Melanoma Awareness Month
May 15, 2020Information
May 17, 2020
Yale Cancer Center
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- 00:04the Beyond Pink campaign aims to empower metastatic breast cancer patients and their loved ones to learn more about their diagnosis and make informed decisions.
- 00:14Learn more at lifebeyondpink.com.
- 00:18Welcome to Yale Cancer Answers with your host
- 00:21Doctor Anees Chagpar.
- 00:22Yale Cancer Answers features the latest information on cancer care by welcoming oncologists and specialists who are on the forefront of the battle to fight cancer. This week
- 00:32it's a conversation about Melanoma research with doctor Jeffrey Ishizuka.
- 00:36Doctor Ishizuka is an Assistant Professor of Medical Oncology at Yale School of Medicine,
- 00:41where Doctor Chagpar is a Professor of Surgical Oncology.
- 00:46Jeff, maybe we could start off by you telling us a little bit about yourself and what you do.
- 00:51I'm a physician-scientist and that means that I spend part of my time treating cancer patients and part of my time in the lab looking
- 01:00for new treatments for those patients.
- 01:02And so tell us a little bit more about the kinds of patients that you treat and the kinds of research that you do.
- 01:09I see Melanoma patients and I'm an immunologist
- 01:12by training. And that means I study ways to
- 01:16make the patient's immune system work better,
- 01:19to attack the cancer.
- 01:22Tell us more about that, we've talked on the show a little bit about immunotherapy and so on,
- 01:27but tell us a little bit more about the broad spectrum of immunotherapy.
- 01:32How exactly does it work and then the role that it plays in Melanoma.
- 01:36There are a couple of types of immunotherapy.
- 01:38And for a long time we knew that the immune system had the potential to control cancer,
- 01:43but I'd say the two big advances that are more recent are on the one hand,
- 01:47CAR T cells. And those are cells that are taken out of the patients body and reprogrammed to go back in and attack the tumor, and immune checkpoint
- 01:55blockade. And these are drugs that cut the brakes on the immune system.
- 01:58Those brakes stop the immune system from attacking the cancer.
- 02:02And when you get rid of them,
- 02:04the cancer is vulnerable to immune attack.
- 02:09Tell us about which of these you work on, and
- 02:12how exactly they work in Melanoma.
- 02:16In Melanoma, immune checkpoint blockade has really been one of the biggest developments
- 02:22really in the last, well maybe ever in the disease.
- 02:27And I think Melanoma was the first disease where
- 02:31these drugs were developed and remains one of the ones where they work the best.
- 02:39Can you talk about this immune checkpoint blockade.
- 02:42Is there more than one molecule that needs to be blocked?
- 02:45How does that work? Why does the immune system have brakes to begin with?
- 02:49These are great questions and they're really at the forefront of the field right now,
- 02:54so there are certainly at least a few molecules that are important.
- 02:58And all of the ones we learned about first are on the surface of T cells,
- 03:02which we know are one of the important cells for controlling cancer.
- 03:07There are a number of molecules that target
- 03:10PD-L1 and that's a major inhibitory pathway in the T cells,
- 03:13and also molecules that target CTL A4,
- 03:15which is another inhibitory pathway in T cells.
- 03:18And what we learned is when you block either one of these and sometimes if you block them both together it works even better.
- 03:25The T cells can get supercharged to attack the cancer.
- 03:28Why is it that
- 03:30they have breaks to begin with?
- 03:32The immune system is supposed to be able to identify foreign stuff in our bodies and get rid of it.
- 03:39So why doesn't that work in cancer?
- 03:42Why is it that we need to take off these brakes?
- 03:45Why do they have breaks to begin with?
- 03:48This is the foundational question of immunology,
- 03:52the distinction between self and nonself.
- 03:55All cells need to be able to get rid of foreign things just as you said,
- 03:59but at the same time
- 04:01they need to have mechanisms to avoid attacking the normal cells in the body that are healthy and so
- 04:10why is it that the immune system thinks that these cancer cells are normal?
- 04:16I think it's really because cancer cells arise from normal cells as normal cells become dysregulated as they acquire genetic errors called mutations.
