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Dr. Manish Shah (Host): Welcome to Weill Cornell Medicine CancerCast, conversations about new developments in medicine, cancer care, and research. I'm your host, Manish Shah. And today, we will be talking about research from the 2025 American Society of Clinical Oncology (ASCO) Annual Meeting.

ASCO is the world's leading organization for physicians and oncology professionals caring for people with cancer, and focuses on collaboration, research, education, and the promotion of high quality, equitable patient care. The ASCO Annual Meeting is the largest international oncology conference in the world and features state-of-the-art research presentations and the latest oncology insights from oncology professionals.

I had a great time as a guest of this annual episode in the past, and I'm excited to continue the tradition of summarizing the exciting research that came out of the ASCO meeting. I will continue to cover solid tumor oncology this year, and my colleague Dr. Sarah Rutherford has joined us to discuss hematologic malignancies.

Dr. Rutherford is an Associate Professor of Clinical Medicine in the Division of Hematology/Oncology at Weill Cornell Medicine. She cares for patients with a variety of lymphomas and her research focuses on improving outcomes in patients with aggressive lymphomas. Dr. Rutherford has received honors from Weill Cornell Medicine, as well as from the American Society of Hematology and support from the New York State Empire Clinical Research Investigative Program for her research in diffuse large B-cell lymphomas. Sarah, welcome to the podcast. It's great to have you.

Dr. Sarah Rutherford: Thank you so much, Manish. It's fitting that we would do this together because we happened to run into each other right outside of ASCO as we were both walking in that Friday, and I was so excited to be there, and it's just been astounding how much progress has been gained over the last several years in all different malignancies. But, you know, of course, my focus is on hematologic malignancies, and I'm really excited to speak with you today about what was presented at ASCO this year.

Dr. Manish Shah: Absolutely. It was great running into you. I think it's really remarkable. I don't know the exact head count. But typically, 45,000 participants join ASCO every year. It's one of the most important meetings that we attend. It's an area where colleagues can see each other. We can connect around research and think about new ideas on where the field is going or what needs to be done. What are your thoughts about the impact of ASCO?

Dr. Sarah Rutherford: I agree with you. One, it's a great place to connect with other people. You know, for example, I saw my co-fellows who were all taking care of patients with different types of malignancies. And I think we can really learn from each other on the different techniques that are being used in these different studies across the types of malignancies. And then, of course, the educational aspect is key. There's always a lot of discussion generated at these meetings. And, again, you come home and take that back and it helps you take care of your patients and also develop ideas for future research projects.

Dr. Manish Shah: I think that's a really key point. I think each of the last several years, there have been some very important research papers and abstracts that have been published that really do change the way we practice medicine even the next day. And just to give people the scope of this, typically the meeting is a five-day meeting. It starts on the first weekend in June, usually on a Friday, and it goes through Tuesday afternoon. So, it is a long meeting. It's a busy meeting. A lot of things happen. And it is really exciting to go through all the data. So, why don't we start with some of the impactful heme malignancy abstracts that were presented. Sarah, what are your thoughts?

Dr. Sarah Rutherford: Yes. I'm really excited and actually you alerted me initially when I saw you that Friday about this polycythemia vera related abstract that was presented in the plenary session. So, this is a rare disease, but it is really key that it was presented in the most important session, a new drug for this disease.

So, polycythemia vera is what's called a myeloproliferative neoplasm. And it's driven by a certain type of mutation called JAK2. It's characterized by excessive production of red blood cells, and that makes people more at risk for blood clots, for example. People often present with an elevated blood count, which we call hematocrit. And one of the mainstays of treatment for years has been to actually do something called therapeutic phlebotomy, where the patients come every couple weeks, maybe sometimes weekly, or hopefully less often, but they have to have blood drawn and discarded, because they have too much of it basically. And that's a very simple way to deal with it. But as you can imagine, it really impacts people's quality of life.

