Cancer Immunotherapy and You Webinar Series – The Cancer Immunotherapy Toolbox: How Does the Immune System Work?

Cancer Immunotherapy and You Webinar Series – The Cancer Immunotherapy Toolbox: How Does the Immune System Work?

Immunotherapy utilizes the body’s own immune system to help patients overcome cancer. But how exactly does the immune system work? Recently, Miriam Merad, MD, PhD, a member of the CRI Scientific Advisory Council who works at the Icahn School of Medicine at Mount Sinai in New York City, joined CRI to explain the basics of the immune system. In conversation with Arthur N. Brodsky, PhD, the associate director of scientific content at CRI, Dr. Merad discussed cancer treatments that leverage the immune system during our CRI webinar, “The Cancer Immunotherapy Toolbox: How Does the Immune System Work?”

In this webinar, Dr. Merad highlights:

• Current cancer treatments that harness the immune system
• Novel immunotherapy strategies that tap into more of the immune system’s power
• How cancer cells can trick and resist the immune system
• The impact of our lifestyles on the immune system, cancer, and our health in general

Dr. Merad serves as the director of the Mark and Jennifer Lipschultz Precision Immunology Institute and the Human Immune Monitoring Center at Mount Sinai. She is an expert in myeloid cells, such as dendritic cells and macrophages that act as the generals of the immune system’s army and inform and activate cancer-fighting T cells. Dr. Merad also highlighted how scientists are now exploring ways to harness these cells to improve the overall effectiveness of immunotherapy.

The Cancer Immunotherapy and You™ webinar series is produced by the Cancer Research Institute and is hosted by our associate director of scientific content, Arthur N. Brodsky, PhD. The 2022 series is made possible with generous support from Bristol Myers Squibb with additional support from Alkermes and Lilly Oncology.

You can access the information-rich and illuminating webinar below:

VIDEO TRANSCRIPT

Arthur Brodsky, PhD 

Hello and welcome to the Cancer Research Institute “Cancer Immunotherapy and You” patient education webinar series. I’m your host, Dr. Arthur Brodsky, associate director of scientific content at the Cancer Research Institute. And today we’re highlighting “The Cancer Immunotherapy Toolbox: How Does the Immune System Work?” First, we’ll learn some immune basics, and then cover some current cancer treatments that utilize the immune system. And then finally discuss novel strategies being explored to fully unlock the immune system’s power against cancer and bring us closer to a world immune to cancer. Before we begin, I’d like to quickly thank the generous sponsors of this webinar series: Bristol Myers Squibb as well as Alkermes and Lilly Oncology. And now it is my pleasure to introduce today’s featured guest. Dr. Miriam Merad is the director of the Mark and Jennifer Lipschultz Precision Immunology Institute and the Human Immune Monitoring Center at the Icahn School of Medicine at Mount Sinai in New York City. Dr. Merad is an internationally acclaimed expert in the biology of myeloid cells, like dendritic cells (DCs) and macrophages, which you’ll learn more about soon. And she’s also a member of the CRI Scientific Advisory Council and has sponsored the research of two CRI postdoctoral fellows. Without further ado, Dr. Merad, I will let you take it from here.

Miriam Merad, MD, PhD 

All right. Thank you, Arthur, for having me today. I’m just going to introduce very briefly what we are trying to do when we manipulate the immune system to treat cancer. First, I want to remind everyone that the immune system is an army of cells that is here to protect us. So, an army of cells with different functions, like the same as in any army. But the goal is to really constantly survey for threats and eliminate them. Here, this is what we are going to try and show you here, the immune system can organize, it has the ability to organize when it senses damage, for example, after any type of trauma, for example, a burn or a heart attack, and will clear it, will eliminate these damaged cells. The same during aging when there is damage that occurs due to accumulated mutations. The immune system knows how to recognize aged cells and eliminate them. Same with microbial infection, any type of microbe can be recognized by the immune system. In fact, it’s probably its main role, to protect us against infection. And similarly, it can recognize cancer cells because the cancer cells look very different from normal cells. And we believe that the immune system is constantly eliminating cells that can become cancerous, and constantly protecting us from cancer progression. But in some cases, the cancer cells know how to stop the immune system or counteract this ability of the immune system to eliminate them. And this is when they progress and the thought was for many years — because of this realization that immune cells weren’t in all tumor lesions, as we might a long time ago. But the idea was that well, if the immune system is, immune cells are here, they accumulate, clearly, they can recognize the cancer cells. But if cancer progresses, then the immune system couldn’t fight it. But that realization really led scientists to think, well, if they recognize it once and were able to eliminate or eliminate some of it, maybe the immune system can be reactivated to fight cancer.