- 04:27And eventually you develop cancer.
- 04:29And because the cancer cell arises from a backdrop of normal cells,
- 04:34doing normal cell things, the immune system has to find specific signals of damage or mutations that
- 04:41look abnormal in order to recognize cancer.
- 04:43So you're telling me that normally it won't do that?
- 04:48Some tumors are recognized by the immune system and the immune system can actually get rid of them,
- 04:54and other aren't. And really what we're trying to understand and at the heart of the field is how can we take tumors that are not well recognized by
- 05:03the immune system and turn them into tumors that the immune system can see and destroy?
- 05:07And so it seems to me that if you take that problem just at its face,
- 05:11there are two ways of doing that.
- 05:13One is to make the tumor look more abnormal so that the immune system
- 05:19realizes, I need to attack it and get rid of it without actually revving up the immune system or getting rid of the
- 05:28brakes and the other is to supercharge the immune system as you put it to make it more sensitive to recognizing what might be abnormal.
- 05:37Yeah, that's right, and I think people are working at both sides of that problem.
- 05:42We and others in the lab, are thinking of strategies both to make tumors put out signs for the immune system, saying,
- 05:49come get me and also looking for new ways to charge the immune system to be more aggressive against cancer.
- 05:56Tell us more about the first,
- 05:58because I think that we've heard a little bit about checkpoint inhibitors,
- 06:05but we really haven't heard a lot about the work that's going on to have tumor cells put out those signs that
- 06:11say, come get me. And it seems to me that might be a way to allow the immune system without getting supercharged to eat up or
- 06:22get rid of these cancer cells,
- 06:25because one of the problems,
- 06:27as you point out, of having a supercharged immune system is that it can then attack its own cells.
- 06:35Yeah, that's a great point and
- 06:38we've been thinking, and others as well,
- 06:43that it comes down to tricking the tumor cell into making inflammatory signals,
- 06:49tricking it into making kind of an antiviral response that recruits anti tumor immune cells into the micro environment,
- 06:56and I think
- 06:57you can go about that by infecting the tumor with a virus or making it think it's infected with a virus or triggering certain danger signals in the micro environment
- 07:07directly around the tumor.
- 07:11Tell us more about that work, is that actually something that's being done?
- 07:16Is it in clinical practice?
- 07:19How do we do that?
- 07:21There are a number of clinical trials now using stimulators of viral pathways that look like DNA or RNA,
- 07:30things that viruses make and that ourselves have dedicated sensors in order to detect,
- 07:37and I think none of them has proven to be the Magic bullet for cancer yet.
- 07:42But there are still some technical hurdles to workout.
- 07:47And I think we're getting there though.
- 07:50Why has that not proven to be as successful as supercharging the immune system?
- 07:56I think one of the challenges is that cancer in many cases can spread to many locations,
- 08:03and when you think about triggering an inflammatory response in the tumor bed,
- 08:09you're really thinking about triggering it,
- 08:12not just at one site,
- 08:14but at many sites all at once,
- 08:16and so finding ways to send drugs
- 08:19to all of the different sites that cancer occupies in the body is one of the major challenges to getting this approach to work.
- 08:26The other approach then is the one that is the mainstay of immunotherapy,
- 08:34which is to quote supercharge the immune system to get rid of the blocks.
- 08:39I always think of it like Harry Potters invisibility cloak,
- 08:43right. The tumor has kind of made itself invisible to the immune system,
- 08:48and it's getting rid of that that cloak and getting the immune system to recognize it and to go after it and two,
- 08:57to be quote supercharged now.
- 09:00You mentioned two molecules, in particular CTL A4 and PDL1, tell us a little bit about the differences between the two.
- 09:10I mean we have drugs that will block either pathway.
- 09:14How do you figure out which one to use?
- 09:18Tell us more about that interplay.
- 09:21I think we still don't fully understand the mechanism of either drug and either pathway.
- 09:29And people have done a lot of good work,
- 09:32in fact, the Nobel Prize was awarded a few years back for some of that work,
- 09:36but I wouldn't say that we completely understand which,
- 09:39even sometimes which cells are being targeted,
- 09:42but certainly which pathways within the cell are being activated.