So, very strikingly over the last decade or a little more, there have been a lot of understanding about the process of iron metabolism in the body. And interestingly, the patients with polycythemia vera, although they have high red blood counts, often actually are low in iron. And so, as a result, their regulation of what we call iron hemostasis is abnormal. There was a phase II trial that had been conducted of this drug called rusfertide, which is called a hepcidin mimetic. It acts like this protein that's normally in the blood and is normally low in polycythemia vera. And basically, by making the body think it has higher levels of this protein, the iron balance is able to be restored. And, as a result, their body is not erroneously absorbing the iron and producing extra blood cells.

So, I know that was a little complicated, but I wanted to go into the details of that. So, this study that was presented in the plenary – the most important session, the key abstracts at ASCO – is called VERIFY. And it was a phase III study that compared the prior type of treatment, which was this therapeutic phlebotomy plus placebo versus the rusfertide. And it just had striking results. So, their main endpoint, the main outcome that they were looking at was what they called a clinical response based on the absence of requiring phlebotomy. And they had a number of other key secondary endpoints, which included quality of life parameters, for example. And they just found striking results, very clear cut, that patients that were receiving the rusfertide, 77% of them were not requiring phlebotomy compared to 33% in those patients who were just getting the traditional strategy of phlebotomy.

And again, like I mentioned, there were also a number of endpoints that showed that this strategy of taking rusfertide compared to therapeutic phlebotomy was much better for people's quality of life. So, I think this is clearly going to be uptaken, I'm sure it already is being uptaken in the clinic, and I think it's going to have a key important impact on patients long-term with this disease, polycythemia vera.

Dr. Manish Shah: That's terrific. So for our listeners, you mentioned something called a therapeutic phlebotomy. Maybe let's just talk through exactly what that means. The main endpoint, as you said, was reducing the need for that. And I think it would be important to know exactly what that is and how often that's done in these patients with polycythemia vera.

Dr. Sarah Rutherford: Basically, people come and they have their blood checked in the clinic. And if their what's called hematocrit, which is basically their blood count, is over a certain percentage, which is usually 45%, they actually go to our infusion center and a nurse draws off a certain amount of blood and discards it. And so, that's the time where they're getting their blood checked, they're getting blood drawn, having to have an IV placed. And then, I think it can vary exactly how long this takes. It could be 30 minutes, it could be an hour. But the bottom line is it's requiring sometimes even weekly or every few weeks of having to have this done. And it is certainly a lot of time for patients.

Dr. Manish Shah: Yeah, exactly. And if I recall, it could be anywhere from 100 ccs to 200 or 300 ccs of blood that need to be removed, which is equivalent of four to eight ounces of blood that are being removed at any given time. And so, going from 33% of people who don't need that anymore to 80% no longer needing that is, I think, a really impactful outcome for this disease.

Dr. Sarah Rutherford: Yes. I'm sure that this is going to be very much preferred by patients moving forward for clear cut reasons that were proven in this large phase III trial.

Dr. Manish Shah: That's terrific. In the plenary, there were two abstracts that focused on immunotherapy. One was in colorectal cancer and the other was in head and neck cancer. And it just reminds me that the first approval for immunotherapy was Keytruda. And that was probably about 10 years ago now, and it's still making waves.

So in colon cancer, the ATOMIC study was presented. Patients with colon cancer that have mismatch repair deficiency, that is a specific genetic mutation, which occurs in about 5-10% of colon cancer. They accumulate new mutations because their cancer DNA isn't able to repair the errors that happen with each cell division. So, these new proteins, they're called neoantigens, they are foreign to the body, and the immune system is primed. It's ripe to attack these cancer cells. And the drug Keytruda, or other checkpoint inhibitors can be given to try to activate the immune system against these mismatch repair-deficient tumors.

So in the ATOMIC study, the drug that was used was a drug called atezolizumab. And that was another drug that is a checkpoint inhibitor, and it was given with chemotherapy compared to chemotherapy alone. And there was a significant improvement in survival, a 10% absolute improvement in survival of three years with the use of atezolizumab. So, that's going to be practice changing. But then, in head and neck cancer, a drug called nivolumab was used for high-risk head and neck cancer that can be resected and that also improved the event-free survival. So, it highlights the really important advantage of actually activating the patient's own immune system against the cancer. And I think we're learning more and more how to do that all the time. So, that was, I think, very interesting and also very practice changing.

