. So even though there is a whole smattering of different mechanisms, they all appear to be going down to the exact same pathway. So it is useful sometimes to understand why patients are progressing on a given therapy. But that doesn’t preclude the fact, even if we don’t know that, we just know by all the studies that we’ve done what the tumor is still dependent on. So in we borrow a lot of evolutionary terms in cancer biology, so we call this convergent evolution, right? And so this is the classic like we learn in biology, that the sharks and the dinosaurs, the reptiles, penguins,dolphins, mammals, looked very different a long time ago, but they all evolved to have a very similar shape, because that was the most efficient when you’re swimming through the water, right? So this idea of kind of multiple different mechanisms to get to the same, the same behavior pattern. So that sets the stage for a number of different strategies. And there are studies looking at Other MAP kinase pathways. There’s a few different ERK studies, so Lilly studies, Asana ERK inhibitors, for example. And then kind of a big study that Novartis is doing, looking at a number of different combinations here. This is a word salad here. I’ll put the PD-1 kind of at the end, and we’ll kind of come back to that one in a minute, because that’s a bit of an outlier in the concepts that we’re discussing in these other items. But the idea here is, how do we learn from these and how do we try to explore what’s going to be best tolerated and give us that best therapeutic window? So we go back to our now slightly tweaked pattern here. This study is actually looking at BRAF, the bratinib, and an erk inhibitor. And so you can see that it’s under my yellow X here. But this is the ltt 462, inhibitor, erk inhibitor, that’s being utilized. And the idea is that we really want to try to block these downstream signaling, but erk inhibitor alone can’t fully shut off signaling, and that that there’s if there’s a lot of signaling from above, there’s still going to be leakage through. So it’s really about, how do you try to tamp down that upstream signaling? And so the three areas that are being looked at are, well, mek, so let’s just BRAF, mek, try to really go downstream. Find best doses for those instead of MEK, there’s others looking at pan RAF. So that’s the LX 254, Pan RAF inhibitor. Remember I said RAF is a family, so it’s kind of ARAF BRAF CRAF so you’re trying to kind of block that bypass where everything upstream is sneaking around, BRAF to get through. So that’s shutting off another leak in the dike, as it were, and then the other is looking at shp2. Now, shp2 is a is kind of an adapter. You also may hear a sauce inhibitors and their sauce MEK combinations being explored, but, but recognizing that there are a number of different rtks, fgfr, EGFR, pdgfr, all these have been implicated at various times or others. And while we think EGFR is a dominant one, certainly we see other ones appearing there for family members as well, and they all feed through shp2 to then activate KRAS. So this is kind of the funnel, you know, it’s a area, and the funnel that, if we hit inhibit shp2 , in essence, where it’s like inhibiting a lot of the receptor tyrosine kinases and so, which is good, but it also can come up with some toxicities, because you’re inhibiting, you know, EGFR and lots of other, you know, her family members and so. So trying to, you know, find these right combinations, our goal then as well. So these are kind of some of the combinations that are being explored in these studies. And this is just showing, you know, the study and how that’s being explored within the water study in particular. But let’s go back to erk inhibitor for just a minute. And again, we’re inhibiting this downstream. And there was some early work, maybe five years ago now, kind of showing in a number in this red box, yellow means more inhibition. That when you give a HERK inhibitor, especially in combination with some of these, that you can improve activity, and that this is another preclinical work now showing that a lot of the doublets here, even the triplets, BRAF mek, EGFR, don’t see a lot of regression in some of these models, but it’s only with the addition of erk top of some of these BRAF targeted strategies that make sense. So you know, there are studies launching looking at BRAF, EGFR, erk, for example, to explore that. And one of the things is that, and this was some really nice work where they looked at Mark good, and this is out of Ryan Corcoran’s Group. So this is a slide from him, where they actually looked at a number of different combinations. And then when they did the combination with the ERK inhibitor, what they could do is prevent outgrowth of some of these clones, right? So the kind of KRAS clones that were present that could prevent those from growing out. So that was, you know, some of the rationale for exploring that. And so I think, you know, just acknowledging, of course, what we know that we need novel therapies. Here we have encorafenib cetuximab. And there’s a lot of work going on about, how do you move into first line or into adjuvant setting? And then some of these, you know, combinations there as well. One final comment about PD-1. So there’s a about 20% of patients with a BRAF metastatic BRAF tumor will also have an MSI high, and that responds well to immunotherapy, but there’s a proportion of patients that progress immediately in immunotherapy and don’t respond. And so there’s a question about, well, what if you target the BRAF, EGFR, and the PD-1, for example, is that something that could be beneficial. And this parallels a whole other area of work that we and others are working on, thinking about PD-1 in a microsatellite stable population. And so there’s NCTN, a large US cooperative group study that’s launching looking at a BEACON regimen and corrective Cetuximab with or without a PD -1 inhibitor for MSS patients. But the Novartis study, for example, is really looking at, can you improve upon outcomes in the MSI high population as well. So there’s a lot of kind of really interesting biology there. So with that, I’ll, I’ll stop and and, you know, take any questions and really make sure I have some time for some discussion around this really interesting area.

Manju George 16:37
Thank you so much for that introduction. So we have got nine questions, and I’ll go through them quickly. The first one was about about the trial design itself. The question was, can the same patient be on two different arms of the trial at two different times, since this is a safety trial,

Dr. Scott Kopetz 16:55
Yep, yeah, there is a safety and then an expansion cohorts in there as well. There’s nothing in the in the trial that prohibits that there are two different cohorts for groups of patients that have not had encorafinib cetuximab before or not any MAP kinase targeted therapies before, and those that have. And so there’s a possibility to go on those that have not had it get treated with it and then potentially re-enroll in the converse. There’s not anything that is in the current version of the protocol that is precluding that, so we’ll certainly be exploring it. The only thing is that if, if a patient has to stop therapy because of toxicities. For example, the you know, ERK caused some toxicities for which one had to stop, then you wouldn’t be able, or wouldn’t, probably want to either kind of go back out of the same regimen. So there is a caveat here.

Manju George 17:55
If a patient has been on the on dabrafinib previously, could they get that on this trial immediately, or is prior dabrafinib an exclusion? If not, do you need to have, okay, okay, so do you need to have an intervening chemo period? Or can they come back?

Dr. Scott Kopetz 18:12
Nope, they can come right in. You know, there’s a requirement that patients have had at least one prior line of chemo therapy. So, yeah, it shouldn’t, shouldn’t be a problem.

Manju George 18:24
Okay, so if they’re on the other like, for example, the -?–emab you know, Dr Corcoran’s trial with the dabrofinib, and they could still come back on the Novartis without any any problems. Okay, okay, good to know. Thank you.

Manju George 18:41
yeah, in between the different trial arms, could you tell us, like, if a patient had to choose, are there particular arms that would be better, and why would you think so?

Dr. Scott Kopetz 18:51
Yeah, that’s a good question. And so, you know, part of it is that with these studies, the way that they tend to work, even a trial that has lots of arms like this, you know, right now, like, if I, you know, somebody that I wanted to put on study this week, there really wouldn’t be any arms available, right? So there’s, you know, the the I think the further we get into the study, the more opportunities and slots, you know, may be available. So it may get to a point where there is a bit of, you know, opportunity to kind of pick and choose, you know, efficacy we just don’t know. And I think the question for all of these is really one of a therapeutic window, meaning how much to inhibit the pathway and really maintain kind of safety. So a lot of work trying to get those doses just right, figure out kind of where things are going to settle down with those treatments. So I think all of them are, you know, based on really good science and good rationale. And I think it’s really going to be a factor of, you know, what doses are achievable and and how effective are we at inhibiting the pathway, and that, unfortunately, just going to come with. Time. So the short answer is, the best arm is the one that you can kind of get on when you need it, you know, I think they’re all very, very reasonable.

Manju George 20:12
Okay, okay, so I’ll just ask one question. So in your talk, you thought that, like with the data, that you showed the BRAF inhibition, the MEK inhibition, and the ERK inhibition, or, you know, this, like that, seems to be having the most, you know, the bars are going down, right? There are some of the arms they’re just taking SHP2. They’re not blocking all the three nodes in a sequence, right?

Dr. Scott Kopetz 20:37
And so acknowledging, of course, that they, you know that one study didn’t, didn’t run, that was in cell culture, right? So there’s some caveats there. And we didn’t really explore all of those different, you know, all of those different combinations, or actually, they didn’t explore all those different combinations. So I, you know, I would be a little hesitant to say that’s absolutely the winner? I think there’s, you know, there’s a lot of thoughts about, well, how do you bring this forward, like, what does the next study look like based on these results? So I’m hopeful that that combination, you know, may be explored, and that’s being explored in other studies, but, but I think trying to think about where one can go with, you know, with a signal like, what is it? What do we need to see in order to move this forward for patients?

Manju George 21:31
Okay, so the next question is, like, we have a patient who has a co occurring, Akt1 e17k mutation. So do you think that particular arm would be better, like with that particular mutation?

Dr. Scott Kopetz 21:43
Yeah, it’s a good question. We don’t have a – it’s a rare mutation, but certainly is activating of that pathway. We can learn from the PIK3CA mutations that have been seen, which is which is slightly upstream of the Akt signal. So the Akt, when it’s activated, PIK3CA, will activate AKT. And when the PIK3CA, when we looked at it, we went into this several years ago, thinking, well, if you had that mutation, conceptually, it seems like maybe the treatments wouldn’t be beneficial. When we looked at some of the earlier data, it actually looked like that for reasons we didn’t understand. The outcomes were even slightly better with the patients who had a PIK3CA, even though you were targeting the MAP kinase pathway and some of the randomized studies that didn’t pan out. So we look at, so I don’t know about the Akt inhibitor alone, but the PIK3CA activating mutations did not appear to be a major, major driver. So, you know, we think about that maybe that mutation was critical early in the development of the cancer, and that as the cancer evolved, it became less of a dominant driver. And it really all became about map kinase pathway,

Manju George 23:07
The next one like I think we have to go quickly so monomer versus dimer, ras inhibitors, and what you know, there is an arm combining both of them along with their inhibitor. If you want to say something about that?

Dr. Scott Kopetz 23:24
So, you know, the idea, obviously, BRAF, we know it targets the oncogene and the wild type BRAF, but you know, the hope for the pan RAFs is that it can help modulate, you know, the other signaling around, kind of the leakage, as we talked about, around that. So, so, you know, that’s, I think, you know, hopeful that some of these pan RAF inhibitors will be more, you know, more effective in this thing. But it still remains to be seen. Again, it comes back to tolerability, right? You know, BRAF’s great because you hit BRAF. And you know your normal skin is okay, you knock out BRAF, but your normal skin has CRAF right? So it can still do what it needs to do with CRAF. So the problem, of course, is if you’re blocking all of RAF, you’re blocking all the raf in the tumor, but you’re blocking all RAF in your skin as well, right? And so or your GI tract, or other areas. So that’s where really trying to make sure that there’s a therapeutic window. So it’s not always what looks great on this simplified signaling diagram, but what is happening in the normal tissues as well.

Manju George 24:29
And safety and toxicity of SHP2 inhibitors. So there’s some data with the KRAS mutant study. So I mean, do you have any advice on what are you seeing?

Dr. Scott Kopetz 24:38
Yeah. I mean, I think shift two is an incredibly interesting class, and I think we’re really kind of excited about the potential there. You know, receptor tyrosine kinases are very ubiquitous throughout the skin, the GI tract as well, and so we need some signaling in our healthy tissue to kind of. Through that. And so again, comes back to the same thing that, you know, it looks great targeting the cancer cells, but it’s, you know, how tolerable is that going to be? And how do we adjust things to look at that we know, for example, EGFR and MEK inhibitors, and we put those together, they’re really difficult to tolerate those two together. Now, turns out, when you look at other different combinations, then it may be a little better, you know, ERK and EGFR may be better. You know, BRAF, MEK, EGFR is much improved because of some of the feedback mechanisms in the skin, for example, so that we know that some of the SHP2 combinations, we may run into some of those same limiting toxicity. So still a little early, but I think very promising.

Manju George 25:53
This was about TKI inhibitors combining with like the BEACON doublet.

Dr. Scott Kopetz 26:00
Yeah. So, yeah. So good question there is, you know, one of the things that Stivarga does is it does have, it’s a multi kinase inhibitor, meaning that predominantly hits a VEGF, so it’s mostly an angiogenic effect. But they also do hit some other pathways, PDGFR right, which is one of those other receptor tyrosine kinases that, in rare cases, can be kind of a dominant feedback. So the concept is certainly, you know, intriguing to think about, you know, regoragenib combined with it. I think that may work in the kind of unique case that PDGFR is the dominant one in a given tumor or patient. But I think the concern is that we see so many other different ways that the tumor evolves and adapts. That concern that it may not be quite as ubiquitous of a solution, although I certainly can acknowledge in a few select patients, it may be.

Manju George 27:04
Letinatinib (?) is also kind of similar in range of targeting multiple…

Dr. Scott Kopetz 27:10
It has maybe a little bit more selectivity than regorafenib, but still very much hits a lot of other things that may actually be driving whatever efficacy we’re seeing outside of that job.

Manju George 27:22
Question about drug availability and addition of slots, for example, in Europe, or –

Dr. Scott Kopetz 27:26
Yeah, so certainly, the largest studies enrolling in Europe, the slot availability is managed worldwide. For this study, like most studies, meaning if there’s no slot in the US, there’s no slot in Europe, there’s not separate slots for for separate separate sites.

Manju George 27:48
We’ve had some off label experiments going on where people have tried, like the BEACON plus ERK inhibitor.

Dr. Scott Kopetz 27:55
Great to hear. And I think, you know, trying that’s the direction I think we need to go as a field to really better understand it.

Manju George 28:04
So when do you expect to report out some of the findings?

Dr. Scott Kopetz 28:07
You know, a lot of these studies are early on, including, you know, Novartis study, a lot of times they’ll want to have the expansion cohorts enrolled before to really understand a little bit better about the safety. So, so it won’t be ASCO gi I think the question will be ASCO, or would it slip into the Fall even?

Manju George 28:33
What about Dr van Morris’s study like the BEACON plus nivolumab? When can we expect some results?

Dr. Scott Kopetz 28:40
Yeah, going very well there. We’ll have some coming out at GI ASCO. I anticipate, again, the results are sufficiently promising that, you know, the follow on randomized study is, is launching, yeah, so the nivolumab for MSS patients, in addition to the Enocrafenib.

Manju George 29:07
So I think the other question is, are you going to add more arms to the Novartis man? Are you expecting more to be added?

Dr. Scott Kopetz 29:12
Yeah, it’s designed for that. So we very well may see some additional arms come in. There’s a lot of arms already, but there’s, it’s designed that new things can come in there, and then the arms will pause at various times when there are efficacy barriers. So, you know, we don’t see a certain amount of activity. An arm may pause enrollment and prioritize other arms as well.

DocTalk
2021
Dr. Kopetz
BRAF

Dr. Kopetz of MD Anderson discusses options for therapy refractory BRAF V600E metastatic colorectal cancer in this Doc Talk, recorded for COLONTOWN in August, 2021.

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The TIL trial for metastatic CRC

The TIL trial for metastatic CRC

DocTalk
2021
Dr. Lou
Dr. Starr
Cell therapy
MSS
Stage IV
Trials

Drs. Emil Lou and Tim Starr from the University of Minnesota discuss the TIL trial for metastatic CRC in this DocTalk, recorded in March, 2021 for COLONTOWN. Dr. Starr opens this discussion with a look at the science behind the trial, including CRISPR, the powerful gene editing tool, and the tumor infiltrating lymphocytes (TILs) that give this trial its name. The second half of the video features Dr. Lou discussing the trial itself.