And that’s really the premise that the cancer immunologists have is how can we reactivate that immune system that has the ability to recognize damage, to make it eliminate cancer cells in the way as I will discuss later, in the way that is first efficient, but also provides memory so that we always remember when cancer comes back. Here is a slide to remind you of extraordinary advances in our immunology knowledge that suggests that an inflammatory response, that immune system that I just described to you is part of all diseases, because as soon as there is an injury, immune cells accumulate, and try to either eliminate injured cells as I just showed you, and therefore, and by trying to eliminate these damaged cells, it will produce what we call inflammatory molecules. And this inflammation is going to contribute to disease outcomes. And in some cases, it improves the disease often during infection, but sometimes it goes too far, and it can be damaging. And we believe that the biggest revolution in medicine is the realization that drugging that inflammatory response can be corrective. The closest example of that are the vaccines against COVID. I’m going to talk about checkpoint therapy in cancer that has been transformative, but there are many other diseases that are benefiting from cancer treatment, such as inflammatory disease and celiac disease, and multiple sclerosis, and this is just to highlight the power of that immune system of ours. 

That immune system is quite complex. And this is what we study, and I’ve been studying for more than 20 years. And it includes two big branches. One, which we call the innate immune system, and the other branch is called the adaptive immune system. So, it’s really the anatomy of cells that just described earlier you know, with many functions, because eliminating the abnormal or eliminating the threat is not an easy task. So, the innate immune system consists of different cell types that have the capacity to just recognize a threat without being exposed to it earlier. It just organizes types of machinery on the right, which you need to organize when something is wrong. And a good example of that, or the best example of that are macrophages, a cell type that I’ve been working on for a long time, they are present in every tissue of our body. And their main goal is to really try to recognize when something is wrong, and when something is wrong. If the cell is damaged, macrophages are going to capture it and try to clear it, but they also release inflammatory molecules to recruit other actors, all other cells of the immune system, which we call the fighter cells to eliminate a threat.

For example, they will recruit neutrophils. Neutrophils are a large cellular compartment, a large number of cells in our blood circulation. The largest number of cells, among the white blood cells that are circulating in the blood and the neutrophils are very good at eliminating a threat and they are recruited when something goes wrong. But there are also these natural killer cells that look like a lymphocyte and are also quite good at eliminating a threat without prior education. Now, there is this other cell type that I’ve been studying for a long time called dendritic cells, and these dendritic cells are also part of the innate immune system. They can also recognize the threat and capture it, but their main role in contrast to macrophages or neutrophils is to bring the threats to lymph nodes, where T cells and B cells are, and really educate the adaptive immune system against this threat. Now, the adaptive immune systems are very — is a novel part of the immune system because it has specificity and recognizes only specific threats, but it also has memory. It remembers a threat and it has that specificity. They can kill really on target, and they will always remember when something is wrong. What dendritic cells do is bring little microbes or tumor cells and educate T cells to recognize the target and eliminate it.