One thing that these studies both highlight though is that we still need to select patients for these drugs. So, in the colon cancer space, the patient selection was by this mismatch repair protein deficiency. And in the head and neck cancer space, there were four or five other studies that were done that were actually in fact negative. But this study was positive. And I think the selection here was in the features that made head and neck cancer high risk. The intermediate and low risk tumors didn't seem to benefit. So, I think patient selection is important. When you have an active drug and you have the right patient, I think that's really the key message. You can really impact survival and have a really good outcome with the right drug and the right patient.

Dr. Sarah Rutherford: I think that's so exciting, Manish. And, you know, as a researcher in Hodgkin lymphoma, I'm really seeing the benefit of nivolumab upfront with chemotherapy in Hodgkin lymphoma, and that was actually presented at the plenary session in ASCO two years ago and has really been practice changing. So, these immunotherapy drugs are just so exciting and improving our patient's outcomes.

Dr. Manish Shah: Oh, terrific. Are there any other abstracts you want to highlight?

Dr. Sarah Rutherford: Multiple myeloma has been a disease that has seen a number of new drugs over the last 20 years or so, I would say. And so, there was an interesting abstract that actually led to a publication in the New England Journal of Medicine called the Phase III MIDAS trial. And these investigators were looking at two different questions, and it's a bit complicated, but I'm going to try to break it down as simply as possible.

So, there's so many active drugs in multiple myeloma now. The regimens for people who are fit and able to tolerate are actually four different drugs, mainly of targeted different strategies. This is a disease that is driven by a type of white blood cell called plasma cell, and it tends to affect bones. It can cause kidney dysfunction and is not viewed as a curable disease for the most part, but there are very effective therapies.

So, basically, this group of investigators, they were looking to answer two questions. One was whether there's a quadruplet regimen, so four different drugs. They're called isatuximab, Kyprolis, Revlimid, and dexamethasone, a steroid, were all being given to a group of patients. And they were trying to answer two questions, and they're related to something called an autologous stem cell transplant. So often, the most aggressive therapy that can be given to patients with multiple myeloma if they have a good response to their upfront therapy, is to give them what's called an autologous stem cell transplant.

We are starting to be able to use minimal residual disease detection in a way that I think that some solid tumor diseases have been using. So, often, for example, using something called circulating tumor DNA. But essentially, they gave all patients six cycles of this treatment and then they collected this blood test for what's called minimal residual disease. And for those who were deemed to meet a threshold to be considered in a standard risk, but a better prognosis, they basically compared continuing that same treatment called IsaKRD compared to doing an autologous stem cell transplant, which would've been the standard of care. And the other group, which was deemed a higher risk group who still had a higher amount of detectable disease in their blood, they either got a transplant, or they got what's called a tandem transplant, which are two stem cell transplants. And what they found is that both groups actually did better with less intense therapy. So, the group that was being randomized to look at transplant versus just continuing the standard targeted agents were found to do just as well. So, transplant is not needed in that group. And then, for those who were being investigated for one transplant versus two transplants, they were deemed equivalent, so those patients would really only need to go through one transplant.

I know this is a very complicated study design, but I think it's really showing the effectiveness of this frontline regimen called isatuximab, Kyprolis, Revlimid, and dexamethasone. I think one downside of this that has been acknowledged by the investigators is that that regimen may not be widely available at this point. But I think it really shows that some of these techniques that we are starting to be able to do, such as minimal residual disease detection, are helping us be able to guide what treatment people need so that we don't overtreat them or we don't undertreat them. In this case, they really found that patients did not need to be overtreated and that certainly will spare patients from toxicity over time.

Dr. Manish Shah: That's really interesting. So, the design was if your minimal residual disease test, the ctDNA was negative, then you were able to maybe deescalate treatment.

Dr. Sarah Rutherford: Yeah, they've proved that those people would not need a transplant. They could continue on for six more months of that treatment without requiring a transplant. And for those who may in the past have needed two transplants, they would just continue on with one instead, based on the results of this trial.