This transcript is automatically generated.

Manju George 0:00
Hello everyone. Welcome to DocTalks. I’m Manju George, the scientific director of COLONTOWN. Today we have with us Dr Ingrid Lou and Dr Tim Starr. Dr Lu is an associate professor of medicine at the Division of hematology, oncology and transplantation. He completed medical school at the State University of New York, and finished his residency from Duke University Medical Center, and he finished oncology and hematology fellowship from Memorial Sloan Kettering, and then a neuro oncology fellowship from Duke University Medical Center. Dr Lou welcome, and we also have with us. Dr Tim Starr. He’s an associate professor in the Department of Obstetrics, Gynecology and women’s health. I was looking at his research, and looks like he’s interested in understanding the genetic basis of cancer in order to develop individualized, targeted therapies. So thank you both for being with us, and welcome Dr Starr

Dr. Starr 1:10
I know everybody here is personally associated with colon cancer. So what we’re going to hear talk about today is a clinical trial that’s led by Dr Lu to treat advanced stage colon cancer, and I’m going to give you the kind of basic science behind the trial. Now you’ll have to bear with me. I am a ex high school teacher, and I’ve also taught a lot of undergraduate and graduates, and I’ve learned from that to start at the very basics and never assume anybody knows anything. So for those of you that know a lot more, bare with it. So first off, the basics of this trial is it’s an adoptive cell therapy trial. And the key here is the therapy is cells, not drugs. And so the basic backbone of an adopted cell therapy is you take cells, and you can take them from the patient or possibly from a donor. In this case, we’re taking them directly from the patient. And for adoptive cell therapy, it can be any types of cells. It could be a T cell. Could be B cells, it could be natural killer cells, stem cells. What we’re focusing on in this trial, we’re calling tumor infiltrating lymphocytes, really just a mish mash of immune cells that are hiding out in the tumor. And then you take the cells out, you do something to make them better at killing the tumor. And this can involve lots of different things. People are trying lots of ways. You could just make more of them, expand them, enrage them somehow, by giving them cytokines, select out the ones you think that are going to do the best killing you can then now add genes and delete genes. We have the technology, which I’m going to talk about a little bit later, and then you treat the patient with those enhanced cells. So that’s the nutshell of adoptive cell therapy, and that’s what this trial is. Now it’s immune cell therapy. So I have to give you the basics. 101, on immune therapy, which I hear you’ve already seen some people give talks on this. So just remember that your body has T cells. T cells have this receptor on their surface. Think of it as a mutation detector. It’s also a virus detector. Turns out that, you know, 1t cell is going to detect one type of mutation or one type of virus. Luckily, you have 1000s to 10s of 1000s to millions of these, each one with a different flavor of a receptor. Now you probably hear the trial in the background there, it’s Wednesday at 1:00. So the way we’ve evolved is that healthy cells actually show their guts to these T cells that are patrolling your body. And the way they do that is they kind of chop up the proteins inside them and put them on these special molecules that display them out to the T cells. Now your T cells have been trained since birth not to recognize healthy cell guts, so any proteins that have been around shouldn’t have a T cell that’s going to try and react with it. So the key here is, with tumor cells, some of these genes get mutated. You know about this, and so the guts are now going to have some mutated proteins, and that mutated protein will get shown and instead of calling it an epitope, now we’re going to call it a NEO epitope, or a NEO antigen. And if the immune system is working, hopefully there’ll be a T cell somewhere that has the matched mutation detector for that mutation, and it will recognize that tumor cell and kill it. Of course, if the tumor is around, it’s probably not working all that well. This is kind of the not so basic so, so when that T cell does recognize that tumor, how does it actually go and kill it? So it turns out there’s a huge slew of proteins inside T cells, signaling pathways that need to be activated, some need to be turned off, for the T cell to actually physically go and try and kill that tumor cell. And it can do that by creating little holes in the tumor cell or throwing molecules at it that kind of tear it apart, apoptosis. So lots of signaling going on. So the basics for our trial is we want to use tumor infiltrating lymphocytes put back in the patient to kill the tumor. But the first thing we want to do is, we want to select out those tumor infiltrating lymphocytes that we think are going to attack the tumor. So here’s the schematic for the trial. We’ll biopsy the patient, so we get a chunk of tumor. The tumor should have these infiltrating lymphocytes in it. Now they’re not working, because this patient has a tumor that’s growing wildly. So they’re there, but they’re not doing so well. So what we do is we cut the tumor into chunks, and we actually grow a little bit of the tumor in its own private well. So we have these 48 well plates, so now that tumor infiltrating lymphocytes that were with that chunk will grow in that well and so forth. And we help them along a little. We encourage all these lymphocytes to grow by giving them a candy they like, called interleukin two, IL2, which stimulates their growth. So we get these wells with these pills growing. Now what we can do is we can actually sprinkle them with the Neo epitopes in the tumors and test to see if they can actually recognize those new epitopes. So I skipped something here. We also take a little piece of that tumor and we sequence it. We sequence it to find all the mutations that are specific to that one patient, and we physically sprinkle those on to the tills. Now this is showing you one plate with six wells. We’re actually doing this in about 100 plates. Each plate has about 96 wells. So it’s a big test. Takes us a little while to do this. But what we do is we find the wells that seem to react to those new epitopes, and then we can pull out those tills, expand them up and throw them back into the patient. And this is kind of what’s been going on for a little while. This was kind of pioneered at the National Cancer Institute by this guy, Steve Rosenberg, so what are we doing to make this even better? So our hope is we can make these TILs better killers. And I date myself here with The $6 million Man Superwoman, and then Dr Lou is a fanatic of The Avengers, so I had to put in an Avenger there for you. Can we? Can we soup these guys up, make them real killers? So here’s the – not going to be too much scientific data. – This is about it, two figures. So our group and others have found this protein, and it’s called sis, stands for inhibitor of cytokine signaling. It’s a protein that actually blocks T cell killing. And here’s the piece of data that kind of proves this to us, is we do these tests in cells, or we do them in mice. So this is a mouse experiment where we give the mice melanoma, and we have a T cell that actually recognizes melanoma, so we can treat the mice with this adoptive cell therapy, but the T cell that recognizes it doesn’t do a very good job. So this is the purple, purple triangles. So this is the size of the tumor in the mouse, and this is the days after we gave them the cell therapy. And you can see the tumor is growing, and pretty soon it grows so big that it kills the mouse. And we have these controls. So these are the normal TILs that have the wild type sis in them. With another set of cells, we can actually knock out the gene sis. And that’s what the SIS minus minus looks like. And when we put these tills in, the tumor stops growing, and this gives us this is a very aggressive mouse melanoma tumor that’s super hard to cure. So this is really exciting data that says, hey, maybe we should try this in humans, and you do some work to try and figure out what’s actually going on inside the cell. So we know that our protein blocks this signaling pathway here, and when it does that in the T cell, the T cell can’t kill the tumor cell. If we knock out the gene and get rid of it, this signaling pathway is activated, and now the T cell is a much better killer, and it can cause the tumor to go into apoptosis, which is our word for killing the tumor cell.

Dr. Starr 9:38
So this is what we want to do to those tills back here, and so what we do physically is we use this new technology that you might have heard of, called CRISPR cast nine and was the science technology of the year. And basically, you take the cells in a dish, you zap them with electricity while you bathe them with. The CRISPR cas9 components, and the zapping causes the cells to kind of break apart a little CRISPR cas9 step gets inside and does its job. So, what is its job? So, another 101, biology. Here, you’ve got your cell, right? You’ve got the nucleus. In the nucleus, you got the chromosomes with the DNA, and part of that DNA is the gene that codes for this ish protein. So we want to get rid of that using CRISPR cas9 so the way CRISPR cas9 works is you give it this enzyme, it’s this big orange blob here called cas9 and you give it this little string of RNA called the guide RNA, which is the CRISPR part. So you give it the CRISPR and the cas9 and what this little string of RNA does is it has the sequence that knows where the CIS gene is, and so it pulls the cas9 enzyme to that exact spot in the genome, and it creates a break. So here’s the DNA. These are the two DNA strands, and it cuts it, and when that cell tries to repair it, it usually doesn’t repair it very well, and it can no longer make the CIS protein. So the last piece of data I’ll show you is what we want to look at. When we take these cells out of the patient, and we run it through that whole process, and we cut them out. We have ways of looking to see if that sis protein is expressed, and it basically shows up as a black blob on a gel that we run that has protein in it. So these are cells that we didn’t put in the CRISPR cast nine, and you can see there’s lots of the SIS protein. These are cells where we did put this in, and there’s almost none. So this is really good. It’s not easy to do this in T cells that you take from patients, but a group working here at the University of Minnesota, especially Brandon Moriarity and Bo Weber have developed this system to get this to work really well in primary cells, which is kind of the limiting factor, which is why people haven’t been doing this before, also because CRISPR cast nine was just invented a little while ago. So now, if we go back to that diagram I showed you, what we do, we’re going to put in this last step before we put the tills back into the patient. So we’re going to take them, we’re going to CRISPR, cast nine, delete out, sis, get the deleted cells, and those are the ones we’re going to infuse back into the patient. So that’s the basic 101. Of the science behind this experiment. And maybe before I pass it over to Dr Lou, if people have any specific questions about this or more technical details they want explained, I’d be happy to do that.

Participant Question 12:48
That does the location of the tumor come into play, as far as delivering

Dr. Starr 12:56
good question. So we when we take the tumor biopsy, we can actually take it from anywhere. So if the patient has a liver metastasis, a lung metastasis, we’ll go in and take it from there, because that’s easier to biopsy. So we haven’t done this obviously, in enough people to know whether it’s going to affect how how many T cells you get out and whether they’re good T cells or bad T cells, but that’s one of the questions we want to ask. So in one of our patients, we’ve done it from a liver biopsy, and one patient, we’ve done it from a lung biopsy, but we could also do it directly from the colon tumor biopsy too, if we needed to. Is that the question?

Participant Question 13:38
Yeah, and the peritoneum is what I’m thinking of, is if you’ve metastasized into the peritoneum, I know everything’s a little more squishy and not so defined in there, and whether that would complicate things, yeah,

Dr. Starr 13:51
What we really want is a, I’m going to call it a healthy piece of tumor. We want a piece of tumor that’s growing well, because that’s where the T cells will have infiltrated into and we want a fairly big one so we can cut it up into many pieces, so we can get a lot of them. So it really depends on this is going to be very end of all individualized for each patient, but we could take it from the peritoneum too.

Dr. Starr 14:13
Thank you.

Manju George 14:14
Thank you very much for that. There are two questions. One is, what is the typical time to grow the tils and then to infuse them. The next question is, are there risks when the TILs are modified that would impact the health of the cells?

Dr. Starr 14:30
Yes, thank you. So first, first question is, we’re trying to get it as fast as possible. But that being said, it takes the time to grow the tills. It takes time to sequence the tumor. It takes time to edit them and pull it out. And right now we’re at about two months, one month to two months we can, we can from the time we take out the biopsy to the time we can infuse them back into the patient, is about that long we can freeze down the cells. So it’s not limited to soon as we get them, we can then put them into the patient, and then the second remind me the second question, what are the risks of this modification to the health of the cells? That’s always an unknown, and that’s that’s the big worry, obviously, for FDA approval and the cells like this have been put into patients, and one nice thing about these cells is they don’t tend to cause a lot of of reaction, like these car T cells that you’ve probably heard of. But this whole idea of cutting out the CIS gene and seeing what happens is really an unknown, and that is a worry of ours. Of course, we’ve done it in mice, and it doesn’t seem to have affected normal, healthy organs like we would be afraid of, but that’s always a possibility. And you know, this is for metastatic colon cancer, so we wouldn’t do this to healthier patients.

Manju George 15:59
The next question is, can you harvest the pills from lymph nodes? Tumor in the lymph nodes,

Dr. Starr 16:05
generally, these tumors, I’ll let probably Emile answer this better. But the tumors don’t, although there might be some tumor cells in the lymph nodes, we really need a good solid junk of tumor. We want a solid piece, and those usually aren’t found in the in the lymph nodes for colon cancer.

Manju George 16:23
Okay, thank you. Great. That seems to be, yeah, go ahead.