There are two big parts of the adaptive immune system: the B cell that makes antibodies, so for example, when you receive your COVID vaccine, that vaccine is going to educate B cells to make antibodies against the virus, but also educate T cells and to recognize potentially virally infected cells and eliminate them. So, how does this killing occur? Going back to the dendritic cells, first in the education. Education is very important because dendritic cells are going to decide how T cells are going to behave. So, for example, in the case of tumor lesions, dendritic cells are capturing tumor cells, then process them, express them on the cell surface in a way that is recognizable by T cells, but also produce additional signals to tell, reinstruct the T cells on what to do. And in most cases, they tell them ‘Go and kill each time you see a cell that expresses that signal. The T cells are going to go back — so they just constantly circulate in our body and when they recognize that signal that they had been educated against, what they do is they kill the cells that express it, so dendritic cells capture tumor cells, and then present the tumor signal to a T cell. T cells recognize the signal on the cancer cells, and they kill it. And it works. It works most of the time. But in some cases, doesn’t work, and this is when cancer grows. And what we realized is that the cancers that grow have learned how to fool those T cells. And they fool them by engaging a signal that stopped their activation and stopped their ability to kill. And those signals are what we call checkpoints.

Checkpoints — for example, the most popular checkpoint is PD-1 — PD-1 is expressed on T cells, and when it’s engaged, it will stop T cells’ ability to kill, and the engagement of these PD-1 can come either from the cancer cells, but also from the dendritic cells or the macrophage themselves. And why is that? Because the immune system has also learned to constantly modulate its ability to respond. Otherwise, let’s say you have a flu infection, if you don’t know how to regulate the immune response, we constantly will be dying of inflammatory response. Regulation is a very big part of the immune response, as important as the activation which I described to you, this ability to educate and kill. At the same time, the dendritic cells are asking T cells to kill, they also constantly modulate this ability to really react against a threat. This is very important for the survival of our species. But sometimes that inhibition goes too far. And this is what we are seeing in cancer. Now, what scientists discovered is that if you inhibit that inhibitory signal, then T cells can again be able to target the cancer cells and kill them. And this is what happens when patients are treated with checkpoint blockade. What we have really built is that instead of now targeting the cancer cells that have proven to be very difficult to target, because cancer cells are completely transformed. It’s a crazy cell. When we give chemotherapy, they know how to really escape that chemotherapy regiment, or the radiation regimen, or these targeted molecules that we’ve been using, for example, in melanoma. Instead, what we are doing is targeting the immune system. The immune system is regulated properly. It’s not transformed, it’s not cancerous, so we can really anticipate how the immune system is going to respond. Cancer treatment has really shifted from cancer-focused treatment towards targeting this immune microenvironment. What we are seeing now is really a combination of treatments where we both target cancer and target the immune microenvironment. This is really the focus of our field is to continue to learn about other molecules that regulate the ability of the immune system to kill cancer cells. Right now, we are really drugging or targeting only three molecules. There are hundreds of molecules that regulate killing, so many of us are trying to identify novel targets and bring them to the clinic. We are also trying to combine additional treatment with immunotherapy. We’re also trying to identify what we call biomarkers of response so that we can identify those patients that are going to respond more favorably to immunotherapy and also many groups are trying to minimize the side effects of immunotherapy.

Arthur Brodsky, PhD 

Thank you very much, Dr. Merad. That was a great overview of the basics of the immune system and checkpoint immunotherapies, which right now are the most successful immunotherapies. But like you mentioned, they still don’t work for a lot of patients, and we still have a lot of work to do to help everybody else. In that light, I thought it was interesting that the PD-1/PD-L1 that you mentioned, involves more than just the T cells. It involves these myeloid cells, these dendritic cells, and macrophages that you mentioned, they can not only educate and stimulate the T cells but also play the other side of the coin of expressing these checkpoints to shut down the T cells. So, because T cells are only part of the puzzle, it makes sense that targeting them would really only account for a fraction of cures, whether it’s through these checkpoints or through the cell therapies that also use engineered T cells. My question is, beyond T cells, how are scientists, how are we starting to look at utilizing other immune cells, especially these antigen-presenting myeloid cells through new approaches and how might those approaches improve the effectiveness of immunotherapy?