- 09:45So a lot of how we figured this out has been empirically.
- 09:48We've done clinical trials with different drugs or different combinations of drugs,
- 09:52and we've seen what's been effective for patients,
- 09:55and the hope is going forward that as we learn more about the immune system,
- 09:59and as we learn more about the tumor that we will be able to do better
- 10:04and even predict the next set of these drugs that could be usefully combined.
- 10:10So tell us more about the differences between CTLA for an PDL1.
- 10:14I get the fact that we've discovered these kind of fortuitously and empirically and have just made drugs that affect each of these pathways,
- 10:24and seeing that they work.
- 10:26But we must know more about these actual molecules.
- 10:30Yeah, they both play an inhibitory role in T cells.
- 10:34I think it's broadly thought
- 10:37that one of them plays more of a role in T cells initially getting primed against the tumor,
- 10:43but maybe plays more of a role in lymph nodes then generating the T cells that are capable of responding whereas the other one,
- 10:52that speedy one may play more of a role in activating the T cells that are already primed against the tumor that already have the capacity to attack the tumor.
- 11:01And I'm going to steer clear of the term of exhaustion because there are a lot of debates about whether T cells
- 11:08are actually exhausted or not,
- 11:10but there's this idea that T cells can, after seeing a lot of tumor antigen stop responding very well that they can become dysfunctional and so one
- 11:21of the things that PDL1 blockade does,
- 11:27is to make the T cells that have become dysfunctional more functional.
- 11:32And so if these two pathways then are complementary,
- 11:36one being more so for priming T cells and one being more so for T cells that are already primed,
- 11:42has there been any work looking into either concurrent therapy or sequential therapy of different immuno therapies that might work better than either in isolation?
- 11:54There has, and in Melanoma combining two drugs,
- 11:57one that targets CTL A4.
- 11:58and one that targets PDL1 seems to be better than using either drug alone and potentially better than using them both in sequence,
- 12:08although the latter is a less clear conclusion.
- 12:17And one of the exciting things in this field has been seeing the slew of approvals for immuno therapies in different cancer types in Melanoma.
- 12:28Certainly it's become standard of care in the frontline for most patients and it's being explored in basically every stage of care of the disease other than for disease that
- 12:39can just be removed and surgically cut out in the early stages and really beyond Melanoma,
- 12:45it spread throughout many many solid tumor types and it's being tried in almost any tumor type you can think of.
- 12:54And so two questions. First question is one of the things you mentioned earlier as being one of the
- 13:00downfalls of some therapies is that it can't always get to all of the cells where the tumors may be hiding.
- 13:08Does immunotherapy have that problem in terms of getting to the T cells and activating them or supercharging them?
- 13:17Or is that concept, this may not work if there's a tumor,
- 13:22for example in the brain?
- 13:24Because this drug can't cross the blood brain barrier?
- 13:28Or does it affect T cells wherever they are?
- 13:32We know that we can get effects certainly in the brain.
- 13:38So you can see effects of these drugs in what are thought of usually as sites of the body that are hard to get to or immune privilege sites but
- 13:51I guess what I don't know for sure,
- 13:53it's hard to say is whether there is a problem activating immune cells somewhere in the body.
- 13:59That is to say, whether we're getting these drugs as effectively as possible to all the immune cells that might be able to be mobilize against the tumor.
- 14:07We're going to learn a lot more about Melanoma immunotherapy right after we take a short break for a medical minute.
- 14:15Please stay tuned to learn more about this research with my guest doctor Jeffrey Ishizuka. Support for Yale Cancer Answers comes from AstraZeneca.
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- 15:23You're listening to Connecticut public radio.
- 15:27Welcome back to Yale Cancer Answers.
- 15:29This is doctor Anees Chagpar andnI'm joined tonight by my guest doctor Jeffrey Ishizuka.
- 15:35We're talking about Melanoma research and in particular we're talking about immunotherapy.