Dr. Lou 16:28
No, I was gonna say I’ve known Tim for nearly a decade, and anytime I hear him speak, I learn a lot. And I wish during his teaching phase, he had been my teacher for biology, I think I would be a whole lot smarter. But thank you. I think, I think what’s really also important is what I had in mind and asking Tim to partner with me for this talk. It’s emblematic of the partnership that occurs for this trial. So I’m a physician scientist. I have an MD and PhD degrees. I do basic science research and translation research, and I treat patients in the clinic, whether it’s with standard of care treatment or clinical trials, when those options are available, and we try the best we can. But you know, the ultimate dream that we that has been said for decades, this term bench to bedside, I think that that term, and that the reality of how that plays out has really evolved over time. It’s not as simple as simple as just taking something from the lab to translation into the clinic, but there’s so many logistical hurdles. And is not just safety, but will something work and but this is this is happening, and that’s what this trial is, really the overall strategy. You know, as Tim said, arising for more from more than half a decade of basic science investigation here at the University of Minnesota, in partnership with those esteemed researchers at the National Cancer Institute who had already done a lot of clinical trial research over the decades, and investigation in the lab for adopted cell therapy in general and tills very specifically. And if we think of this as a next generation of that, I think we’re very proud. I think I speak for Tim and really our whole team that really under the proverbial roof of this gigantic campus in Minneapolis, Minnesota, that allow the basic science research that arose out of here, and collaborators, the NCI, we’ve been able to take from that bench so called to the clinic and have this trial open is really, I think, really puts us at the next frontier. And I’m not saying just at the University of Minnesota, but just as a field of gastrointestinal oncology, we’ve seen from afar that our colleagues who treat patients with hematologic malignancies like lymphoma, leukemia, and they’ve had all these fancy immunotherapy and cellular therapies on the horizon, and they’ve been able to treat patients with this type of therapy, and we’ve been very envious, and there have been Things like immune checkpoint inhibitors, which I’m sure you’re everyone in COLONTOWN has heard a lot about for patients with microli and stable disease, which only comprises barely 5% or maybe a little bit more, of all treatment of all patients, but who qualify for colorectal cancer, but what about the other 85 to 95% of patients? We need to do better, and this scientific effort from bench to bedside as an effort to do that. And there will be more other studies. There will be other studies, maybe looking at sis knockout using CRISPR and other types of immune cells, but here looking at tumor infiltrating lymphocytes, this trial brings, brings across several novelties, and I think we’re going to discover things together. And I think at any clinical trial, if we had the answer already, it would no longer be on clinical trial. I’d have the luxury of being able to treat it, treat patients as standard of care. But maybe the answer for this and other new, innovative treatments will be different, and hopefully it will be two years from now, three years from now, five years and 10 years and decades to come. So I’ll go ahead and share my screen if it’s possible, and I will do slideshow view. So consider this the second half of discussion from Dr starr, and I do want to take a moment so dr Manju, George, thank you so much for the opportunity to meet everybody. I follow COLONTOWN from afar online, and I know you and other. Other members have participated in the ACRS, the American Association for Cancer Research Scientist survivor program, which is 20 plus years strong, welcoming advocates to the AC annual meeting to learn about the science. And I think you and everybody in colintown are are not just advocates from afar, but deeply immersed in learning the science, and not just about clinical trials, but the actual science of it. And I think that’s an immense endeavor. So I really am full of admiration, and I’m particularly grateful to have this opportunity during the onset of colorectal cancer awareness month. So March and blue, we wear the blue as a symbol of support for anyone who has been diagnosed with colorectal cancer of any stage going through treatment now, has gone through treatment. And those who have yet to be diagnosed and yet to go through treatment that will benefit from clinical trials like this one and others, so that the trial itself has a long name. And if you go to clinical trials.gov I can show you that page at the end, briefly, if we have time, this is the NCT number. It’s called a phase one two trial in patients with metastatic gastrointestinal epithelial cancers, administering cancer administering tumor infiltrating lymphocytes, in which the gene encoding sis was inactivated using the CRISPR cast nine system. And thanks to Tim’s in depth discussion, you have the context for where that title comes from. There are many, many dozens of people here at the university who make this work, and that’s from within the labs and from the different centers that I’ll talk about briefly, and also throughout the clinics. I have the great pleasure of leading this investigation, which is here at the University of Minnesota, and some of my co pilots, or CO investigators include Dr David McKenna, who is the head of our molecular and cellular therapeutics department, and we’ll talk about that that’s crucial to how we can produce the T cells and expand them for treatment here at the University Jeff Dr Jeff Miller is a renowned bone marrow transplant specialist at cancer researcher Dr starr here, along with when he mentioned Dr Bo Weber and Dr Brandon mayordi, who have been instrumental to developing the CRISPR cast nine system with great efficiency, and specifically looking at sis, and that’s in collaboration with the National Cancer Institute team. So this is a little bit kind of picking up the baton, but it’s in the context that it’s not that no one has ever used tumor infiltrating lymphocytes or tills or adoptive cell therapy in solid tumors before, but as I said, you know, the hematologic malignancies have been little bit more at the forefront, and we’re catching up. But in previous studies at the National Cancer Institute led by Dr Steven Rosenberg and his colleagues, they really blazed a trail for developing protocols for how this can be used, developing safety, better understanding of the toxicities that were observed that were really coming from the high dose lympha depletion, chemotherapy given prior to administration of the or infusion of the tills, and also high dose IL2. So this is the part of translation from what Tim said he described to you and showed you the in picture form that the T cells were fed by the IL two. He called it the candy. And I like that analogy, because il two is a inflammatory stimulant that the cells, the T cells thrive on, and they can replicate and really be robust and last longer. And that’s part of the clinical protocols as developed that have developed over the course of the last decade or two at the NCI, and it’s preceded by chemotherapy that normally would be given by our colleagues who are treating aggressive leukemias or lymphomas. So it’s not the usual standard of fare for patients with colorectal cancer, but in this case, it’s designed to try and prepare the bone marrow to not just receive the T cells allow them to engraft or and ultimately thrive. And so that combination of the lympho depletion, chemotherapy, providing the tills, and then following that with high dose il two is designed to not just build upon the CRISPR engineering part, which is gene editing as Gene scissors. It’s not just the principle of adding to just giving T cells, but in addition knocking out SIS to magnify and amplify its effect. But to even do it further, you can think of those steps so mutation, reactive, kill, act therapy in patients with progressive metastatic gastrointestinal epithelial cancers, NIH has shown promising efficacy signals now, in terms of what type of cancers that means that’s a long, drawn out description, metastatic obviously means having spread far away from where it started. In other words, stage four disease. Gastrointestinal is self explanatory, basically from mouth to anus, but epithelial cancer is really hones in, for example, carcinomas of the esophagus, stomach, pancreatic adenocarcinoma. I think the key there is it’s not going to include pancreatic neuroendocrine tumor that despite anatomic site being in common, it’s really, in many ways, so many, so much of a different biologic cancer. But in terms of the efficacy, what’s been seen in preclinical The reason is to include epithelial, but not neuroendocrine, and continuing along the digestive tract, small intestine, of course, colony, rectum. Um, and so the adenocarcinomas, when they metastasize and refractory to therapy, would make someone eligible for this study. So some of the additional background in the third line setting that data suggests that about 15% of patients with mest act gi associated carcinomas can obtain objective clinical responses when neoantigen selected tills are part of the equation, even just without the benefit of sis modification. And as Tim mentioned, such as an acronym, means fancy form of regulation of T cell receptor signaling to the patients, at least for the patients, and maybe that’s one of the patients that you mentioned earlier in the conversation. Menju to the patients, remain without evidence of disease, no evidence of disease greater than three years after treatment. And I think this is probably one of the crowds I don’t need to preach to and to explain how remarkable that is, and that’s really going from the exception, and we want to make it the rule with more innovative treatments. Pre clinically, CSG knockout has been shown to improve important cancer selling function, cancer killing functions of T cells and mice and humans. And so the next step, of course, is to go from cells in dishes to animal models, and now we’re at human clinical trials. So this is a single center trial here at the University of Minnesota. It’s a combined phase one two study, because we’re looking to answer the questions, many of which I’ve already heard, which you undoubtedly may have, or anyone watching this as recording may have later, really want to not just look and answer the question, Does this new treatment work in individual patients? But we have to prize most and first and foremost. And what keeps me at night up at night, more than any other endeavor I’ve ever undertaken as an oncologist is we are the ward of patients that have entrusted us with their safety, and we have to make sure to do this as safely as possible. So the purpose of the study is to determine the safety of administering these mutation reactive autologous lymphocytes that, in addition to prior studies, has knocked out the CIS gene, and in addition, has used CRISPR cast nine editing to do this. And the patient population, as specified, are patients with metastatic gi epithelial cancers, not when they’re first diagnosed, but further along in treatment, starting with progression on first line therapy or the equivalent. And as the GI oncologist, I added the term maintenance therapy, which it can often be given. For example, after FOLFOX you can achieve stable disease, and just do 5FU to spare further injury from oxaliplatin is just one example. There will be up to five dose levels initially, of this sis, which I reviewed, the acronym for in kale, means knockout. I’m knocking them out using CRISPR cas9 of the tills. And we want to escalate the dose as is as we’re able to do safely. And if we can prove we can do it safely. We can go to higher doses, then we can then establish a dose and concentration of the T cells that are safe enough to proceed for the remainder of the patients, primarily in the phase two version. So instead of bench to bedside, I think the way some of that paradigm has evolved is clinic to lab, back to clinic. And that’s the strategy and the tactic and the approach for this trial, it starts in the clinic, because everything starts in the clinic. Our observations, how we help patients, and when we receive patients who are interested, or if we identify patients who may be eligible for the trial that we can offer to we have a very extensive screening process with my team in the clinical trials office, from point of entry, from the first phone call to welcoming them into clinic, to determining from a long list of eligibility of whether or not there would be good candidates. And so much of that is predicated on safety. As you know many of you, if you’ve investigated clinical trials, you know it’s, it’s nothing to do with personality or where someone lives. It’s, it’s always the underlying strategy is safety, but sometimes it could be laboratory values that need to meet criteria to indicate safety. It could be how well someone is able to, for example, walk and be able to do activities of daily living, such as showering themselves, be able to feed themselves, make basic foods. These are basic measures of safety going in to this kind of process. So when we identify patients and they meet eligibility criteria, we can consent them and welcome them onto this protocol. Then the protocol begins. Tim mentioned the tumor harvest, and he fielded some questions on that. And so patients, if benestac disease, whether it really depends on intensive discussion of myself and our multidisciplinary team, including our surgeons who are integral if the tumor, in this case, colorectal cancer, has gone to the liver, then we call upon our expert liver surgeons. If it’s gone to the lung, then we call upon our expert thoracic lung surgeons. And if it deals with the primary tumor or other areas, we call upon expert surgeons. But when the surgery is performed, we hold chemotherapy for a bit to make it safe to proceed with surgery. And then the surgery is performed, and then, as we say, we transition from the clinic back to the lab. And there’s a large, vast team that does this. And it’s not just a wet bench lab, but it’s also a core facility, molecular and cellular therapeutics I mentioned earlier, led by Dr David McKenna. And this is one of five NCI sponsored such facilities in the nation, and I think that’s. One of the aspects that makes our program, our university and this trial unique is that rather than having to send this to a different site, we do this at the university, basically on the premises, and so in collaboration with Dr Starr and Dr maherdi and Dr Weber Dr McKenna and their vast team members, there are different things going on at different points of a next month or multiple months, however long it takes to be able to derive TILs, hopefully successfully and hopefully robust. I noted a question about lymph nodes. And lymph nodes tend to be scant and couldn’t be necrotic. But the key here with infiltration is you need enough tumor tissue, and there has to be enough size there. So usually solid tumors in the we call the organ parenchyma, inside an actual organ are usually ones most likely to yield enough tills to expand they undergo genomic sequencing, and much of which I appreciate from Tim so I don’t have to expand upon this too much, but then also being able to grow them to enough numbers and also energize them with the candy that Has il two and of course, a CRISPR assist Knockout is an essential part of that process that makes this trial unique, above and beyond the studies that were done in the NCI. And then we go back into the clinic. That’s a proverbial clinic, because much of that happens at an inpatient hospital stay that we’ll go over. So the overall schema is that when someone is admitted into the study and meets eligibility for safety. They undergo apheresis, they undergo tumor resection, and we do the leukapheresis prior to the resection, and also later on, about six weeks after till infusion to compare, and also just to ensure that the tills are persisting, primarily because want to make sure that this is not just something that’s going to last a few days, a few hours, a few days or just a few weeks, but rather be a long lasting form of treatment, if it’s going to work, and hopefully will persist over time and be very efficacious long term. That is the intent, or the intent to cure, is something that’s an ambitious goal of this, but trying to go for something above and beyond the normal standard of care, such a cytotoxic chemotherapy, and even even in combination with biologic agents that are not capable of eliminating or producing a cure or completely removing tumors, rather, are able to achieve stable disease for a prescribed period of time before tumors evolve and eventually become human resistant. This is basically verbiage that describes what I showed in the schema, and the key is, when someone recovers from the tumor harvest surgery, they can receive the protocol allows for either no chemotherapy or standard of care chemotherapy, and that can be comprised of any standard of care FDA approved drugs, such as fall Fox full theory, combination of five fu based therapy with or without biologic agents or other targeted agents. And that is done in consultation with me. And if, obviously, if someone doesn’t live in Minnesota, we don’t bind them for that several month period to live here, but whether it’s winter or summer or not, but integral to all this is close collaboration between me, my entire team, and the home oncologist, working together, and that we welcome that person into the team, the local oncology team, but the imaging for disease response has to be done here, because we want to make sure it’s uniform and get as accurate as read as possible. For patients who want to know, did this treatment actually work once the autologous sis knockout, till product passes final lot release, inquire preserved the treatment with tail product maybe may go forward. So it’s not going to happen in the exact day, because some of it’s unpredictable. It will take some time to recognize the antigens to expand. And then we also have to coordinate many, many moving parts, among which is, when does the patient start chemotherapy safely after the tumor harvest, and when can they stop? But a key to that, like almost pretty much any clinical trial you can imagine or have seen, a 28 day or, in other words, four week washout is required of this trial, as it is standard in so many clinical trials, before beginning the lympha depletion chemotherapy. And again, that part of that is a lot of logistic working out with the oncologist, or if they’re under my care here, that I work that out with my team, and we’re very cognizant of that. So leading up to that, after the minimum 28 day washout comes the time which I call the centerpiece of the treatment, which is actually getting the tills. And I think, if I don’t get to say it outright later, the centerpiece, the absolute centerpiece, what we call Day Zero, literally, is the infusion of tills. And the tills is not a repeat administration. It is a single, one time administration for everything leading up to that one day and everything to follow that is surveillance to determine safety and efficacy is not going to be a repeated administration. This is intended and built to last, and that is the great hope of what we’re trying to discover on this trial. But if we call that day zero retroactive to that seven days prior is when a patient’s admitted, it may not be on a Monday, but just to make it logistically make sense as an example, if someone were to be admitted on Monday, they may receive five consecutive days of chemotherapy, which is high dose, and these drugs are things that are probably not familiar to you, because the average someone, anyone caregiver or an actual patient who receives treatment with chemotherapy for colorectal cancer may not see these unless they know someone with leukemia or lymphoma. But these are part of the. Basically the same borrowing from the same regimen, the same drugs and same dosing and schedule and frequency as what was done at the NCI. And so this is done in in supreme collaboration with our bone marrow transplant colleagues. The University of Minnesota has over half a century of experience in adult and pediatric bone marrow transplant, a very prolific and esteemed group, and they have partnered with me and Dr Jeff Miller, who I mentioned as my co investigator, is integral to that for safety when we admit these patients to our bone marrow transplant unit, but the multidisciplinary team is taking care of them, but the day to day to the doctor who rounds will be a bone marrow transplant specialist, because they have a lot of experience with these type of high dose chemotherapies. And seven days from admission, if all goes well, then we anticipate day zero would be the infusion of the tills, which is in some measure almost anticlimactic, can take an hour, it can take two hours, but a couple of hours, and then what happens at that point later in that same day, and the several days that happens after is up to six doses of the high dose, il two. It’s also called aldose Lucan, if you end up googling at home and it’s we do safety intensive safety monitoring to see if it’s safe to administer the IL two because certainly there are potential for strong side effects there. But again, the intent, just like it is in the lab, is to boost the energy of these teal cells once they’re infused into the human patient, and to make sure that they last for a long time. So by day 28 so we asked them, approximate amount of time that someone might be in the hospital as a very gross estimate, maybe two weeks, but it’s definitely not a couple of days and someone goes home, it could exceed 14 days. It may be slightly under 14 days, but I think 14 days is a good frame of reference. And when someone is discharged safely from the hospital, following this, then we have a very close follow up in our outpatient clinic, hand in hand with our bone marrow transplant and solid tumor oncology colleagues. So the patients will be seen twice a week in our outpatient clinic here at the university, and then until day 28 and day 28 measures 28 days plus or minus one day since the infusion of tills, and we will obtain scans and we will do a six week non mobilized leukophoresis to help to detect and confirm persistence of the tills. And then we will do CT scans, or other forms of scans, that might be appropriate at close intervals for the several for several months, and then spacing it out every several months after that, per our protocol. And so at the time, if disease progression occurs, then I consult with the referring physician, or if they’re under my care for anything appropriate. But we would like to continue long term follow up study again looking for long term follow up of safety as well as efficacy. There’s a long list of inclusion criteria that are fully available on the clinical trials.gov so I won’t touch on every single one, but probably the things that people want to know in general, definitely for a metastatic gastrointestinal epithelial cancers, patients who’ve had progressive disease after at least one line of therapy. And so that first line of therapy, for example, if Colorectal cancer is diagnosed and a stage four diagnosis, just as one standard of care, example might be FOLFOX with Avastin, if someone has progression disease on that would potentially be eligible. And I would love to hear from patients at that stage. And then maybe someone has received two lines of treatment. And that’s also an opportunity to inquire about eligibility, if it’s not for pediatric patients, and it’s not for patients who are elderly and maybe have a poor performance status, but 18 to 70, as per the trial, to respect those parameters. And you know, standard for any clinical trial hematologic and adequate liver and kidney function of the organ function, we want to look at more than four weeks elapsing from prior systemic therapy for that 20 day washout period. And respect to the fact that we’ve we’ve encountered many inquiries, not just from Minnesota, around the world, around the country. We understand and plan for the fact that not everyone on this trial will be from Minnesota, per se, but for the first 28 days, at least until the end of treatment, visit, patients must agree to be remain within a one hour drive of the University Minnesota. I would say, we want to work with patients and partner with patients, but I would say that’s not something for safety reasons that we could change. It has to be something that someone has to be willing and so one of the early questions that I trained my team in taking to ask is if someone feels that realistically, they would not come to Minnesota for more than a few days. And I say this is definitely not something that would be appropriate for them, or maybe not be of interest to them. So due to a 10 to 12 week or more delay between study enrollment, start of study treatment that could be variable based on the tills, we have to reassess performance status, just to make sure, again, for safety purposes, that someone is healthy enough to proceed, that hematologic parameters and blood count and other organ function, as demonstrated by labs and scans, is safe to pull forward. There’s a long list of eligibility, and also just ensuring that people don’t have other types of viral infections that could make til infusion or the lympha depletion chemotherapy in particular, more dangerous. Just ensuring that women with child bearing age are not pregnant, and just testing for that any changes in medical status or. Social situation that would make study participation not in the best interest of the patient and the opinion of the role investigator. So some of that might be if they have interim hospitalizations, if they’re extremely ill, may not be good time. But as Tim mentioned, if someone were to cover the tills are frozen and could be thought if appropriate, at a later time and in social situation. I think honestly, just for as many bone marrow transplant candidates, it’s an intensive process that requires a lot of social and family or caregiver of any kind support. I think that holds here, and it’s not something that any individual can physically or in many cases, do alone, but would need help. And so that’s something that would be really important to help arrange continuing to agree to remain within the Twin Cities area for 28 days, as I mentioned, and for informed written consent for any clinic trial. This is a brief schema. This is showing in schema format, the number of days what chemo therapies will be given. And this is the example, Monday through Friday. I gave cyclophosphamide given on the second and third day, but fludarabine is an intensive drug given five days in a row, started the day of admission, a little bit break of two days, and then anticipated till what we call Day Zero, followed by il two for up to several days, but a maximum of six doses. So I think vigilance is essential for safety. And so to answer some of the questions that people will naturally have upon hearing of this trial, there are a couple of novel areas, and with great novelty and innovation come responsibility to to understand what the potential side effects might be, some of which we know, and many of which from the NCI experience, can be attributed to either effects of the aisle, two such as high fevers or rigors or chills and the level of depletion chemotherapy, which essentially brings its goal is to bring the bone marrow and wipe out the existing immune system, to replace it with the immune system supplemented by the tills. I anticipate you may have, as many people might have, also in the news read about the so called cytokine storm, also called cytokine release syndrome, that has been associated mostly with car almost all with car T cells as an example. FDA approved for pediatric and some forms of adult liquid malignancies, but not found to be an experience to date, particularly since all that seems to be at the NCI. — but not seen and experienced, a date at the NCI with tills or another centers, nearly, pretty much the entirety of expected, . The entirety of side effects are anticipated are from the high dose lymphodepletion chemotherapy in il two that’s something that does differentiate this form of therapy from adoptive cell therapy off so called off the shelf car T cells, of course, we might discover because we’re at the cutting edge of innovation. Sis, immune checkpoint abrogation with CRISPR, cast nine produces one or two factors that we’re going to discover whether or not that rule might be different, or if that will hold for T cells that have been altered in this way, but we will do very careful monitoring of sign, of sign, vital signs, and these are some of the potential side effects of cell infusion that we want to look out for, and others. So I emphasized earlier that patients will receive a single course of treatment, including live with depletion chemotherapy, followed by the tills and then the aisle two, up to six doses. But we have to predicate on safety, and so I say up to eight doses of aisle two, and that might be one, that might be six, it might be three, might be zero, if it is not deemed safe. And that’s me on the premises constantly, every eight hours, getting calls from our inpatient team to assess that, as well as in person assessment. And then a treatment visit occurs on day plus 28 there’s a long list of assessments that, of course, to understand safety and to be vigilant about that. I said vigilance is required for safety. There’s a lot people will get to know our staff in the clinic, in our hospital, and through phone calls, a lot, including virtual visits in this day and age. So we have intensive mechanisms of reporting for governing bodies that ever incident monitoring and documentation through our Clinical Trials Office, we have overall experience with cellular therapy trials. And so this is just the new wave of evolution for that. And so having gained the experience, having opened the trial in the past year, in 2020 we’ve already gained a valuable experience, and also in close collaboration with a lot of colleagues who have experience at other centers. So I think from a logistical standpoint, some people may have questioned about, how would I find out more? We funnel the input system for patients not already at the university, but certainly, if patients are already treated at the university, can find out more or in the region or in the world or anywhere else in the country. You can look up clinical trials.gov NCT number, and we are funneling the inquiries to our expert clinical trial nurse navigator, who’s on the other end of these phone numbers, the phone number and the email. And so I appreciate sometimes people want to find my name or find other. People’s name and look up because it’s easy to do that Internet, and I appreciate that. What I don’t want is for referrals to get lost in the process, and also, in some measure, some of it is not HIPAA compliant by standard email. We want to respect privacy and ensure that. So the best mechanism I could recommend, and this is the same information copied from the clinical trials.gov website, is this phone number goes directly to our clinical trial nurse navigator, specifically for this trial and others, but primarily for this trial. And this is the email address. So I think of having worked with the ACR scientists survivor program for better part of the last decade, I’ve really come to have extreme admiration for patient advocates for a few years as yourself, because I know it’s not easy. It takes time. And I think, you know, having had loved ones with cancer, I feel like it’s almost a full time, or at least a part time job, just to navigate complex health systems, to navigate treatment for yourself, and deal with insurance companies and so people who take time out of the normal life, so to speak, to do this. I don’t know why I do it, and I have, I think, of immense courage. And the fact that even want to know this level of detail is never ceased to amaze me, but it shows the vast investment. And there’s nobody who has better investment than patients and their caregivers to find something better than what already exists, to find the next generation of cures. And so when patients volunteer for clinical trials, I’m always just left just very with very much with profound admiration. I’m gonna pause there. I don’t want to get too emotional on that, but I think bring cutting edge of care is the dream of scientists like Dr starr, Dr minority, Dr Weber, physicians like me who can help bridge that this, this is, this is something we’ve all dreamed of. We didn’t know about CRISPR cast nine until exposed and invented to the world in the last decade. But things like this are why we do cancer research. People like you are the reason we do all this. And so whether it’s an endeavor that takes up our days and nights and we lose sleep over we know that the end goal is to really do this, and it takes a village, and we want to bring it with great safety to everyone. I will bring over here. If you can see, this is the clinical trial.gov page. This is the information at the bottom, saying, recruiting. If any one of you has interest in the actual references, some which Tim alluded to, you can click on here and you can be taken that set of information, the long list of eligibility I basically took verbatim here, so it’s all included, and also any more information. The basic description This summarizes nicely the essence of what I’ve described. And it’s the same title that I described on the title slide, so I know we have just a few remaining minutes together, and I’d be very happy or to tag team with Dr Starr or any appropriate questions that I can answer.