Miriam Merad, MD, PhD 

This is a very important point because something we didn’t discuss is that the tumor cells know also how to escape these T-cell responses by just not expressing a lot of these targets. Sometimes you can educate it, she says very well, but the tumor cells know how to not express the right target or dampen them. Finding other ways of killing a tumor is a big focus of the field. Let’s talk about non-T cell immune cells, immune cells that can kill cancer, but are not T cells and there are two of them. Natural killer (NK) cells are quite good at killing the tumor cells without recognizing the specific target. Macrophages are very good at eliminating any type of damage threats. Several groups are focusing on reactivating macrophages’ ability to kill. What’s extraordinary about macrophages is that they are the dominant immune cells in every cancer lesion. Sometimes there are more macrophages than there are tumor cells. It’s the definition of an inflamed site. Each time you have anything that goes wrong, you have this big accumulation of macrophages. Several groups are trying to harness macrophages’ ability to kill and use them as cures. Others are harvesting NK cells, and there are very, very interesting results now with NK cell therapy where we manipulate NK cells and inject them and have them migrate to the tumor lesions and kill tumor cells. I didn’t talk a lot, but in case I should have, I put them in that innate immune system, which means that they recognize without being educated. And that is because the tumor can potentially dampen some of the signals they put on the T cell, on the cell surface, that can be recognizable by T cells, but they very rarely can completely shut down all the danger molecules that can be recognized by macrophages and NK cells. It would be very difficult for them to remain alive, and not present some of these molecules.

We think these are very, very interesting paths to really harness. Another big focus of the field is the immune microenvironment because what we’ve realized is that sometimes you can educate T cells as much as you want. And education happens in the lymph node. We didn’t discuss that Arthur, but maybe we should just remind the public. So, those lymph nodes, pretty sure that people know but lymph nodes are really appendixes that are attached to every organ of ours. And the education of a good response really occurs in lymph nodes. So, for example, let’s say we have lung cancer. Dendritic cells will capture a piece of the lung cancer, bring it to the lymph node, educate the T cells, and that can happen very well. T cells go back to the lung cancer, and there are macrophages trying to repair, they need to repair because macrophages think ‘okay, I have to now stop the wounds.’ They are fooled by cancer, which gives them signals to really try not to clear us, but rather repair us, and cancer knows how to say that to macrophages. This is something also I should have said about these macrophages is that they have an ability to clear, but a very strong ability to repair. And when they repair, what they do is promote tumor progression. They are bringing vessels that are going to repair, bringing vessels and therefore bringing oxygen, preventing T cells to kill, to go induce more damage. Because macrophages do that, initially they kill and then they try to repair. They constantly do that all the time in our bodies. And they are fooled by the tumor. They think that it’s a little wound, okay we got rid of the most dangerous cells. And now we have to repair and those macrophages are fooled, are the ones that are fooled the most by the tumor. And for a long time, we focused on those T cells, but now we realize that macrophages in their desire to repair are really preventing T cell function. So, I showed that PD-L1 is also expressed by macrophages, and macrophages are very numerous so they’re always trying to stop T cell function, but macrophages are also preventing T cell killing by many other modalities, which we are trying to identify and block.

Arthur Brodsky, PhD 

You mentioned a lot there and I wanted to clarify something for our audience. In addition to your slides, where you showed that the macrophages and dendritic cells can play a support role or act as the generals of the immune system, they tell the T cells what to do, they, as you just discussed, can set the stage, they really determine what the behavior of whether that environment is going to be shut down with the immune system, or whether it’s going to allow the immune system to respond, so that’s the supportive role, I guess you could say, but then also, as you mentioned, they can directly attack cancer cells through a process called phagocytosis. With these various roles, could you speak a little bit about how they might be useful on their own, as well as how they might be used in combination, not only with checkpoint immunotherapies, but also with other potential treatments today?