- 15:41Jeff, right before the break we were talking a little bit about immunotherapy in terms of,
- 15:47really getting the immune system to attack cancer cells,
- 15:52which it may not recognize because as you put it,
- 15:55these cancer cells come from normal cells and that
- 15:58may not be as foreign looking to the immune system to really trigger it and we talked a little bit about two separate pathways,
- 16:08CTL A4 and PDL1 and the fact that we now have drugs,
- 16:12this explosion of drugs in immunotherapy targeting these two pathways and how this really has become the mainstay of therapy,
- 16:21particularly for cancers like Melanoma.
- 16:24I had a few questions to kind of follow up on that.
- 16:28The first is, tell us a little bit about the side effects.
- 16:32We think about
- 16:35chemotherapy, and you know, traditionally,
- 16:40chemotherapy was therapy that kills off cancer cells and was really thought to be therapy that switches off
- 16:47rapidly dividing cells and so people ended up losing hair and maybe getting sick because it effects your GI lining,
- 16:55which are rapidly turning over cells.
- 16:58Do you get the same kind of thing in immunotherapy,
- 17:01or are there other side effects that are the results of
- 17:06kind of supercharging this immune system and getting the immune system to attack healthy cells?
- 17:12So I think that's it exactly.
- 17:14Many of the side effects that you get from immunotherapy are actually side effects of supercharging the immune system,
- 17:20so the immune system can accidentally attack different areas of the body.
- 17:24Some of the things we see are inflammation in the lungs,
- 17:27inflammation in the GI system we see inflammation of the endocrine system,
- 17:32and when we first started seeing these side effects,
- 17:34there wasn't a good sense of how you treat them,
- 17:37how you manage them, or even how you monitor.
- 17:40We didn't really know what to look for.
- 17:42But I will say that as experience with these agents has progressed,
- 17:46we've gotten better at detecting these side effects as they occur,
- 17:50and managing them, usually using immunosuppressives and one of the questions that comes up when you start saying,
- 17:56well, you're using drugs to charge the immune system and at the same time to shut down the immune system,
- 18:02is that going to be is going to be bad for the patients.
- 18:06Are they going to have that outcomes and the data isn't really completely mature on this yet,
- 18:11but it certainly appears from the early data that
- 18:14you can safely give these immunosuppressives and that you don't at least don't clearly make their responses against the cancer
- 18:22worse.
- 18:26That's really interesting. Why would that be the case? I can imagine that when we think about people who are immunosuppressed,
- 18:32people who for example have HIV or other things that turn off their immune system,
- 18:38they are more at risk of developing cancer,
- 18:41and I guess for the same reason that you talked about before the break,
- 18:45which is your immune system,
- 18:47unbeknownst to you, might be getting rid of little cancers that you don't know you have because it recognizes them and it gets rid of them,
- 18:56and so if you are immuno compromised you're at increased risk of getting cancer,
- 19:02and that's the whole point of
- 19:04supercharging the immune system to get rid of these cancers.
- 19:11Why is it that giving people an immunosuppresant at the same time as an immuno supercharger doesn't seem to affect the cancer in a bad way?
- 19:22A couple of potential thoughts here.
- 19:25The first one is that I want to be careful we don't know for sure that it doesn't affect the
- 19:32response to therapy in a negative way.
- 19:35I think what we can say is that
- 19:37at first blush, patients who needed immunosuppressives because they had these bad immune effects and got them didn't do obviously worse,
- 19:45at least in the early studies
- 19:46then patients who didn't need them in the first place and that actually could be a kind of selection bias issue where the patients who needed the immunosuppressives
- 19:55actually were having the strongest immune responses to begin with,
- 19:59and so I think we have to do some careful experiments in a controlled setting to see whether it was really true that the immunosuppressives weren't having any effect there.
- 20:08And I think that's probably the main thing that I would think about for that issue.
- 20:15The other question that I have is, these autoimmune side effects,
- 20:21the side effects of people's immune system now attacking their own normal cells,
- 20:26are those permanent? Are
- 20:29they forever or are they short lived? I mean when you get chemotherapy and you lose your hair,
- 20:38your hair will grow back.
- 20:39Is it the same with immunotherapy that this is a short term thing?
- 20:45Or when your immune system attacks your lungs,
- 20:47now you've got pulmonary fibrosis forever?