Manju George 47:45
Thank you so much. Excellent. That was excellent. That was a very good introduction. You know, great introduction. And thank you, Doctor starr. I mean you your your explanations at the stage. So I think that like for us in our group, because we have the til trial, and, you know, we have people who have been posting about what they’re going through, like, the whole chemo regimen, and what they have experienced, and when they got the kills, what happened, and when they got the ILQ, what happened. So I think that lots of people maybe on this call may be familiar, because, you know, this is an advantage in having these groups right, that they explained like so this, you know, so I hope that the listeners were able to kind of place what you spoke in the context of what they’ve heard in the group. So for me, I think there is some concern about the chill trials in our group because of, you know, the cytokine storm and things like that. And, you know, one of the things I think people feel very comfortable is that they would be at NIH and it has the, you know, that they would get a lot of care and all of that. And I think that the way you have explained with the your university’s experience in bone marrow transplantation and all that you it looks like you have a similar team and the same setup and all the monitoring and everything, right? I think in my mind, that’s what I’ve heard the most common concern that, you know, how safe is it? And I mean, your study is exactly looking for that, right?

Dr Lou 49:10
I’ll tell you, I never set for the state of Minnesota until I interviewed for position here, and lo and behold, here I am, and that’s a decade later. So, you know, I think maybe allow me just provide some context so I have the background here. So there were approximately, I think now, over 60, if not more, National Cancer instituted designated comprehensive cancer centers. That’s basically a designation given for cancer centers of excellence and academic settings that have the full spectrum of Premier clinical care as well as cancer research and things in between. And there’s, there’s a large application process every five years to get this gigantic grant to have this designation. And the Cancer Center, which is called the Masonic Cancer Center at the University of Minnesota, has been an NCI designated Comprehensive Cancer Center for many decades. And there’s a specific reason. It’s not that. By accident, and it’s not only because of the basic science research here at the university that we have this trial. We were brought the opportunity to have this trial in partnership because of the renowned and because we had everything under one roof. So it was gi oncology expertise. And that’s not just me, obviously, it’s a whole team of people, and that includes expert surgeons, oncologists, radiologists, radiotherapists every everything, and then the basic science also, and then also the Molecular Cellular therapeutics group, which is one of only five NCI sponsored groups in the country. And you know what? The BMT group is one facet of that, but it’s crucial. And I think something that’s been that we were told, and one of the reasons we were asked to take on this trial is that the NCI is, you know, my best friend’s mom died of pancreas cancer in the early 90s, and that was a time where that was a last ditch effort. But in the NCI has certain capabilities, and certain capabilities it does not have. Is it premier center, and a lot of great research comes out of there, but they’re not a tertiary care referral center. They are there. And many times, for patients who have exhausted all available options and nothing else available to them, or cannot pursue anything else, they might go the NCI. Whereas here at the University of Minnesota, from the beginning, when someone is first diagnosed, when a colonoscopy is first performed, here or at our affiliate sites in the region or throughout the state, they are diagnosed colorectal cancer, they have access to our Clinical Trials Network. They have access to us. They can meet with me when first diagnosed, and maybe for the right patient, I might meet the right patient and think this patient 612, months down the road might be a good candidate for this trial, because we’re running this trial here and all the way to enrollment. We have not just the basic ability capacity. We have the outstanding capacity to take excellent care of these patients. So I think I just want to reassure people, maybe are not familiar with the state of Minnesota, not familiar with the University of Minnesota. I understand that there’s a at least one other center that may be more famous, but we have this trial. And I think there’s a reason why we have this trial, and not to say other centers won’t in the future or not, can’t or don’t have great trials themselves, but this is an innovative trial, and I think it’s because of our expertise as a multi disciplinary team that we have the opportunity to do this. And it’s a great undertaking. It’s years in the making, not just the basic science, it’s years to get the point we could even open the clinical trial, years of clinical work to get to this point, we could do this safely.

Manju George 52:22
Okay, I have one question, Would you be open to having tele, tele health visits with patients? Because I can imagine that after they watch the videos, they probably want to have, you know, initial consult with you before they, you know, decide to come. Is that something that you will be interested in doing?

Dr. Starr 52:38
I’m certainly interested. I have to work within the boundaries of what I’m allowed to do within our health system, as in many, nearly all states. Well, we, with the onset of COVID, a year ago, we plunged into the world of virtual medicine. I’m doing that almost exclusively. I still encourage you as a first point again, funneling to the clinical trial nurse navigator, the phone call and also the or email, because what the trial nurse does is she helps gather all the information. I can’t make an assessment video or not, wherever someone in the world is without proper information, and our team meets multiple times per month, led by me, but our whole team to go through scans, to go through information. I spend a great deal of my time, day and night, doing that, to try and not waste people’s time at the same time. Practically, we are not allowed to do virtual visits for people in other states, aside from Wisconsin. So unfortunately, although you think you know FaceTime and zoom and HIPAA compliant versions of virtual visits break down boundaries. Legally, I’m not allowed to this is a state government level. It’s not our institution even to to do that unless someone is physically in state of Minnesota. I acquired a a temporary license for the state of Wisconsin for the remainder of the year in order to take care of patients, my patients, and other future patients who live in Wisconsin. So we don’t have to physically come over. But if someone lives in Hawaii, for example, unfortunately, I’m not able to, but I’m open to discussion, because I don’t want to waste people’s time and have them come over here. But we do a lot of homework behind the scenes, but that’s starting by spending a lot of time obtaining the records. So I would encourage you, if you have interest, please don’t reach out to me directly, not because I wouldn’t love to hear from everybody, but we have a system in place to ensure we don’t miss any information, and my team helps me do that. Okay,

Manju George 54:22
that makes sense. And then you said that the dose of the til was one time. Are you guys also planning -??- own cells, and is there any any plan later to be using them, or something like that?

Manju George 54:39
I was wondering if you will be also freezing down cells in addition to infusing

Dr. Lou 54:46
so we are the administration clinically for the patient on the trials. It was intended to be one time for the current time, maybe future iterations of the trial might do different. But we are also doing extensive research in what we call correlate biomarkers, and that effort is led by doctors. Are. Our whole team is doing that with blood and tumor samples to determine, once we have the clinical outcomes and see who whose tumors respond best, try and identify specific factors of why that is, and maybe to refine the trial further. But for this iteration of trial, the administration of the tills is is intended to be one time. It’s intended to be hard hit, however you want to call it unintended, for this to be built to last and to have a durable, effective response while also being safe.

Manju George 55:27
So my other question is, thank you very much for that answer. My other question is, on the clinical trial website, you have a list of mutations listed right? So Should people with only those mutations reach out to this clinical trial coordinator, or is it?

Dr. Lou 55:45
There are some team mutations and the chaos mutations and all of those listed. Yeah this is independent. So that’s a great question, because so much of in the era of molecular profiling and molecular oncology basket trials, or umbrella trials, whatever we wish to call them, predicated on a tumor harboring a certain mutation at a certain time in tumors evolution. This is independent. So it has nothing to do with Pdl, one if you’re if you’re interested or read about that is nothing to do with micro satellite instability, presence or absence of K RAS mutation, BRAF mutation N RAS is independent. So it’s really more predicated, as Dr starr said, on the new antigens, and being able to stimulate the new antigens to be productive and be recognized, but is independent of any of the status that we normally would identify on standard of care genomic profiling,

Manju George 56:32
okay, I think I see one question here. It is like, can you comment on vitals without the CIS blockade are not very effective in solid tumors.

Dr. Lou 56:44
Well, I think the numbers, we don’t have 1000s of experience, but some of the studies from the NCI, I mean our limited number, and I think logistically, these are very, very difficult to try out, to carry out, and they’ve been step wise over time. So it’s not that they don’t respond without sis knockout. But this effort to knock out sis is an effort to improve further upon efficacy. I mean, the golden prize. We would love it. We would love it if 100% of time we did a treatment that it worked, we know that that’s not the case for any form of targeted therapy, regular chemotherapy or immunotherapy or cellular therapy yet. But if this strategy works, would sis be the next level? Would it improve? It double or triple fold? That would be great. So I don’t think it’s a till that don’t work, but really it’s a first step, and what probably probably be many steps in the years and decades to come.