Dr. Manish Shah: That's really terrific. So actually, that leads perfectly to an advance in breast cancer that was presented at ASCO as well. That was the SERENA-6 study. And here, they used the same technology, the minimal residual disease or ctDNA technology to guide therapy again.

So, historically, people often they're familiar with blood tests called tumor markers where you look for a certain protein in the blood and you use that to track the disease. So, in colon cancer for example, there's a protein called CEA that you might draw a test for. The technology that we're talking about is actually much more refined than that. So, there are pieces of DNA that are floating in the blood that will eventually get cleared by your body. And when you do a regular blood draw using precision instruments, you're able to isolate this DNA and then look at what the mutations are in the genes that are on this small piece of DNA. And sometimes you're able to find mutations that shouldn't exist in the blood and really should only come from the tumor that may be in your body. And so, if you are able to identify these mutations in the DNA that's found in the blood, then you would be considered as having some circulating tumor DNA. DNA that came from the tumor that's in your blood. And that's turned out to be very, very informative.

In many solid tumors, and I think also in some heme malignancies, if you had a cancer and you're treated either with surgery or some other kind of treatment, maybe a transplant, if this circulating tumor DNA becomes positive later in the future, then it means that there might be some residual cancer in your body and that will predict or portend a recurrence. So, that data exists. And what's kind of the future is can we use that information where you're basically having microscopic evidence of tumor recurrence? Can we use that to guide therapy?

And it sounds like this is exactly what was done in this trial that Dr. Rutherford mentioned. In the SERENA-6 trial, they examined this as well. So specifically, this was a study of a drug called camizestrant, which is a next generation drug that blocks the androgen receptor. And this is given in patients that have resistance to the standard androgen receptor inhibitors. And this is given with the CDK4/6 inhibitor.

So in this trial, what they did is that patients received the standard treatment and then, if they had evidence of this circulating tumor DNA, a mutation in this gene called ESR1, then they were switched to camizestrant or not.  Camizestrant is a next generation oral drug that blocks the ER receptor, both the wild type and the mutant receptor. And patients who were switched to camizestrant when they had the positive mutation for ESR1, they had a significant improvement in survival. The progression-free survival was 60% with  camizestrant versus 33% without. So, almost a doubling of the progression-free survival by using a ctDNA-guided approach. It's just an exciting area where we can apply this new technology and improve patient outcomes because we can identify the disease earlier and earlier.

Dr. Sarah Rutherford: That's really exciting, Manish, for our breast cancer patients to have such good results from that study. I actually wanted to tell you about two abstracts on the same study for CLL, chronic lymphocytic leukemia, which is a disease that I treat. And because this disease is often found in the blood, has been one that has been able to use these types of techniques for a number of years. It's more accessible to be able to access this type of minimal residual disease when you're just easily able to detect it from the blood. But basically, this disease, CLL, tends to be one with a very good prognosis. Many people don't even need treatment for many years. People tend to live a long time and have good full lives. But there is one subset of patients that have traditionally not done as well with standard treatments. And those are ones that have a chromosome abnormality called deletion 17p or sometimes it can be associated with mutation called TP53.

So, about over a decade ago, there's been a new type of therapy approved for CLL called BTK or Bruton's tyrosine kinase inhibitor, which targets directly to the B cell receptor, which is what drives CLL. And so, the first approved drug of that category was called ibrutinib. And so, more research studies have been done in this disease over time, and we now have a very potent version of a BTK inhibitor, considered the third generation, called zanubrutinib. And there was a really exciting results, specifically in this patient population.

So, many of the studies for CLL have not been able to directly enroll just patients with this abnormality. But this SEQUOIA trial had four different arms. And in particular, I'm going to mention arm C, which was enrolling the deletion 17p-related CLL. And I do want to mention this drug zanubrutinib is very well established to be safe. Honestly, from an anecdotal standpoint, patients often tell me that aside from having to take the pills, they don't even realize they're taking a medicine much of the time. It really does not have that many side effects. But the primary endpoint of the study was progression-free survival.