Miriam Merad, MD, PhD 

As I mentioned, the extraordinary things about macrophages and dendritic cells, and I assume this is why you invited me to talk about these cells in particular, is that they have many different roles. They eat the cancer cells, present them on the cell surface, and educate T cells, but in some cases, they also inhibit T cell function. So, if they are surrounded by tumor cells, we improve or enhance the ability of macrophages to capture these pieces of tumor cells. For example, with chemotherapy, we may enhance their ability to present so we realize already that with chemotherapy and the right chemotherapy, the ones that don’t kill T cells so much but kill tumor cells mainly, can provide more of what we call the cargo antigen to macrophages. So, there are many groups that are trying to combine chemotherapy and potentially immunotherapy, how can we harness more of those macrophages and dendritic cells by making them more active or less sensitive to tumors’ ability to dampen their function, we have also identified how the tumor cells dampen their ability to instruct the T cell killing function. So, this is a bit complex, but bear with me here, so I’m talking to the audience here. Our body is so extraordinarily well-organized. The dendritic cells and macrophages are also sensitive to tumor cues. They are sensitive to any damage cues, so let’s say we have an infection, dendritic cells and macrophages are going to capture the, let’s say COVID, and they know that things are really not going well, so they are super active and are presenting the COVID antigen, but also producing lots of signals to tell the T cells where to go and kill in some cases. And in the case of tumors, they are going to present but they present in a way where they are telling the T cells ‘well don’t kill, in fact.’ They make them what we call regulatory, they tell the T cells ‘do not kill the tumor.’ This is because they receive the cue, as I explained before, that tells them we are in repair mode now. And this is how the tumor is thinking about them. What my lab is doing, for example, is really targeting these cues. Blocking tumors’ ability to tell dendritic cells and macrophages that they are in repair mode, like being kind. Tell the T cells not to kill us, because we want to repair our tissue. What we are trying to do is bring a signal to the tumor microenvironment with the DCs and macrophages that are in this microenvironment, to tell them there are very bad things that are happening here. And those signals come from our understanding of an infectious response. We know that dendritic cells and macrophages are not fooled by microbes. They can be fooled also during chronic infection, but they know how to recognize microbes. And all this knowledge is being used to devise novel therapies to target dendritic cells and macrophages, make them a resistor to tumors’ ability to help them to be in repair mode, and make sure that they will constantly activate T cells and not make them what we call regulatory and also identify other checkpoints. I’ve told you that those PD-L1 checkpoints that engage in the checkpoint on the T cells identified other molecules that engage checkpoints on T cells. In fact, we have identified many new regulatory molecules by really looking at dendritic cells. So, we’ll use high-dimensional technology to really look at the molecular level of how dendritic cells behave in tumors. And we’ve identified many other regulatory molecules beyond the PD-1/PD-L1 that we’re targeting right now.

Arthur Brodsky, PhD 

That’s awesome to hear. It’s definitely a very exciting time. Thus far, we’ve been talking about established tumors, patients that are already in the hospital and need to get treatment for large established tumors. But we’re also starting to appreciate the role that other immune cells and the immune system in general play during the development of cancer and the progression of cancer, in addition to how it responds to treatment. So, as we’re learning more about the immune system and the role that it plays during the development of tumors, what opportunities might there be for treating cancer earlier, and potentially even preventing it altogether?

Miriam Merad, MD, PhD  

This is where the excitement resides really, is to go as early as possible because what we all want is to cure cancer, right? We want to eliminate those cells and prevent them from coming back. And we think that if we go early, during cancer progression, this is where we maximize our chances of curing the disease, although we are also trying to cure established tumors, and we are having great success, we think we can continue to build on the success. Early seems easier. And there are already data that suggests that this is happening already. So, for example, in this early squamous cell cancer, cancer of the skin, we know that activating a very strong immune response is sufficient to eliminate cancer cells. We know it, for example, in bladder cancer also, when we had superficial bladder cancer BCG therapy, which is really a way of providing a microbial signal, as if you have tuberculosis in your bladder, so, we provide a microbial signal that just activates the immune system. Of course, we are not providing microbes, we are just providing things that look like microbes. And this is sufficient to activate the immune system. And this is in turn eliminating cancer cells. We know that this is possible. At my institution, Mount Sinai School of Medicine, we are now the largest hospital in New York City, and we have put enormous, we have invested enormous means to really develop a very solid screening protocol. And we, the cancer immunology program, are very attached to the screening program. And so, we want to have screens, during the screening process, this is where we identify these very small tumors. And our hope is that by activating very strongly the immune system, we can more easily eliminate those cancer cells. That’s a big part of the focus of our group and many other groups in the world. And CRI is very interested in funding these types of studies. Another big hope of ours is to prevent cancer progression. And this is a little bit more complex. It requires different types of thinking, and we are going to predict that if we can, let’s say vaccinate against some common tumor antigen, we may prevent tumor progression in some organs. And there’s lots of effort also being done to identify those common tumor antigens that are commonly used and commonly expressed by most tumor cells, or at least tumor cells in specific organs, and how we can vaccinate against them. These are really the two pockets of studies that are being done now with the hope of curing cancer in the future.