Manju George 57:34
Okay? Thank you. So I think Dr Star had answered about the size of the tumor. He said about 10 grams. So how much like do you? Do you have? Like, I know it’s not like a fair question to ask, but what size match would be approximately? Is it like five, six centimeter cube lesion, or do you have any? Ideally,

Dr. Lou 57:55
I would say, as much as safely could be possible, but very grossly. I won’t stick to it exactly, but like, if you imagine a centimeter or something in centimeter or more in size, when I connect with our surgeons, we look at it and it really it’s kind of a game time decision, because a lot of time tumors that are treated or grow rapidly can become necrotic, meaning they die, which is good. It could be because of tumor so large that the interior part dies, or because the chemotherapy has been so effective, but if the cell portion is dead, it doesn’t have the tills that we can extract. So in that case, we may need to extract more tumor, and we also want to do some for research purposes as well. So minimum, I guesstimate, like a centimeter, and we try to get as much as safely can be removed. But also, just as we round up the discussion and appreciate your time. Is that the surgery for tumor harvest is not done with intent to cure or remove the entire tumor, but rather with intent of getting enough to make the till extraction feasible. I appreciate your time. I do have to move on, but I’m very grateful for the opportunity to come meet with everybody. Thank you, Manju, thank you. Thank you. Dr star for helping me out. Dr George as well,

Manju George 59:03
yeah, thank you. Dr Lou, thank you. Dr Starr, this is great. Thank you very much.

DocTalk
2021
Dr. Lou
Dr. Starr
Cell therapy
MSS
Stage IV
Trials

Drs. Emil Lou and Tim Starr from the University of Minnesota discuss the TIL trial for metastatic CRC in this DocTalk, recorded in March, 2021 for COLONTOWN. Dr. Starr opens this discussion with a look at the science behind the trial, including CRISPR, the powerful gene editing tool, and the tumor infiltrating lymphocytes (TILs) that give this trial its name. The second half of the video features Dr. Lou discussing the trial itself.

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BRAF V600E research update

BRAF V600E research update

DocTalk
2020
Dr. Corcoran
BRAF

Dr. Ryan Corcoran of Massachusetts General Hospital provides a look at current options and research for BRAF V600E colorectal cancer in this COLONTOWN Doc Talk, recorded in August 2020.

Dr. Morris 00:00
Yeah, thank you guys for inviting me in, as you refer to, we really appreciate just the support of COLONTOWN in general. This goes beyond just kind of, as you mentioned, your support for the COBRA trial, and in the BRAF trials as well, which you guys are obviously incredible in mobilizing patients, through social media, but I will say more experientially as well, you know, this group means a lot to my patients. And it’s common for me to have that patient come to MD Anderson, who’s newly diagnosed with colon cancer and is very understandably afraid and, to hear kind of their testimonies with how helpful COLONTOWN has been, and helping them and other patient advocacy groups who have been in helping them to understand kind of what’s going on with the shock of this news in their lives. So we just want to say we as oncologists appreciate your commitment to helping patients in this effort we’re all fighting against. I will say, you know, I realized that Dr. Corcoran had presented I think, a week or so ago. So some of this may overlap, I’ll try to kind of interject my own opinions about this, but there will be some overlap. There may be some slides that we haven’t published yet. But I did want to share these just share our data. So when I hit the slides, I want to share that kind of why we think what we think, but also just maybe ask for those particular slides, just kind of keeping those confidential, because we haven’t really published this data yet. I’m gonna be talking about kind of combining targeted therapies with immunotherapy. And maybe not using a one-size-fits-all approach for the management of BRAF-mutated metastatic colorectal cancer.

So I always just feel that it’s important to start out with, a patient presentation just to kind of put into context what we’re up against here, and this was a patient that I met during my first year on faculty at MD Anderson. She was a 35-year-old lady from the valley in southern Texas who presented to the ER, with abdominal pain, no past medical history at all. She had a 13-year-old son, a single mother. When she presented with abdominal pain her surgeons locally felt that she had issues with their gallbladder and took her to surgery to remove the gallbladder and were surprised, instead, to find a large transverse colon mass with diffuse metastatic disease in the peritoneum that was responsible for the abdominal pain. The pathology ultimately showed a microsatellite-stable BRAF-mutated CRC tumor. She then came to MD Anderson, where, by the time she arrived at MD Anderson, she already had evolved a large bowel obstruction from her tumor. So this was in 2016, we started her on treatment with FOLFOXFIRI. And she had some initial clinical improvement, but unfortunately, within three months of what is really throwing the kitchen sink at this tumor, in terms of cytotoxic chemotherapy, she was already developing signs of clinical and radiographic progression. Within four months of her initial presentation, the single mother was transferred to hospice and it was horrific to watch this unfold as a new oncologist at that point in time, and I think it just really speaks to the challenge we face with BRAF-mutated colorectal cancer, we recognize that this is a unique population with regards to clinical outcomes. As I’ve alluded to, the responses to chemotherapy aren’t great as we’re used to seeing our BRAF wild-type patients, we recognize the unique pathology here just in terms of where these tumors commonly arise from and how they look under the microscope. And with the genome as well we’ll talk about later the high tumor burden may extend beyond the association with MSI high into the MSS setting as well. But also it’s unique with regard to the epigenome and we recognize these to be hypermethylated tumors. I think that this still represents an untapped biology, that is potentially targetable with regards to this particular subpopulation of colorectal cancer, and possibly, with respect to the transcriptome as well, and we’ll talk kind of about CMS correlations a little bit later, too. So we’re seeing a unique but challenging, but potentially intervenable, clinical presentation. And I’ll kind of go through these slides quickly, because we all recognize that the BRAF mutations, even though it’s typically called an uncommon subpopulation of CRC, when you still consider it’s 5 to 10% of all the patients who have CRC and colorectal cancer represents one of the top causes for cancer mortality in the United States. By absolute numbers, it’s still a large fraction of patients who are faced with the challenge of BRAF-mutated, metastatic CRC. And unfortunately, as we all know here the successes of targeted therapies in terms of response rates that other cancer types see with the same exact BRAF mutation, we just don’t see those in data that Dr. Kopetz and then Dr. Corcoran had shown with BRAF monotherapy and BRAF MEK combination therapy, it just we don’t see either the response rates or the survival outcomes, that we’re accustomed to seeing in the context of other solid tumors as well. So this, oftentimes, when I hear people say that we should be treating tumors agnostically to the primary and according to the molecular subtype, I always just cringe when I hear that, because I think that again, that’s a one-size-fits-all approach. And I think that the BRAF V600E story for colorectal cancer is a very good example of why we can’t practice under such an umbrella. This is just kind of data that, again, we’re all familiar with, from eight years ago now, just kind of showing why in the context of CRC, blocking the BRAF V600E oncoprotein with agents that work in other contexts doesn’t work as well, to kind of have this upregulation of MAP kinase signaling, you get kind of this constitutive activation of… I think I say this to say it again, I don’t… correct me if I’m wrong here, but I think I can probably go pretty quickly through the next couple of slides. I think this group fully understands the recent clinical trials, which have led to clinical outcomes, or new clinical options for these patients; but it was really exciting, I think, to be involved early on with Dr. Kopetz as a fellow even, and working on the SWOG protocol, and seeing this translate from an idea in the data that was coming out of the lab, to showing some benefit in patients.

We looked at a model too that is a different model that was initially had disease control with Vemurafenib and Cetuximab. And we saw similar results in PDX, as we were seeing acquisition of acquired KRAS mutations. This is something that in the Vemurafenib study, when they went to the baseline samples of these patients and looked in their plasma, droplet digital PCR sequencing showed the presence of very, very low allelic frequency of KRAS mutants, you can see 0.21%, 0.31% that were present at baseline that are oftentimes below the limit of detection of assays that were available at that time. When we looked at patients who were treated on a phase one trial at MD Anderson with Vemurafenib, Cetuximab and Irinotecan, we saw that in the black here, you see the relative allelic frequency of the BRAF V600e gene in ctDNA. But again, we were finding in patients the same thing that we had seen in the PDX models, that there were these acquired oncogenes showing up in the resistant setting that had not been present in the pretreatment specimens. So our question then, at that time, and this is the data that we took to Array when Kopetz was pitching the BEACON approach, was: can the addition of the MEK inhibitor overcome the resistance to BRAF, EGFR targeted therapies. I also think with the SHP and SOS inhibitors, which are coming out as well, this also kind of represents something we’re thinking about moving forward as well. And again, what we saw on our PDX was, again, when these tumors grew resistant to the Vemurafenib and Cetuximab, if we added a MEK inhibitor, we could see sensitivity; and I think that Corcoran and his group beat us to the punch in publishing this data, but we certainly felt that what we’re seeing in the lab were being validated by his group as well. And so again, it made a lot of sense to us. So, as we all know, these thoughts led to the creation of the BEACON study. This is kind of flipped here, but the overall response rate of 26% with the triplet, and the 20%, with the doublet, beat that of Irinotecan and Cetuximab. And as you guys are all aware, the addition of the MEK inhibitor didn’t add any overall survival difference between BRAF EGFR and, very excitingly, (oh, this should actually be changed)… Encorafenib, Cetuximab, in February or April 2020, became FDA approved. So this was obviously super exciting for us, and for our patients as well. So one of the questions that comes up with our patients when we talk about this in the clinic is binimetinib, is it a non-viable option for the management of patients with BRAF mutated colorectal cancer? And I honestly don’t fully know how to answer this question because I struggle with the idea that there’s a one-size-fits-all approach for patients with BRAF-mutated metastatic colorectal cancer. You know, I think that we realize, clinically, these are heterogeneous patients, and they’re probably biologically these are heterogeneous patients as well, and just kind of talking out loud, it just seems like when we manage these patients, we oftentimes get a lot of more mixed responses and the BRAF mutated context than we do in maybe the BRAF wild-type, I don’t know, if that’s a thing, I’m actually just kind of talking out loud right now, saying that I haven’t really looked into it, but it’s, you just see this more, I think, than kind of in the BRAF wild type where if patients are going to progress, all of their spots are going to be kind of progressing together. Whereas, oftentimes you’ll have responses in two-thirds of the lesions and then massive changes in the opposite direction in the other third. So, again, I think the underlying biologic heterogeneity, as well, is very interesting, and it points to the challenge of treating this disease. We presented this data at ASCO last year. It’s under review right now for a manuscript.

We looked at our cohort of patients at MD Anderson, if you had been evaluated since 2005. And we found 187 patients with BRAF-mutated metastatic CRC. If you were evaluated at our institution, and we just asked a simple question: if we take both ends of the spectrum and compare the differences what do we see? It wasn’t surprising that in the better survival group there were more MSI-high patients; almost 50% of the patients in whom we had data on had MSI-high tumors. But I think that one of the really interesting things as well, is that the median survival from the time of metastatic disease, and this longest survival, was eighty-four months, and in the lowest survival, it was 8.6. And I think that when we, as oncologists see the BRAF mutation, our minds automatically go to this lower end of the spectrum. But I think that we have to kind of keep open minds that there are patients who do have good survival outcomes. When we looked at what is driving out survival in this longest survival group, – what’s driving the long survival outcome? And we saw that was also heterogeneous as well. Some of these patients were able to go to surgery. And as you can see, in the black line here, many of these patients remained disease-free despite having an initial diagnosis of BRAF mutated, metastatic CRC, you know, 5, 6, 7 years out. But interestingly, and as we would expect, as immunotherapy has unfolded, patients who are MSI-high, were also seeing good long-term outcomes. Interestingly, one of these patients had an MSS tumor. But again, there were seven patients that we found who were doing fairly well for long periods of time on MAP-kinase targeted therapies, this included BRAF EGFR options, BRAF MEK options and BRAF inhibitors alone. So, there is some suggestion here to us that there may be a subpopulation of the BRAF mutated who just need targeting in their MAP-kinase, in their particular tumor is addicted to MAP-kinase signaling in the same way that perhaps an EGFR-mutated lung cancer may be addicted to that EGFR mutation, and being equally sensitive to tyrosine kinase inhibition in that context as well. So, I say that to say that even the drivers for favorable outcomes in the study are heterogeneous and do not always conform to what providers can assume. So, I talked about how this is still ongoing, I think, bench to bedside to bench and back to bedside success story, but how can we lift that tale further.

Obviously, in the MSI setting, response rates, even with a concomitant BRAF V600E mutation, is very good for anti-PD1 with or without anti-CTLA4 therapy. But unfortunately, still within the BRAF V600E context, we feel that the MSI-highs, that concomitant microsatellite instability is still a minority of the patients with BRAF V600E tumors. So, this is where we start getting a little bit more in-depth to our data, which we haven’t published yet, but I did want to share with you. It’s a majority of… we think of BRAF V600E tumors as being kind of high tumor mutation burden. And oftentimes I think the assumption is that, well, there’s this association between microsatellite instability, we all know that MSI tumors have higher mutation burdens and so that’s the reason that BRAF V600E tumors carry this association with having high tumor mutational burdens. We actually looked at four datasets that were available to us: the nursing health data from Memorial Sloan Kettering, data from the TCGA, and then from internal data, we had it at MD Anderson, and we said, let’s pull out the MSI high tumors. And let’s look at just the MSS tumors. And look at the patients and compare BRAF-mutated tumors with the BRAF wild types. We saw the same trends across all four datasets that in general MSS, BRAFV600E mutated tumors harbor higher tumor mutation burdens relative to their MSS, BRAF wild-type counterparts. So this may not be something that’s just MSI-high-driven. And if that’s the case, this may argue for some role of immunotherapy as a component for the MSS BRAF V600E story. We’re also excited to see data that was published in Science last year from Dr. Bardelli’s group in Milan, where they looked at BRAFV600E CRC cell lines and showed that when you treat these with dual BRAF EGFR targeting, you induce, in terms of expression, a loss of expression of the mismatch repair of proteins and can kind of create this transient and MSI-high like state. So, if that’s the case, you know, does that make sense that dual, or I guess, triplet, BRAF EGFR plus PD-1 therapy would make sense in this context. And this is something that we’ve seen as well. This is data we haven’t published yet, but this is from an expansion cohort of patients who were treated with vemurafenib, Irinotecan and cetuximab, – patients with BRAFV600E metastatic CRC. This is an example of a patient with a microsatellite stable tumor, but you can see prior to treatment, you don’t see a lot of immune reactive T cells within the tumor microenvironment, but that upon treatment with a BRAF EGFR inhibitor, you do see recruitment of activated CD8 positive cytotoxic T cells within the microenvironment. So that suggested to us that there may be a role for BRAF EGFR plus immune checkpoint therapy when we were pitching these concepts years ago in our initial letters of intent.

Let’s talk about CMS, you know, we all I think all recognize the role of CMS biology and that again, CMS1 is kind of the immune active group of a subset of CRC tumors, again, often associated with microsatellite instability. We also recognize that BRAFV600E tumors kind of aggregate to CMS1 oftentimes as well. And so our question again was is this association uniquely inherent to this association between MSI high CRC with BRAF V 600E mutations or can you see this in the MSS setting as well. So, we looked at data from the SWOG 1406. And again, it hasn’t been published yet either, but will be kind of forthcoming. And we looked specifically at in the red here from the from the SWOG study. And within the MSS context, the relative distribution of BRAFV600E tumors and as again, as you can see almost half of the MSS BRAF tumors were CMS1, the other kind of large proportion was CMS4. And this is different than what we had seen with an internal cohort of patients at MD Anderson who had MSS BRAF wild types, where you see a very low fraction of CMS1 within the BRAF of wild-type MSS contexts. So again what we’re seeing here is that within this MSS CRC population of patients, there may be some enrichment for a group, at least of BRAFV600E MSS tumors, for this more kind of immunologically hot CMS1 phenotype. We recognize from data that was published by several groups several years ago that already signatures can indeed for their subcategorized, BRAFV600E tumors, BM1, the B RAF mutation, one subgroup, it tends to be more of a kind of KRAS MAP kinase. Whereas the BM2 is more consistent with cell cycle gene regulation. And again, you can see here kind of when they look by CMS subtypes as well you see kind of what we had seen in the in the prior slide in the group where you have more MSS, BRAF mutated tumors, you start seeing more CM4 as well. And I think that it’s a little bit early to know how this will kind of play out but again, kind of argues for the heterogeneous subpopulations within the BRAF V600E contexts.