And they have found that Brukinsa, which is the brand name, or zanubrutinib, the generic name, has very similar outcomes with this 17p deleted subset than patients without that mutation status or without that chromosome abnormality. And I think we knew, again, just from taking care of patients over the years and using this drug, that it's very effective in most patients. But now, we have very objective information indicating that this therapy is very effective even in patients who historically would have less favorable prognoses. So, we're just so happy that we have more to offer for these patients now that historically would not have responded as well to chemotherapy, for example.

Dr. Manish Shah: That's really terrific. I mean, I think that's really been a revolution over the last decade. The idea of having targeted therapies. And so, maybe for our listeners, how would you describe a targeted therapy like the BTK6 inhibitor versus chemotherapy. Just from a very basic standpoint, I think that's very important for people to understand.

Dr. Sarah Rutherford: Yeah, I think it's a great question. It comes up a lot in my practice. So basically, chemotherapy works by killing cells that are dividing, and it can be quite effective. So for example, in one of the diseases I treat frequently called diffuse large B-cell lymphoma, it's a fast-growing cancer and the chemotherapy interferes with the cell cycle as the cells are dividing quickly. But it's not specific just for the lymphoma cells and that's why people have other symptoms. For example, hair loss and often neuropathy and other symptoms like that, because of this non-specific nature of chemotherapy.

We're seeing more and more cancers that we're finding of a specific reason why this cancer develops and then treatments have been developed that actually kill that cell at that place so that the cancer can be eliminated as opposed to the non-specific way that chemotherapy works. There still is a role for chemotherapy, certainly in lymphomas. And I think what we're trying to work to do is figure out, for example, with this minimal residual disease type detection, is can we give people just enough chemotherapy to get the disease under control. And then, favor using these what I think of as smarter agents, the targeted agents, maybe to maintain a response, for example.

Dr. Manish Shah: Absolutely. And thank you for explaining that. So, I think it also explains some of the challenges that there are with drug development. So, historically, let's say, for large B-cell lymphoma, an early trial, you would enroll everybody that has that diagnosis. It looks like a large B-cell lymphoma under the microscope. But now, and this is true in solid tumors as well, instead of just having a histologic diagnosis, you also need to know the molecular features because there are some lymphomas that you would treat one way, other lymphomas you treat another way, with the different targets. And I think the specificity increases. But then, it also makes it more challenging because, to run that kind of a trial, you need to screen thousands of patients to find the right one that meets that target that you want to examine.

Dr. Sarah Rutherford: Right. I agree. Actually, maybe we can do a future podcast on this. I'm going to be doing an ASH education session. So, this is the American Society of Hematology meeting, which will be in December of 2025, specifically on what you're just talking about, targeting treatment by molecular subtype and there's five different types of molecular subtypes of that disease I mentioned diffuse large B-cell lymphoma. And now, we have a way to be able to pretty reliably put people into these different categories. And there's a clinical trial that's being planned through the inner group, through the National Cancer Institute run by the ECOG group to actually treat newly diagnosed patients with diffuse large B-cell lymphoma into five different arms based on their subtype. So, I think we're seeing a lot of exciting research to come in lymphomas and all different hematologic malignancies.

Dr. Manish Shah: That is terrific. And you just bought yourself another date with us on the podcast. Let's think about any other lesser publicized studies, anything that you might think that we should keep an eye on.

Dr. Sarah Rutherford: I wanted to mention another disease, myelodysplastic syndrome, which can be managed sometimes at its lowest risk state with transfusion support. These are people who have errors – they’re not able to fully make normal amounts of all different types of blood cells.

So, there was an injection called luspatercept, which is showing actually a survival improvement over a traditional type of injection called epoetin alfa, which helps red blood cell stimulation. That trial's called the COMMANDS trial. So, I think that's something to look out for. And I, of course, with an interest in Hodgkin lymphoma, clinical care and research, I'm really excited about a new trial that was looking at a new immunotherapy approach for people who've already received prior immunotherapies. I've already indicated that nivolumab and pembrolizumab, as well, are effective in Hodgkin lymphoma. It was called the LuminICE-203 study that's looking at a new drug called a bispecific antibody that targets both Hodgkin lymphoma cells and then what's called natural killer cells, which are part of our immune system, and it's a combined type therapy that had very impressive early results in safety in Hodgkin lymphoma. So, from my practice, that was probably the abstract I was the most excited about for my patients in the future.