Arthur Brodsky, PhD 

I want to zoom out a little more now. We’ve been talking about the immune system’s impact throughout the course of cancer. But as your slides showed at the beginning, the immune system and inflammation, or lack of inflammation, play a role in almost all diseases that we know of. And I know it’s still really an early field. But I wanted to bring in some of the more recent and surprising findings, especially with regard to the microbiome and diet and things like that. The microbiome, for our audience, is the microbial species that live in and on our bodies, mostly in the skin and especially in our intestines. Bacteria mainly, but also viruses and fungi, which can prime the immune system and determine how the immune system acts. Again, it is still very early in these explorations, but what do we know about how our lifestyles and other factors influence our immune system, not only in the context of cancer but impacting other diseases and even our health in general?

Miriam Merad, MD, PhD 

Yeah. I just want to emphasize what you said again because this is definitely a big focus also of the institute that I lead here at Mount Sinai, which is really thinking about how the immune system can cause diseases. And also, how can we learn from really studying the immune response to different diseases? We’ve seen that cancer immunology has helped tremendously in our fight against COVID. Because COVID patients were dying from this bad inflammation. And in fact, oncologists have studied inflammation for a long time. And we’re quite active in trying to modulate immune responses in organs. And it’s played an extraordinary role in the design of vaccines, but also in clinical trials and in our fight against this pathogenic inflammation. So, it’s very important that we study the immune responses that cause different diseases because we could learn if we can bring principles from one organ and one disease to another. And that can really always facilitate and accelerate progress.

You had this specific question of the microbiome, which is one aspect where we can, through nutrition or other external influences, modulate. The microbiome is all these microbes, trillions of microbes that populate our intestine, but are also present in the skin, potentially in our nose, in our ears, in our mouth, and are playing a very important role in producing metabolites that we know shape the immune response. And we have seen in cancer patients that specific microbes are associated with good responses to immunotherapy. And now there are interventional studies, where cancer patients are being fed or sometimes with different therapeutic strategies, we provide different types of microbes in their intestines and see whether by changing the microbial composition, we can modulate cancer treatment. And we have some early successes that are very encouraging. But we also know that what we eat defines our microbial composition. There are several studies showing that for example, eating red meat has a very big impact on what we call biomass, the number of microbes. Microbes love meat, so the more red meat you eat, the more microbes you have.

We also know that fibers change almost completely the behavior of microbes, so we know that microbial composition and potential function can respond to different nutritional elements and there is lots of work in this area trying to shape. Now there are very serious studies where we are trying to modulate the composition of microbes and definitely eat strategically, I was going to say, but maybe there are better words for that. It can have an impact on our microbiome. And because we modify the microbiome, you can modify what we call metabolites, and you can impact your immune system. But we know also that exercise is an extraordinarily potent way of stimulating your immune system.

We know also that sleep has a dramatic impact on what we call the wellness or the fitness of our immune system. The less you sleep, the less your immune cells are really fit to respond properly to cues. There are also studies, for example, here from Sinai and from other groups showing that jetlag can also impact the release of immune cells from the bone marrow. The immune cells are produced in the bone marrow and released in the blood, and from the blood, they go to all organs and that release of immune cells is significantly impacted by jetlag. My lab showed that eating impacts the release of immune cells. We showed that each time you eat, you release immune cells. But this excess release is not very good for you, because you shouldn’t release so many immune cells in your blood circulation. Since then, I eat much less. I eat once or twice a day, but I used to eat at different times during the day, and it’s probably not so good because humans we’re not used to eating all the time. We used to eat when we were hungry and now eat — food being so easy to find, the tendency is to eat all the time, and our body is not used to this way. There are many ways where you can control potentially the number and composition of the immune system. And I will say now clearly food, sleep, and exercise are the best way to really maintain a healthy immune system.