So I think that, this was the reason that we were thinking, about the BRAF, EGFR PD1 combination, and we’re very excited to kind of see Dr. Corcoran’s data that he presented earlier this summer in virtual Barcelona and then I think to you guys, it sounds like in the recent past here, looking at the Dabrafenib Trametinib Spartalizumab combination. So not exactly the same ideas or it’s just kind of given the mechanism of the BRAF but, I think that one of the things that really stuck out to us was the fact that you don’t see a whole lot of kind of toxicity with this combination. When we approached Array and BMS with this idea several years ago, I think that they internally were worried a lot about the skin toxicity that you were going to see with these combinations. And I think that his early data suggests that, this is a fairly well-tolerated regimen. But very interestingly even though the data are still very early and immature, the gross numbers, just comparing the same BRAF MEK combination with or without a PD1 I mean, it’s really encouraging, like, and it’s very encouraging. And similarly, I think that he saw, kind of with this slide, similar to what I had shown you guys with our multiplex immunofluorescence slide, or data several slides back, but again, that BRAF MEK PD1 does seem to recruit active T cells to the tumor microenvironment for hopeful cytotoxicity. So, this kind of led us to our concept at MD Anderson, which is now enrolling, you know, it’s a trial looking specifically at MSS BRAFV600E mutated CRC for patients who have not had prior BRAF, EGFR, MEK therapies or immunotherapy, I think his trial may have been a little more broader, and its eligibility criteria. But, this was the population we wanted to look at first, to kind of see signal and we put 11 patients on kind of amidst the COVID pandemic and having to stop it for 2 30-day windows to evaluate toxicity. And given the fact that this combination hadn’t been looked at before. And so we’ve enrolled, you know, fairly quickly under this trial, and what we’re seeing is that just kind of as Dr. Corcoran has shown, the safety data is very promising for this combination as well. This is the kind of the selected eligibility criteria for study again, MSS BRAF V600E adenocarcinoma of the colon or rectum, at least one but no more than two prior lines of systemic therapy, and then excluding prior BRAF, MEK or other anti EGFR therapies or immunotherapy. So that trial, like I said, is enrolling kind of at the same time, as we were about to launch, Dr. Atreya at UCSF was interested in looking at a BRAF MEK PD1 combination in the same setting. So we’ve worked with her to kind of get these trials going up in parallel, I believe her trial is open now. And I think that they’re kind of talking to her they’ve been enrolling too. Sorry, I actually don’t know what the safety data is of this combination yet. I haven’t heard that from her. But we presume that it’s going to be well tolerated.

So I want to circle back just to how we can learn from what we’re doing in the lab, and move that forward in this context, as well. We love using PDX models at MD Anderson kind of as I’ve talked about earlier, we feel that these kind of help us to pitch concepts for clinical trials to the NCI and pharmaceutical companies. And we’ve shown again, in data that hasn’t been published yet that what happens clinically, the patients on BRAF, EGFR therapies match what happens in their matched mouse avatar. So we looked at five patients who were treated on the SWOG 1406 study and characterized them by their clinical responses either having stable disease or partial response. And what you can see is that the overall trends for the stable disease patients in the blue mirror that for what was happening in the matched mouse whereas what was happening in the patients who responded clinically to the combination, you see have greater reductions, kind of in the tumor size in their mouse avatars as well. One of the interesting things just kind of anecdotally, just to kind of point out here as well, is that, in some of these mouse models, this was just looking at this one, the patient had a response to vemurafenib, irinotecan and cetuximab. You can see that in this mouse model for this patient, the BRAF EGFR, you know, it developed resistance but then when we added the irinotecan you see a drastic reduction in tumor size, there’s also a trend towards the irinotecan being different than that of the BRAF EGFR. Similarly, here, this mouse model, this patient responded to the combination, the mouse didn’t really benefit from irinotecan alone. But when we added all three, we saw that there was improvement. So, again, it may point, that just the one size doesn’t fit all. And also kind of points to the fact that this heterogeneity that I’m talking about. There is a trial, you know, that’s being developed in moving forward looking at chemo with or without encorafenib cetuximab in the frontline setting. And I think that data like this kind of points, the idea that, hey, maybe there’s some meaningful interaction with chemotherapy and targeted therapies in this context that that we will see. The problem is when it comes to mouse models, these are immunocompromised. So the the ability to study, the encorafenib nivolumab cetuximab combination would be limited in traditional PDX models. So, Dr. Karla in our group at MD Anderson’s, all star, his work to develop these humanized PDX models where tumor tissue from a patient and matched blood is used to create these mouse avatars. And we have funding that’s through an early career SPORE award at MD Anderson to do a clinical trial for our study, to look to see if what happens again in the patient mirrors what happens in with the same treatment combination in a developed humanized PDX model. And likewise, if what you see happening immunologically, in terms of changes, matches what happens in the matched humanized PDX model as well. This was funny, I got through the SPORE award the mentor here is John Allison, who won the Nobel Prize for his work in developing immunotherapy for patients with cancer. And it’s been really exciting to have the chance to work with Dr. Allison on and get his input on the design and science of what’s going on here. This was just kind of work showing some stuff we’re doing with Dr. Tusayan in collaboration with her on this trial, I would also ask this to be confidential and not shared as well, out of respect to her developing technology, but what we’re doing is we’re getting her slices of tumor, from pretreatment biopsies taken from patients on this study. And then she’s slicing these tumors and putting them into individual plates. And we’re testing what’s happening, with various combinations. And this is a patient who responded on our study to the triple combination. And what we saw was that when she treated the small slices of the tumor with encorafenib, and cetuximab by day 18, there was some reduction of tumor cell viability with the BRAF EGFR combination. When we added nivolumab, to that combination, we saw a much deeper reduction in cell viability, I didn’t put the nivolumab here as well, but it was that bar was here. So you didn’t see it wasn’t single-agent nivolumab down here either. So it was interesting to us because we felt that her model could likewise when you have the patient’s own immune cells present within the microenvironment may reflect what’s happening in the matched patient, but also that there may be in some patients some meaningful benefits to the addition of nivolumab. So, I hope that I provided here some rationale for why adding immunotherapy to BRAF, EGFR targeted therapies in MSS BRAF mutated setting makes sense, when these patients historically have been unresponsive to immunotherapy alone. I think we’re all encouraged by Dr. Corcoran’s work. And our hope would be that given the recent FDA indication of encorafenib and cetuximab we can build upon that success with a similar approach, and are certainly working to that and then I think that this will be informed further by preclinical and translational work that remains ongoing.

I was asked just to talk a little bit about atypical BRAF mutations in CRC. These are slides that I borrowed, full disclosure from Dr. Benny Johnson in our group at MD Anderson who really has led our group’s efforts, very valiantly to kind of work. This is a slide I think, had come from maybe Dr. Yeager at Memorial, I’m just kind of showing how the different mechanisms have the traditional RAS independence, BRAF V600E monomer, we associate with a class I, the dimerized. BRAF mutants, we see kind of with class II, and then kind of the, the BRAF inert, class IIIs that kind of has been characterized is these more atypical BRAF mutations. Again, we recognize that, as you can see, in all three of these, the atypical BRAFs tend to fare better than the BRAF V600Es and I would say I don’t think that this is something that all oncologists realize it’s not uncommon, so you get a referral or a call from outside doctors saying, hey, I have a patient with the BRAF mutation can I send them for your trial, and then we find out that it’s like a D594G mutation, kind of one of these more atypicals. So I think this is something we’re really trying to get the word out with oncologists as well, kind of as we learn more. And this is kind of, again, Dr. Johnson here, who I really just want to plug I think, has really had a passion for leading this effort in our group at MD Anderson, but just kind of some of the novel approaches that we’re trying to take at MD Anderson for kind of how we triage patients to various trials, according to their specific BRAF mutation, whether it’s a V600E, or a non V600E. So that kind of sums up what I had to say. I try to be active on Twitter, if you have any questions, please just let me know.

Manju George 37:06
So if I can, I’m going to start the questions, you can hear me, right?

Dr. Morris 37:12
Yes, I can. Yeah.

Manju George 37:13
So you were talking about the heterogeneity, so I was kind of wondering, in the unpublished data that you have, can you said that one part was the MAP kinase signaling pathway, and the other one was a different, you know, cell cycle and all of those pathways? So are you in your different trials are you attempting to find out what those different groups are? And in the reason I asked is, just like you said, we in our group, we find a lot of heterogeneity in how people respond to the different treatments for the BRAF V600E mutation. So it will make sense to us to if we could know what they were, because most of the patients, they already have their genomic testing done. And then if there’s some way to know upfront that you are in the 8.4 months category, not in the 84-month category, then you can plan accordingly how you have to prioritize treatment, right?

Dr. Morris 38:14
Yeah. So I think we’re looking at that we’re certainly collecting biopsies, to look at the transcriptome in RNA sequencing of these patients, and that may kind of inform on what their CMS classifications or BM1 BM2 classifications. I believe that Pfizer is looking at that on the patients who were on the Beacon study as well. So I think it’ll be very interesting if you see here that the BM1 patients are the ones who maybe had more benefit with the triplet, if there was a preferential added benefit with the addition of the MEK inhibitors that the BM1s than the BM twos. So, I’m very interested in this question as well and I hope that we’ll get some information from Pfizer about that. I think that Corcoran had published from his triplet, the dabrafenib, tremetinib, panitumumab work earlier this summer in clinical cancer research some signal kind of saying that, but I think it’ll be very interesting, in a larger cohort in a randomized trial to look at that in a kind of post hoc analysis.

Manju George 39:33
And then my other question would be like, there is this test called immuno score, right? Do you think those kinds of tests can tell you more, I was kind of wondering that if there was any efforts to develop some kind of assays so that you can look at a BRAF patient and say that this would be more BM1 or BM2, even the consensus molecular subtypes if there is, do you know if there is something like that being developed or going on?

Dr. Morris 40:02
I mean, not that I’m aware of I’m sure that it probably is being worked on. And it’s a really good point. But it’s not something that we’re actively working on now.

Manju George 40:13
Okay. And then the other person that you’re collaborating with Houston Yun, like the tissue culture thing. So it’s like an entire section of the biopsies is grown in the wells and you’re seeing that, when you try the combination treatment with the immunotherapy, just with that not inside an animal, you’re still seeing a response. Right? That’s what you said?

Dr. Morris 40:40
Yeah, that’s right. So, I mean, again, like, we’ve put only 11 patients on our trial thus far. And I mean, in full disclosure, with the pandemic, we had to shut down understandably, all optional biopsies for several months. So this limited our ability, thus far to look at this in high numbers, but it is something that we’re opening back up now. And we’ll be looking more stringently to see is there a signal? You always see kind of in the presentations, the N of one? So it’s hard to know for sure iff that’s truly representative, or if people cherry-pick the best for you to show? I don’t know,

Manju George 41:26
Okay. And then you have some results by GI-ASCO. Is that right?

Dr. Morris 41:36
Yeah, I mean, if so, it’d be a late-breaking abstract. I think we have 26 patients that we would plan on putting on study, so we’re just about halfway there. So it would either be a late-breaking, or probably the ASCO next year, we’ll see. We’re moving forward. And we talked to the NCI about what the next step would look like in a more definitive fashion.

Manju George 42:03
So, thank you, let’s see if others have questions. Questions, anyone?

COLONTOWN Member 42:29
Know, I feel like I need to, like, listen to this all again and consume so much information here, it’s been very helpful. But I was really interested to hear about some of the other mutations, you know, that we’re seeing, that are driving when BRAF you know, kind of becomes, you know, less important. So, while you know, I’m, again, I kind of feel like I need to, like review all of that, again, because I don’t think I caught it all. But you know, any other thoughts you have around that? And how we should think about how does treatment progress, as you know, maybe get to the end of what targeted BRAF therapy can do how do you make the decision to move forward from there?

Dr. Morris 43:10
Yeah, I mean, I think it’s a really good question. I think one of the things that hasn’t been fully looked at yet is with what you see in a RAS wild-type setting where there’s this idea of, these patients developing these acquired RAS, KRAS NRAS mutations. And then when you pull away the anti-EGFR therapy, that selective pressure is lost, and that acquired mechanism of resistance decays back down. Dr. Christine, Parsighian in our group had a really nice paper just kind of showing the kinetics of in the acquire resistance study to anti-EGFR therapy, the median half-life is about four to five months. So, before by the time you see 50% of that acquired resistance mechanism go away and then you can re-challenge these patients and see some benefit, and that’s being looked at in multiple clinical trials right now. And then the question is when a patient progresses on BRAF EGFR therapy, is that the end ever in their story and journey for EGFR therapy, or is there a role for rechallenge? None of us knows that. And I think it would be really, really interesting to look at. So I mean, yeah, like I think that’s something we’ve thought about, and I’m not aware of any data out there that’s shown that that’s successful or not successful.

COLONTOWN Member 44:53
Thank you, Manju. Dr. Morris, My name is Rashmi and I’m a caregiver to my husband with BRAF. My question to you is we know the pathway of the BRAF and the EGFR and the MEK and Erk. Looking at the three trials between Dr. Corcoran’s Dr. Kopetz and Dr. Atreya’s it seems that the BRAF and immunotherapy are similar. What’s different is the EGFR versus the MEK. Would you speak something to that? Is there I mean, your study is leaning towards the EGFR versus Dr. Corcoran’s is looking more at the MEK inhibitor?

Dr. Morris 45:39
Yeah, I mean, I think that’s what he’s seeing and the rationale for what we did what we did was similar, I don’t think that we know that BRAF, EGFR PD1 is any better or worse than BRAF MEK PD1, I think for us we realized several years ago that with the SWOG data that probably BRAF EGFR was going to get approved. And how we were going to be able to develop a strategy to, if successful to roll this out to our patients. It made sense in the context of a BRAF EGFR setting. So that’s why we we kind of went with that for approach years ago. He ‘s done a lot of work in the BRAF, MEK. I mean, I can’t speak to why they chose that, but I don’t think that we know that there’s a difference or why or if there’s a difference. Thank you.

Manju George 46:54
Okay, again, I’m going back to the CMS1 and CMS4 subtypes. So in our group, we have patients, we have one patient who has been almost NED, she’s been on the Beacon triplet, and she’s that one patient,who has gotten a phenomenal response. For most of the patients, we see that they’re on the triplet for a certain time, and then you know, things start growing, and then they get back on FOLFIRI + bev and that seems to work really well. So we have a group of patients for whom the FOLFIRI plus bev or FOLFOXIRI plus bev seems to give the best response. So again, I was kind of wondering whether, you know, that goes back to what you said about the BRAF, MEK, ERK pathway being important versus the cell cycle one, because then in that case, the cell cycle one would be more susceptible to chemo, right.?

Dr. Morris 48:01
Yeah, I mean, in theory, yes, but kind of given the fact that, these patients don’t respond in a treatment-refractory setting very well to chemotherapy, whether that translates into, clinical reality, I don’t think we know yet.

Manju George 48:22
Again, like, my push will be to if there could be an assay to tell you what kind of BRAF you are, from a patient perspective, that could make a big difference to patients as to how they approach the different treatments.

Dr. Morris 48:33
It would help us to Yeah, I mean, I think we’re very interested in understanding the different biologies, because again, we recognize it’s not a one-size-fits-all approach here.