Dr. Manish Shah: That's very exciting. I agree with you. So, this class of drugs is actually one of the next generation things that will change practice. Our listeners have heard about monoclonal antibody therapies where the antibody targets a specific receptor or antigen or something like that. A bispecific is where they can engineer the antibody to target two different things. And so, one might be PDL1, which is a checkpoint inhibitor. And then, one might be VEGF, which is an anti-angiogenic type of agent. And if you combine them and you target them both, you might even have more effective therapy. So, I think this area of research is really going to grow and I think might be something that we need to talk about in the future.

There are two lesser publicized abstracts that I think are really interesting that I wanted to mention. One is in pancreatic cancer. It's called the PANOVA-3 trial. And what they did is that they used a contraption, something that you would wear around your waist and this device would deliver, they're called TT fields, so tumor treating fields. These are electric fields that disrupt the processes that are important for cell division. And this device is able to directly deliver these fields to the tumor. It's almost like wearing a belt with a little fanny pack on your side or on your front. People would wear this 14 to 16 hours a day on this trial. But the trial was a chemotherapy trial with or without these tumor treatment fields. And it was really remarkable. There was an improvement in survival in patients who use these fields. So, somehow local electric field treatment to the tumor improve survival. This is pretty interesting. I looked this up actually afterwards because I was so fascinated, and it turns out that this wasn't a one-off. Tumor treatment fields has efficacy in gliomas, so in brain cancers, as well as in lung cancer. So, I think there is definitely an effect on, if you can disrupt the tumor itself, you might be able to treat it better when you combine it with chemotherapy.

And then, the other trial that I really am quite excited by is actually a trial of exercise in colon cancer. So, this was called the CHALLENGE trial. And in colon cancer after surgery, if you have stage III colon cancer or some patients with a higher risk of stage II colon cancer, the standard treatment is chemotherapy. This trial gave people the chemotherapy, but they randomly assigned patients to also receive a structured exercise program. And the structured exercise program included in-person mandatory sessions plus supervised sessions, plus counseling. And this was over six months. And then, the next phase was recommended sessions over the next six months and then, surveillance over the next two years. The target was to increase the physical activity by about 10 MET hours per week. A MET hour is the energy expended by sitting for one hour. So, walking briskly for one hour is four MET hours. So, this was two and a half hours of brisk walking, essentially equivalent of that. And patients who were able to go on the exercise program-- this is a randomized study-- they had a significant improvement in disease-free survival and recurrence. And this was not only an improvement in colon cancer recurrence, but also an improvement in the recurrence rates of other cancers like liver cancer or lung cancer. So, it's actually really, really quite remarkable. So, I think we've all recommended exercise, but now we have actual data that in a randomized setting that says that if you exercise in a structured way, it can help reduce your risk of recurrence of cancer.

Dr. Sarah Rutherford: I think that's so fascinating, Manish. There also have been some studies, not to that extent, but in lymphomas showing benefits. There must be some clear mechanism that's helping, and it also helps people psychologically, I think, to exercise as well. And all my patients ask me, "What can I do?" And I think that that likely applies to a lot of other type of cancer. So, I hope similar research will be done in other areas.

Dr. Manish Shah: Yeah, absolutely. I think it's really exciting. I think one thing that I really feel is that, for many years in oncology, the advances were primarily in the area of cytotoxic therapy, like new chemotherapy agents, new drugs and things like that. And then, there's a shift toward targeted agents as you were saying earlier, what are the specific mutations that drive a tumor? And if you can target those mutations, you can have an outcome that's beneficial. Now we're also getting in an area of other things like exercise or there was an abstract that was presented that actually the timing of immunotherapy, if you give immunotherapy before three in the afternoon-- which is kind of maybe the morning hours, your immune system is a little more awake and more energized-- that was better than giving immunotherapy after three in the afternoon. These kinds of things are exciting because it really places cancer and treatment in the context of our lives.