Arthur Brodsky, PhD 

You mentioned at the beginning, how unlike other treatments, chemotherapy, and radiation that act directly on the cancer cell, with immunotherapy, with us trying to strengthen the immune system and get the immune system to do the job if our immune system is compromised to begin with, that’s going to make it a lot less effective in treating cancer, even with the help of immunotherapy.

Miriam Merad, MD, PhD 

Oh, absolutely. And also, something we didn’t mention at all is how this bad immune system can also promote cancer progression. We know that bad inflammation, an immune system that is not doing well, or potentially inflammation that persists because you constantly have some type of damage and your immune system is not responding very well to it, can also contribute to tumor cause. Something I didn’t discuss because I wasn’t sure whether it would be too complicated to explain but in our prevention strategies, one thing that cancer immunologists are also doing is really trying to learn how to recognize these what we call pro-tumorigenic inflammatory responses and block them. We know, for example, that in a disease called NASH, for non-alcoholic steatohepatitis, we have a fatty liver that can predispose patients to liver cancer. And we know that it’s not the fat that’s inducing cancer, it’s the response to that fat that is really going at some point because there is this chronic and persistent inflammation that can induce cancer progression, and this works in complicated ways. At some point, the cells being constantly exposed to this inflammatory signal become dysregulated and start to have this abnormal ability to multiply. This is something that also can be prevented, maybe by proper nutrition and exercise.

Arthur Brodsky, PhD 

Now before we go, I just wanted to give you a chance to offer your take-home message about where the current research in the field is leading us and what the future of cancer treatment might look like.

Miriam Merad, MD, PhD 

I think that cancer treatment is going to change — or has changed already forever. Every single patient with cancer is going to be treated at some point with immunotherapy. It’s an extraordinary time in medicine and cancer care, but also in medicine in general. This realization that we had this whole, as I described, army of cells that had been protecting us, protecting, in fact, the human species and more living species for so long, and we have really not taken advantage of that. Knowledge of the regulation of the immune system is going to have a dramatic impact, in general, and on cancer patients in particular. What we have to do is really take advantage of another revolution that’s happening in medicine, which is the technology revolution. Technology is now enabling us to understand how the immune system is wired, or how it’s being fooled by cancer as I discussed earlier, in a way that was never possible before. The realization of immunotherapy being potentially curative, and the technology enabling those to really study the immune system in patients with extreme granularity and depth is going to be transformative. It is a fantastic time in medicine.

Arthur Brodsky, PhD 

I wholeheartedly agree. That is all the time that we have for today. Thank you so much, Dr. Merad, for sharing your time and insights with us.

Miriam Merad, MD, PhD 

My pleasure. Thank you for having me.

Arthur Brodsky, PhD 

For more of our webinars and the additional resources we have for patients and caregivers as part of CRI’s Answer 2 Cancer educational programs, we encourage you to check out our website at cancerresearch.org/patients. Here you can read and watch stories shared by others who have received immunotherapy. You can browse our entire library of past webinars and Immunotherapy Patient Summit Series, access other informational resources on treatment, emotional support, and financial assistance, and find help locating an immunotherapy clinical trial. I’d like to thank our sponsors one last time, Bristol Myers Squibb as well as Alkermes and Lilly Oncology, for making this webinar series possible. And thank you all for your attention today. I hope you found today’s webinar interesting and informative. And again, you can watch this and all of our other webinars on our website at cancerresearch.org/webinars. Finally, Dr. Merad, thank you again so much and we wish you the best of luck.

Miriam Merad, MD, PhD 

My pleasure.