Manju George 48:53
I think if there are no more questions, thank you very much for your time, and I guess that people, there are about 250 members many of them will watch the video because we’re going to post this in our group. And then there may be more questions, so then I’ll probably get them to you either by email or on Twitter. And thank you so much for your time.

Dr. Morris 49:20
Thank you, I appreciate it so much.

Manju George 49:23
Bye. Bye. Thanks, everyone.

DocTalk
2020
Dr. Corcoran
BRAF

Dr. Ryan Corcoran of Massachusetts General Hospital provides a look at current options and research for BRAF V600E colorectal cancer in this COLONTOWN Doc Talk, recorded in August 2020.

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Targeted therapies and immunotherapy

Targeted therapies and immunotherapy

DocTalk
2020
Dr. Morris
BRAF
Immunotherapy

Dr. Van Morris from MD Anderson discussed combining targeted therapies and immunotherapy for BRAF patients in this COLONTOWN Doc Talk, recorded in August 2020. 

Dr. Morris 00:00
Yeah, thank you guys for inviting me in, as you refer to, we really appreciate just the support of COLONTOWN in general. This goes beyond just kind of, as you mentioned, your support for the COBRA trial, and in the BRAF trials as well, which you guys are obviously incredible in mobilizing patients, through social media, but I will say more experientially as well, you know, this group means a lot to my patients. And it’s common for me to have that patient come to MD Anderson, who’s newly diagnosed with colon cancer and is very understandably afraid and, to hear kind of their testimonies with how helpful COLONTOWN has been, and helping them and other patient advocacy groups who have been in helping them to understand kind of what’s going on with the shock of this news in their lives. So we just want to say we as oncologists appreciate your commitment to helping patients in this effort we’re all fighting against. I will say, you know, I realized that Dr. Corcoran had presented I think, a week or so ago. So some of this may overlap, I’ll try to kind of interject my own opinions about this, but there will be some overlap. There may be some slides that we haven’t published yet. But I did want to share these just share our data. So when I hit the slides, I want to share that kind of why we think what we think, but also just maybe ask for those particular slides, just kind of keeping those confidential, because we haven’t really published this data yet. I’m gonna be talking about kind of combining targeted therapies with immunotherapy. And maybe not using a one-size-fits-all approach for the management of BRAF-mutated metastatic colorectal cancer.

So I always just feel that it’s important to start out with, a patient presentation just to kind of put into context what we’re up against here, and this was a patient that I met during my first year on faculty at MD Anderson. She was a 35-year-old lady from the valley in southern Texas who presented to the ER, with abdominal pain, no past medical history at all. She had a 13-year-old son, a single mother. When she presented with abdominal pain her surgeons locally felt that she had issues with their gallbladder and took her to surgery to remove the gallbladder and were surprised, instead, to find a large transverse colon mass with diffuse metastatic disease in the peritoneum that was responsible for the abdominal pain. The pathology ultimately showed a microsatellite-stable BRAF-mutated CRC tumor. She then came to MD Anderson, where, by the time she arrived at MD Anderson, she already had evolved a large bowel obstruction from her tumor. So this was in 2016, we started her on treatment with FOLFOXFIRI. And she had some initial clinical improvement, but unfortunately, within three months of what is really throwing the kitchen sink at this tumor, in terms of cytotoxic chemotherapy, she was already developing signs of clinical and radiographic progression. Within four months of her initial presentation, the single mother was transferred to hospice and it was horrific to watch this unfold as a new oncologist at that point in time, and I think it just really speaks to the challenge we face with BRAF-mutated colorectal cancer, we recognize that this is a unique population with regards to clinical outcomes. As I’ve alluded to, the responses to chemotherapy aren’t great as we’re used to seeing our BRAF wild-type patients, we recognize the unique pathology here just in terms of where these tumors commonly arise from and how they look under the microscope. And with the genome as well we’ll talk about later the high tumor burden may extend beyond the association with MSI high into the MSS setting as well. But also it’s unique with regard to the epigenome and we recognize these to be hypermethylated tumors. I think that this still represents an untapped biology, that is potentially targetable with regards to this particular subpopulation of colorectal cancer, and possibly, with respect to the transcriptome as well, and we’ll talk kind of about CMS correlations a little bit later, too. So we’re seeing a unique but challenging, but potentially intervenable, clinical presentation. And I’ll kind of go through these slides quickly, because we all recognize that the BRAF mutations, even though it’s typically called an uncommon subpopulation of CRC, when you still consider it’s 5 to 10% of all the patients who have CRC and colorectal cancer represents one of the top causes for cancer mortality in the United States. By absolute numbers, it’s still a large fraction of patients who are faced with the challenge of BRAF-mutated, metastatic CRC. And unfortunately, as we all know here the successes of targeted therapies in terms of response rates that other cancer types see with the same exact BRAF mutation, we just don’t see those in data that Dr. Kopetz and then Dr. Corcoran had shown with BRAF monotherapy and BRAF MEK combination therapy, it just we don’t see either the response rates or the survival outcomes, that we’re accustomed to seeing in the context of other solid tumors as well. So this, oftentimes, when I hear people say that we should be treating tumors agnostically to the primary and according to the molecular subtype, I always just cringe when I hear that, because I think that again, that’s a one-size-fits-all approach. And I think that the BRAF V600E story for colorectal cancer is a very good example of why we can’t practice under such an umbrella. This is just kind of data that, again, we’re all familiar with, from eight years ago now, just kind of showing why in the context of CRC, blocking the BRAF V600E oncoprotein with agents that work in other contexts doesn’t work as well, to kind of have this upregulation of MAP kinase signaling, you get kind of this constitutive activation of… I think I say this to say it again, I don’t… correct me if I’m wrong here, but I think I can probably go pretty quickly through the next couple of slides. I think this group fully understands the recent clinical trials, which have led to clinical outcomes, or new clinical options for these patients; but it was really exciting, I think, to be involved early on with Dr. Kopetz as a fellow even, and working on the SWOG protocol, and seeing this translate from an idea in the data that was coming out of the lab, to showing some benefit in patients.

We looked at a model too that is a different model that was initially had disease control with Vemurafenib and Cetuximab. And we saw similar results in PDX, as we were seeing acquisition of acquired KRAS mutations. This is something that in the Vemurafenib study, when they went to the baseline samples of these patients and looked in their plasma, droplet digital PCR sequencing showed the presence of very, very low allelic frequency of KRAS mutants, you can see 0.21%, 0.31% that were present at baseline that are oftentimes below the limit of detection of assays that were available at that time. When we looked at patients who were treated on a phase one trial at MD Anderson with Vemurafenib, Cetuximab and Irinotecan, we saw that in the black here, you see the relative allelic frequency of the BRAF V600e gene in ctDNA. But again, we were finding in patients the same thing that we had seen in the PDX models, that there were these acquired oncogenes showing up in the resistant setting that had not been present in the pretreatment specimens. So our question then, at that time, and this is the data that we took to Array when Kopetz was pitching the BEACON approach, was: can the addition of the MEK inhibitor overcome the resistance to BRAF, EGFR targeted therapies. I also think with the SHP and SOS inhibitors, which are coming out as well, this also kind of represents something we’re thinking about moving forward as well. And again, what we saw on our PDX was, again, when these tumors grew resistant to the Vemurafenib and Cetuximab, if we added a MEK inhibitor, we could see sensitivity; and I think that Corcoran and his group beat us to the punch in publishing this data, but we certainly felt that what we’re seeing in the lab were being validated by his group as well. And so again, it made a lot of sense to us. So, as we all know, these thoughts led to the creation of the BEACON study. This is kind of flipped here, but the overall response rate of 26% with the triplet, and the 20%, with the doublet, beat that of Irinotecan and Cetuximab. And as you guys are all aware, the addition of the MEK inhibitor didn’t add any overall survival difference between BRAF EGFR and, very excitingly, (oh, this should actually be changed)… Encorafenib, Cetuximab, in February or April 2020, became FDA approved. So this was obviously super exciting for us, and for our patients as well. So one of the questions that comes up with our patients when we talk about this in the clinic is binimetinib, is it a non-viable option for the management of patients with BRAF mutated colorectal cancer? And I honestly don’t fully know how to answer this question because I struggle with the idea that there’s a one-size-fits-all approach for patients with BRAF-mutated metastatic colorectal cancer. You know, I think that we realize, clinically, these are heterogeneous patients, and they’re probably biologically these are heterogeneous patients as well, and just kind of talking out loud, it just seems like when we manage these patients, we oftentimes get a lot of more mixed responses and the BRAF mutated context than we do in maybe the BRAF wild-type, I don’t know, if that’s a thing, I’m actually just kind of talking out loud right now, saying that I haven’t really looked into it, but it’s, you just see this more, I think, than kind of in the BRAF wild type where if patients are going to progress, all of their spots are going to be kind of progressing together. Whereas, oftentimes you’ll have responses in two-thirds of the lesions and then massive changes in the opposite direction in the other third. So, again, I think the underlying biologic heterogeneity, as well, is very interesting, and it points to the challenge of treating this disease. We presented this data at ASCO last year. It’s under review right now for a manuscript.

We looked at our cohort of patients at MD Anderson, if you had been evaluated since 2005. And we found 187 patients with BRAF-mutated metastatic CRC. If you were evaluated at our institution, and we just asked a simple question: if we take both ends of the spectrum and compare the differences what do we see? It wasn’t surprising that in the better survival group there were more MSI-high patients; almost 50% of the patients in whom we had data on had MSI-high tumors. But I think that one of the really interesting things as well, is that the median survival from the time of metastatic disease, and this longest survival, was eighty-four months, and in the lowest survival, it was 8.6. And I think that when we, as oncologists see the BRAF mutation, our minds automatically go to this lower end of the spectrum. But I think that we have to kind of keep open minds that there are patients who do have good survival outcomes. When we looked at what is driving out survival in this longest survival group, – what’s driving the long survival outcome? And we saw that was also heterogeneous as well. Some of these patients were able to go to surgery. And as you can see, in the black line here, many of these patients remained disease-free despite having an initial diagnosis of BRAF mutated, metastatic CRC, you know, 5, 6, 7 years out. But interestingly, and as we would expect, as immunotherapy has unfolded, patients who are MSI-high, were also seeing good long-term outcomes. Interestingly, one of these patients had an MSS tumor. But again, there were seven patients that we found who were doing fairly well for long periods of time on MAP-kinase targeted therapies, this included BRAF EGFR options, BRAF MEK options and BRAF inhibitors alone. So, there is some suggestion here to us that there may be a subpopulation of the BRAF mutated who just need targeting in their MAP-kinase, in their particular tumor is addicted to MAP-kinase signaling in the same way that perhaps an EGFR-mutated lung cancer may be addicted to that EGFR mutation, and being equally sensitive to tyrosine kinase inhibition in that context as well. So, I say that to say that even the drivers for favorable outcomes in the study are heterogeneous and do not always conform to what providers can assume. So, I talked about how this is still ongoing, I think, bench to bedside to bench and back to bedside success story, but how can we lift that tale further.

Obviously, in the MSI setting, response rates, even with a concomitant BRAF V600E mutation, is very good for anti-PD1 with or without anti-CTLA4 therapy. But unfortunately, still within the BRAF V600E context, we feel that the MSI-highs, that concomitant microsatellite instability is still a minority of the patients with BRAF V600E tumors. So, this is where we start getting a little bit more in-depth to our data, which we haven’t published yet, but I did want to share with you. It’s a majority of… we think of BRAF V600E tumors as being kind of high tumor mutation burden. And oftentimes I think the assumption is that, well, there’s this association between microsatellite instability, we all know that MSI tumors have higher mutation burdens and so that’s the reason that BRAF V600E tumors carry this association with having high tumor mutational burdens. We actually looked at four datasets that were available to us: the nursing health data from Memorial Sloan Kettering, data from the TCGA, and then from internal data, we had it at MD Anderson, and we said, let’s pull out the MSI high tumors. And let’s look at just the MSS tumors. And look at the patients and compare BRAF-mutated tumors with the BRAF wild types. We saw the same trends across all four datasets that in general MSS, BRAFV600E mutated tumors harbor higher tumor mutation burdens relative to their MSS, BRAF wild-type counterparts. So this may not be something that’s just MSI-high-driven. And if that’s the case, this may argue for some role of immunotherapy as a component for the MSS BRAF V600E story. We’re also excited to see data that was published in Science last year from Dr. Bardelli’s group in Milan, where they looked at BRAFV600E CRC cell lines and showed that when you treat these with dual BRAF EGFR targeting, you induce, in terms of expression, a loss of expression of the mismatch repair of proteins and can kind of create this transient and MSI-high like state. So, if that’s the case, you know, does that make sense that dual, or I guess, triplet, BRAF EGFR plus PD-1 therapy would make sense in this context. And this is something that we’ve seen as well. This is data we haven’t published yet, but this is from an expansion cohort of patients who were treated with vemurafenib, Irinotecan and cetuximab, – patients with BRAFV600E metastatic CRC. This is an example of a patient with a microsatellite stable tumor, but you can see prior to treatment, you don’t see a lot of immune reactive T cells within the tumor microenvironment, but that upon treatment with a BRAF EGFR inhibitor, you do see recruitment of activated CD8 positive cytotoxic T cells within the microenvironment. So that suggested to us that there may be a role for BRAF EGFR plus immune checkpoint therapy when we were pitching these concepts years ago in our initial letters of intent.

Let’s talk about CMS, you know, we all I think all recognize the role of CMS biology and that again, CMS1 is kind of the immune active group of a subset of CRC tumors, again, often associated with microsatellite instability. We also recognize that BRAFV600E tumors kind of aggregate to CMS1 oftentimes as well. And so our question again was is this association uniquely inherent to this association between MSI high CRC with BRAF V 600E mutations or can you see this in the MSS setting as well. So, we looked at data from the SWOG 1406. And again, it hasn’t been published yet either, but will be kind of forthcoming. And we looked specifically at in the red here from the from the SWOG study. And within the MSS context, the relative distribution of BRAFV600E tumors and as again, as you can see almost half of the MSS BRAF tumors were CMS1, the other kind of large proportion was CMS4. And this is different than what we had seen with an internal cohort of patients at MD Anderson who had MSS BRAF wild types, where you see a very low fraction of CMS1 within the BRAF of wild-type MSS contexts. So again what we’re seeing here is that within this MSS CRC population of patients, there may be some enrichment for a group, at least of BRAFV600E MSS tumors, for this more kind of immunologically hot CMS1 phenotype. We recognize from data that was published by several groups several years ago that already signatures can indeed for their subcategorized, BRAFV600E tumors, BM1, the B RAF mutation, one subgroup, it tends to be more of a kind of KRAS MAP kinase. Whereas the BM2 is more consistent with cell cycle gene regulation. And again, you can see here kind of when they look by CMS subtypes as well you see kind of what we had seen in the in the prior slide in the group where you have more MSS, BRAF mutated tumors, you start seeing more CM4 as well. And I think that it’s a little bit early to know how this will kind of play out but again, kind of argues for the heterogeneous subpopulations within the BRAF V600E contexts.