- 20:51I think it depends on the type of immune side effect that we're talking about.
- 20:56I think many of them,
- 20:57if they're controlled with immunosuppressives,
- 21:00and if you take the patient off of the immunotherapy, will actually go away.
- 21:04So we see this in a lot of cases,
- 21:06inflammation in the colon, or inflammation in the lungs.
- 21:10I think the case in which this isn't necessarily true is when the immune system attacks the cell type
- 21:17that produces hormones in the body and destroys all of that cell type because in that case you may not really know what's going on until the cell type
- 21:26is gone, and after that there's really no bringing it back.
- 21:30So in most cases we actually have been able to give hormone replacement.
- 21:37It's extremely bad if it's not detected,
- 21:40but in a lot of cases it can be solved by giving a pill a day.
- 21:45When you talk about hormones,
- 21:47are you talking about thyroid are you talking about ovaries, what hormones are we talking about?
- 21:54Yeah, so thyroid is one that you certainly see,
- 21:58but you see actually a number of other hormones that are produced in the brain that can also be altered,
- 22:05and these can be be more rare,
- 22:07but can be pretty dramatic if you see them.
- 22:10So given the side effects of immunotherapy,
- 22:14is immunotherapy really better than classic chemotherapy?
- 22:18You had mentioned that immunotherapy has now become standard of care for Melanoma.
- 22:24Is it better than what we used to do?
- 22:29We used to give chemotherapy for Melanoma,
- 22:31right?
- 22:33And Melanoma is not particularly responsive to chemotherapy,
- 22:37and I think what excited everyone in the field and it's given us all
- 22:41a lot of excitement and a lot of hope is not even that
- 22:45everyone responds to these immunotherapy's because they don't,
- 22:48not enough patients do, and that's something we don't really understand.
- 22:52We're trying to understand it in the lab,
- 22:55but it's that some of the patients who respond seem to just keep responding,
- 22:59and some of them respond so well and for so long that we've actually started to believe that we can take the patients off of the drugs,
- 23:07the immunotherapy drugs, and that the cancer won't return.
- 23:10And this is true even in some cases for very aggressive disease.
- 23:15And so seeing those effects are the ones that have really made everybody excited.
- 23:20And you see that in clinical trials when we study how patients survive on different drugs and
- 23:27it was no contest between the immunotherapy's and chemotherapy.
- 23:31When we talk about therapy for cancer a lot of times we're talking about personalized medicine and we're talking about how we can figure out what a cancer likes to
- 23:44eat, what receptors cancer has,
- 23:48what genes are turned on and turned off,
- 23:51and then we target our therapy accordingly.
- 23:55Talk about immunotherapy. It seems to me like we're talking about a blanket turning on supercharging the immune system,
- 24:04is that right, or are there ways where we're actually tailoring this therapy?
- 24:10Are we looking at who those people are that are super responsive to immunotherapy versus the people who are not super responsive to immunotherapy?
- 24:20And which immunotherapy might work better in particular patients?
- 24:25Yeah, so this question is near and dear to my heart.
- 24:29We in general don't do a great job of selecting patients to get particular immunotherapy, there is one biomarker which is the expression of PDL1 in the tumor as
- 24:39we talked about PDL1 and PD1 is one of these key pathways,
- 24:43so if you have PDL1 expressed in the tumor microenvironment either by immune cells in the micro environment or by the tumor,
- 24:51we know that you are more likely to have a response to targeting the PD1 PDL1 axis.
- 24:58But basically everyone in the field spends a lot of time complaining about this biomarker because we know there are a lot of patients who will have PDL1 expression
- 25:08in their tumor who won't respond well to these drugs.
- 25:11And conversely, there are a lot of patients who won't have PDL1 expression in the tumor who will still respond to these drugs.
- 25:18So what's the point of the biomarker then?
- 25:20We know it's better than not using it in terms of you have some predictive value and in some cases you might not even be able to see
- 25:29a signal of the drug working in a patient population and unless,
- 25:32you used a biomarker, and also it's a stand in because we haven't done a good enough job yet of
- 25:37finding better ones.