So I think that, this was the reason that we were thinking, about the BRAF, EGFR PD1 combination, and we’re very excited to kind of see Dr. Corcoran’s data that he presented earlier this summer in virtual Barcelona and then I think to you guys, it sounds like in the recent past here, looking at the Dabrafenib Trametinib Spartalizumab combination. So not exactly the same ideas or it’s just kind of given the mechanism of the BRAF but, I think that one of the things that really stuck out to us was the fact that you don’t see a whole lot of kind of toxicity with this combination. When we approached Array and BMS with this idea several years ago, I think that they internally were worried a lot about the skin toxicity that you were going to see with these combinations. And I think that his early data suggests that, this is a fairly well-tolerated regimen. But very interestingly even though the data are still very early and immature, the gross numbers, just comparing the same BRAF MEK combination with or without a PD1 I mean, it’s really encouraging, like, and it’s very encouraging. And similarly, I think that he saw, kind of with this slide, similar to what I had shown you guys with our multiplex immunofluorescence slide, or data several slides back, but again, that BRAF MEK PD1 does seem to recruit active T cells to the tumor microenvironment for hopeful cytotoxicity. So, this kind of led us to our concept at MD Anderson, which is now enrolling, you know, it’s a trial looking specifically at MSS BRAFV600E mutated CRC for patients who have not had prior BRAF, EGFR, MEK therapies or immunotherapy, I think his trial may have been a little more broader, and its eligibility criteria. But, this was the population we wanted to look at first, to kind of see signal and we put 11 patients on kind of amidst the COVID pandemic and having to stop it for 2 30-day windows to evaluate toxicity. And given the fact that this combination hadn’t been looked at before. And so we’ve enrolled, you know, fairly quickly under this trial, and what we’re seeing is that just kind of as Dr. Corcoran has shown, the safety data is very promising for this combination as well. This is the kind of the selected eligibility criteria for study again, MSS BRAF V600E adenocarcinoma of the colon or rectum, at least one but no more than two prior lines of systemic therapy, and then excluding prior BRAF, MEK or other anti EGFR therapies or immunotherapy. So that trial, like I said, is enrolling kind of at the same time, as we were about to launch, Dr. Atreya at UCSF was interested in looking at a BRAF MEK PD1 combination in the same setting. So we’ve worked with her to kind of get these trials going up in parallel, I believe her trial is open now. And I think that they’re kind of talking to her they’ve been enrolling too. Sorry, I actually don’t know what the safety data is of this combination yet. I haven’t heard that from her. But we presume that it’s going to be well tolerated.

So I want to circle back just to how we can learn from what we’re doing in the lab, and move that forward in this context, as well. We love using PDX models at MD Anderson kind of as I’ve talked about earlier, we feel that these kind of help us to pitch concepts for clinical trials to the NCI and pharmaceutical companies. And we’ve shown again, in data that hasn’t been published yet that what happens clinically, the patients on BRAF, EGFR therapies match what happens in their matched mouse avatar. So we looked at five patients who were treated on the SWOG 1406 study and characterized them by their clinical responses either having stable disease or partial response. And what you can see is that the overall trends for the stable disease patients in the blue mirror that for what was happening in the matched mouse whereas what was happening in the patients who responded clinically to the combination, you see have greater reductions, kind of in the tumor size in their mouse avatars as well. One of the interesting things just kind of anecdotally, just to kind of point out here as well, is that, in some of these mouse models, this was just looking at this one, the patient had a response to vemurafenib, irinotecan and cetuximab. You can see that in this mouse model for this patient, the BRAF EGFR, you know, it developed resistance but then when we added the irinotecan you see a drastic reduction in tumor size, there’s also a trend towards the irinotecan being different than that of the BRAF EGFR. Similarly, here, this mouse model, this patient responded to the combination, the mouse didn’t really benefit from irinotecan alone. But when we added all three, we saw that there was improvement. So, again, it may point, that just the one size doesn’t fit all. And also kind of points to the fact that this heterogeneity that I’m talking about. There is a trial, you know, that’s being developed in moving forward looking at chemo with or without encorafenib cetuximab in the frontline setting. And I think that data like this kind of points, the idea that, hey, maybe there’s some meaningful interaction with chemotherapy and targeted therapies in this context that that we will see. The problem is when it comes to mouse models, these are immunocompromised. So the the ability to study, the encorafenib nivolumab cetuximab combination would be limited in traditional PDX models. So, Dr. Karla in our group at MD Anderson’s, all star, his work to develop these humanized PDX models where tumor tissue from a patient and matched blood is used to create these mouse avatars. And we have funding that’s through an early career SPORE award at MD Anderson to do a clinical trial for our study, to look to see if what happens again in the patient mirrors what happens in with the same treatment combination in a developed humanized PDX model. And likewise, if what you see happening immunologically, in terms of changes, matches what happens in the matched humanized PDX model as well. This was funny, I got through the SPORE award the mentor here is John Allison, who won the Nobel Prize for his work in developing immunotherapy for patients with cancer. And it’s been really exciting to have the chance to work with Dr. Allison on and get his input on the design and science of what’s going on here. This was just kind of work showing some stuff we’re doing with Dr. Tusayan in collaboration with her on this trial, I would also ask this to be confidential and not shared as well, out of respect to her developing technology, but what we’re doing is we’re getting her slices of tumor, from pretreatment biopsies taken from patients on this study. And then she’s slicing these tumors and putting them into individual plates. And we’re testing what’s happening, with various combinations. And this is a patient who responded on our study to the triple combination. And what we saw was that when she treated the small slices of the tumor with encorafenib, and cetuximab by day 18, there was some reduction of tumor cell viability with the BRAF EGFR combination. When we added nivolumab, to that combination, we saw a much deeper reduction in cell viability, I didn’t put the nivolumab here as well, but it was that bar was here. So you didn’t see it wasn’t single-agent nivolumab down here either. So it was interesting to us because we felt that her model could likewise when you have the patient’s own immune cells present within the microenvironment may reflect what’s happening in the matched patient, but also that there may be in some patients some meaningful benefits to the addition of nivolumab. So, I hope that I provided here some rationale for why adding immunotherapy to BRAF, EGFR targeted therapies in MSS BRAF mutated setting makes sense, when these patients historically have been unresponsive to immunotherapy alone. I think we’re all encouraged by Dr. Corcoran’s work. And our hope would be that given the recent FDA indication of encorafenib and cetuximab we can build upon that success with a similar approach, and are certainly working to that and then I think that this will be informed further by preclinical and translational work that remains ongoing.

I was asked just to talk a little bit about atypical BRAF mutations in CRC. These are slides that I borrowed, full disclosure from Dr. Benny Johnson in our group at MD Anderson who really has led our group’s efforts, very valiantly to kind of work. This is a slide I think, had come from maybe Dr. Yeager at Memorial, I’m just kind of showing how the different mechanisms have the traditional RAS independence, BRAF V600E monomer, we associate with a class I, the dimerized. BRAF mutants, we see kind of with class II, and then kind of the, the BRAF inert, class IIIs that kind of has been characterized is these more atypical BRAF mutations. Again, we recognize that, as you can see, in all three of these, the atypical BRAFs tend to fare better than the BRAF V600Es and I would say I don’t think that this is something that all oncologists realize it’s not uncommon, so you get a referral or a call from outside doctors saying, hey, I have a patient with the BRAF mutation can I send them for your trial, and then we find out that it’s like a D594G mutation, kind of one of these more atypicals. So I think this is something we’re really trying to get the word out with oncologists as well, kind of as we learn more. And this is kind of, again, Dr. Johnson here, who I really just want to plug I think, has really had a passion for leading this effort in our group at MD Anderson, but just kind of some of the novel approaches that we’re trying to take at MD Anderson for kind of how we triage patients to various trials, according to their specific BRAF mutation, whether it’s a V600E, or a non V600E. So that kind of sums up what I had to say. I try to be active on Twitter, if you have any questions, please just let me know.

Manju George 37:06
So if I can, I’m going to start the questions, you can hear me, right?

Dr. Morris 37:12
Yes, I can. Yeah.

Manju George 37:13
So you were talking about the heterogeneity, so I was kind of wondering, in the unpublished data that you have, can you said that one part was the MAP kinase signaling pathway, and the other one was a different, you know, cell cycle and all of those pathways? So are you in your different trials are you attempting to find out what those different groups are? And in the reason I asked is, just like you said, we in our group, we find a lot of heterogeneity in how people respond to the different treatments for the BRAF V600E mutation. So it will make sense to us to if we could know what they were, because most of the patients, they already have their genomic testing done. And then if there’s some way to know upfront that you are in the 8.4 months category, not in the 84-month category, then you can plan accordingly how you have to prioritize treatment, right?

Dr. Morris 38:14
Yeah. So I think we’re looking at that we’re certainly collecting biopsies, to look at the transcriptome in RNA sequencing of these patients, and that may kind of inform on what their CMS classifications or BM1 BM2 classifications. I believe that Pfizer is looking at that on the patients who were on the Beacon study as well. So I think it’ll be very interesting if you see here that the BM1 patients are the ones who maybe had more benefit with the triplet, if there was a preferential added benefit with the addition of the MEK inhibitors that the BM1s than the BM twos. So, I’m very interested in this question as well and I hope that we’ll get some information from Pfizer about that. I think that Corcoran had published from his triplet, the dabrafenib, tremetinib, panitumumab work earlier this summer in clinical cancer research some signal kind of saying that, but I think it’ll be very interesting, in a larger cohort in a randomized trial to look at that in a kind of post hoc analysis.

Manju George 39:33
And then my other question would be like, there is this test called immuno score, right? Do you think those kinds of tests can tell you more, I was kind of wondering that if there was any efforts to develop some kind of assays so that you can look at a BRAF patient and say that this would be more BM1 or BM2, even the consensus molecular subtypes if there is, do you know if there is something like that being developed or going on?

Dr. Morris 40:02
I mean, not that I’m aware of I’m sure that it probably is being worked on. And it’s a really good point. But it’s not something that we’re actively working on now.

Manju George 40:13
Okay. And then the other person that you’re collaborating with Houston Yun, like the tissue culture thing. So it’s like an entire section of the biopsies is grown in the wells and you’re seeing that, when you try the combination treatment with the immunotherapy, just with that not inside an animal, you’re still seeing a response. Right? That’s what you said?

Dr. Morris 40:40
Yeah, that’s right. So, I mean, again, like, we’ve put only 11 patients on our trial thus far. And I mean, in full disclosure, with the pandemic, we had to shut down understandably, all optional biopsies for several months. So this limited our ability, thus far to look at this in high numbers, but it is something that we’re opening back up now. And we’ll be looking more stringently to see is there a signal? You always see kind of in the presentations, the N of one? So it’s hard to know for sure iff that’s truly representative, or if people cherry-pick the best for you to show? I don’t know,

Manju George 41:26
Okay. And then you have some results by GI-ASCO. Is that right?

Dr. Morris 41:36
Yeah, I mean, if so, it’d be a late-breaking abstract. I think we have 26 patients that we would plan on putting on study, so we’re just about halfway there. So it would either be a late-breaking, or probably the ASCO next year, we’ll see. We’re moving forward. And we talked to the NCI about what the next step would look like in a more definitive fashion.

Manju George 42:03
So, thank you, let’s see if others have questions. Questions, anyone?

COLONTOWN Member 42:29
Know, I feel like I need to, like, listen to this all again and consume so much information here, it’s been very helpful. But I was really interested to hear about some of the other mutations, you know, that we’re seeing, that are driving when BRAF you know, kind of becomes, you know, less important. So, while you know, I’m, again, I kind of feel like I need to, like review all of that, again, because I don’t think I caught it all. But you know, any other thoughts you have around that? And how we should think about how does treatment progress, as you know, maybe get to the end of what targeted BRAF therapy can do how do you make the decision to move forward from there?

Dr. Morris 43:10
Yeah, I mean, I think it’s a really good question. I think one of the things that hasn’t been fully looked at yet is with what you see in a RAS wild-type setting where there’s this idea of, these patients developing these acquired RAS, KRAS NRAS mutations. And then when you pull away the anti-EGFR therapy, that selective pressure is lost, and that acquired mechanism of resistance decays back down. Dr. Christine, Parsighian in our group had a really nice paper just kind of showing the kinetics of in the acquire resistance study to anti-EGFR therapy, the median half-life is about four to five months. So, before by the time you see 50% of that acquired resistance mechanism go away and then you can re-challenge these patients and see some benefit, and that’s being looked at in multiple clinical trials right now. And then the question is when a patient progresses on BRAF EGFR therapy, is that the end ever in their story and journey for EGFR therapy, or is there a role for rechallenge? None of us knows that. And I think it would be really, really interesting to look at. So I mean, yeah, like I think that’s something we’ve thought about, and I’m not aware of any data out there that’s shown that that’s successful or not successful.

COLONTOWN Member 44:53
Thank you, Manju. Dr. Morris, My name is Rashmi and I’m a caregiver to my husband with BRAF. My question to you is we know the pathway of the BRAF and the EGFR and the MEK and Erk. Looking at the three trials between Dr. Corcoran’s Dr. Kopetz and Dr. Atreya’s it seems that the BRAF and immunotherapy are similar. What’s different is the EGFR versus the MEK. Would you speak something to that? Is there I mean, your study is leaning towards the EGFR versus Dr. Corcoran’s is looking more at the MEK inhibitor?

Dr. Morris 45:39
Yeah, I mean, I think that’s what he’s seeing and the rationale for what we did what we did was similar, I don’t think that we know that BRAF, EGFR PD1 is any better or worse than BRAF MEK PD1, I think for us we realized several years ago that with the SWOG data that probably BRAF EGFR was going to get approved. And how we were going to be able to develop a strategy to, if successful to roll this out to our patients. It made sense in the context of a BRAF EGFR setting. So that’s why we we kind of went with that for approach years ago. He ‘s done a lot of work in the BRAF, MEK. I mean, I can’t speak to why they chose that, but I don’t think that we know that there’s a difference or why or if there’s a difference. Thank you.

Manju George 46:54
Okay, again, I’m going back to the CMS1 and CMS4 subtypes. So in our group, we have patients, we have one patient who has been almost NED, she’s been on the Beacon triplet, and she’s that one patient,who has gotten a phenomenal response. For most of the patients, we see that they’re on the triplet for a certain time, and then you know, things start growing, and then they get back on FOLFIRI + bev and that seems to work really well. So we have a group of patients for whom the FOLFIRI plus bev or FOLFOXIRI plus bev seems to give the best response. So again, I was kind of wondering whether, you know, that goes back to what you said about the BRAF, MEK, ERK pathway being important versus the cell cycle one, because then in that case, the cell cycle one would be more susceptible to chemo, right.?

Dr. Morris 48:01
Yeah, I mean, in theory, yes, but kind of given the fact that, these patients don’t respond in a treatment-refractory setting very well to chemotherapy, whether that translates into, clinical reality, I don’t think we know yet.

Manju George 48:22
Again, like, my push will be to if there could be an assay to tell you what kind of BRAF you are, from a patient perspective, that could make a big difference to patients as to how they approach the different treatments.

Dr. Morris 48:33
It would help us to Yeah, I mean, I think we’re very interested in understanding the different biologies, because again, we recognize it’s not a one-size-fits-all approach here.

Manju George 48:53
I think if there are no more questions, thank you very much for your time, and I guess that people, there are about 250 members many of them will watch the video because we’re going to post this in our group. And then there may be more questions, so then I’ll probably get them to you either by email or on Twitter. And thank you so much for your time.

Dr. Morris 49:20
Thank you, I appreciate it so much.

Manju George 49:23
Bye. Bye. Thanks, everyone.

DocTalk
2020
Dr. Morris
BRAF
Immunotherapy

Dr. Van Morris from MD Anderson discussed combining targeted therapies and immunotherapy for BRAF patients in this COLONTOWN Doc Talk, recorded in August 2020. 

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