- 25:41So we have this biomarker that if you have it,
- 25:44you won't necessarily respond to the immunotherapy, if you don't have it,
- 25:49you may still respond to the therapy,
- 25:52so either way you're likely going to get immunotherapy if you have Melanoma,
- 25:57regardless of whether you have the biomarker or not.
- 26:01That's true, and that's where I think we have the potential to do much better,
- 26:07particularly as we talked about these two pathways,
- 26:11there are a lot of other immuno regulatory pathways that can activate immune cells or can activate the tumor to recruit immune cells.
- 26:20And we're still at the beginning of understanding these.
- 26:24But as these drugs come out and as they are available we have the potential to start thinking about OK for a given patient.
- 26:32How can we assess that patients immune system and how can we understand the tumor,
- 26:37the genomics, the genetics of the tumor in such a way that we can find the best combination of drugs to work for that patient.
- 26:46That sounds really interesting,
- 26:49because that sounds like the stuff that we've been doing for awhile now in terms of cancer and looking at cancers in figuring out which therapy is going to work
- 26:59better. What targeted pathways are turned on versus turned off.
- 27:03Should you be using, you know an anti HER-2 agent in somebody who's got a HER-2-positive breast cancer?
- 27:10Or should you be targeting KRAS in lung cancer?
- 27:13Sounds like you're moving in the same direction in Melanoma.
- 27:17But looking at it from an immune perspective,
- 27:19and I should say this is mostly on the research side,
- 27:24right now we're trying to understand the flavors of inflammation in the tumor microenvironment.
- 27:30The composition of the immune cells that are there and why they're there,
- 27:35and then once we understand that, we're simultaneously starting to look at OK if we take pieces of the tumor and study them in tissue culture,
- 27:44if we study them in a dish and treat them
- 27:47with different immunotherapy drugs, can we see patterns of response from some patients but not from others?
- 27:53Those are things that we're working on here,
- 27:56and others are working on as well that we think could lead to the development of better biomarkers.
- 28:01That's one kind of major approach.
- 28:03Another one is focusing on the technologies that have emerged to sequence patient genomes.
- 28:09The immune cells from patient genomes.
- 28:11We do technologies now to look at individual cells in sequence.
- 28:15Everything that that cell is expressing.
- 28:17Basically everything it's doing and we can do that for a bunch of cells in the micro environment all at once,
- 28:25and the thought is that we may find particular genetic lesions in the tumor that lead to a better response to immunotherapy A versus B.
- 28:34We may find particular features of the immune system that interact with the tumor as well that predict that,
- 28:41and so I think that in the next 5 or 10 years we're likely to see progress in this direction.
- 28:47Whether that will translate affectively into
- 28:50guiding precise therapy choice for a patients
- 28:54Melanoma, I'm not sure.
- 29:00When you talk about,
- 29:02essentially taking tumors and looking at the micro environment and seeing the composition of these cancer cells,
- 29:09and what kinds of immune therapy they may benefit from,
- 29:13you can also look at the immune system and see,
- 29:17maybe my immune system is different from your immune system in terms of attacking a particular cell.
- 29:24Is that on the right track?
- 29:26It's exactly on the right track,
- 29:29and you know, even taking a step back when we first started to see that these therapies could work for patients,
- 29:37people started to ask,
- 29:38why do they work for some patients but not for others?
- 29:42And we started to look inside patient tumors and one of the things that was clear is that some patients have a lot of attacking immune cells
- 29:51even prior to immunotherapy and others don't.
- 29:54And just unpacking that basic
- 29:57observation is something we're still doing,
- 30:00but as I was mentioning, as we start to understand it as we start to understand the chemical signals that the tumor in the immune system makes.
- 30:09It's giving us a lot of inputs to try to determine which drugs could be affective in each case,
- 30:15and what the basic flavors of immune micro environment are.
- 30:19Doctor Jeffrey Ishizuka is an Assistant Professor of Medical Oncology at the Yale School of Medicine.
- 30:25If you have questions, the address is canceranswers@yale.edu and past editions of the program are available in audio and written form at Yalecancercenter.org.
- 30:35We hope you'll join us next week to learn more about the fight against cancer
- 30:40here on Connecticut Public Radio.