Dr. Sarah Rutherford: It's exciting that we have these strategies that are being developed. And I'm astounded by how much progress has been made already. I'm an optimist, but I still just wouldn't have even expected so much progress to have been made in the last 10 years. I think we're going to just see it continue on like this as we move forward.

Dr. Manish Shah: Are there any exciting treatments or technologies that you're looking forward to in the horizon?

Dr. Sarah Rutherford: Yeah, I think we already hit on it with the ctDNA, so specifically in Hodgkin lymphoma and diffuse large B-cell lymphoma where it hasn't been used. That's what I'm most excited about right now for our field. And I've been talking to some of your colleagues in colon cancer to really understand how the impact of that has been on your disease that you treat.

Dr. Manish Shah: With every new technology, there is a learning period. And also, we are learning a little bit about the limitations as well, right? So, I'm sure this happens to you. But just recently, for example, we've been following one of my patients', their ctDNA. And we look at it together with the magnifying glass. And then, one thing that comes up is that, sometimes, if you're not looking for mutations that are specific to the tumor, but sort of common mutations, you can identify something called CHIP, right? Which is mutations that could be not related to your cancer, but for other causes. And I think we'll do a podcast on what CHIP means, but not every mutation that's found in the blood is related to cancer. And it's something that we need to keep in mind as we move this technology forward.

Dr. Sarah Rutherford: Right. Agree. I think Dr. Pinkal Desai can talk to you more about CHIP in a future podcast as well.

Dr. Manish Shah: Exactly. So, is there anything else that you want to touch on as a takeaway or wrap up? Like what are the main things that you think that we should think about as a patient or as a caregiver?

Dr. Sarah Rutherford: From a general standpoint, you've really introduced this from the beginning. Part of the reason we go to these meetings like ASCO is we learn about all these exciting trials that are moving forward the science and the outcomes for patients. And for patients, I think it's important to explore clinical trial options when you have a diagnosis that requires treatment. And there also are clinical trials that don't even involve treatment. But I think that's a key.

So if you're out there listening and you have a cancer diagnosis, I think it's important to ask your doctor about trials or we're happy at Weill Cornell Medicine to talk to you about trials that we have open. Because often you can actually get treatment that may be better than what is available commercially by going onto a clinical trial. We actually hit on a lot of the exciting research specifically that I'm interested in for hematologic malignancies moving forward.

And one of them I think very clearly is the bispecific antibodies. I think those are really well-tolerated. Overall, most patients are eligible for them. We have them approved for third line and people who've had two other types of treatment in a number of different hematologic malignancies.

And I think one actually really exciting aspect of that type of treatment is that it doesn't necessarily require a more nuanced understanding of that specific tumor, at least in hematologic malignancies. We call it sometimes subtype agnostic, that it's likely to work in most patients with a certain type of lymphoma, for example. So from a therapeutic standpoint, I think that's the type of agent that I'm most excited about right now.

Dr. Manish Shah: I think we touched on a lot of the exciting areas with the ctDNA and the bispecifics. And one thing that I think is important for our listeners to understand is that oncology, whether it's solid tumor or lymphoma, it doesn't really happen in a vacuum anymore. You really require teams of people to work with you to try to help navigate your care. I think that's definitely true with regard to solid tumors where often you're thinking about interventional radiologist or a surgeon or radiation oncology, like there's so many different disciplines that could impact your care that you wouldn't have thought of previously. So, I think, this kind of multidisciplinary approach to care is actually really, really important to oncology care.

Dr. Sarah Rutherford: Right. I agree.

Dr. Manish Shah: So with that, I think, it's been really a terrific discussion with you, Dr. Rutherford. It's so many exciting things that have happened at ASCO, and it's really a pleasure to update our listeners on the best of ASCO 2025. You can download, subscribe, rate, and review CancerCast on Apple Podcasts, Spotify, or online at weillcornell.org. We also encourage you to write to us at cancercast@med.cornell.edu with questions, comments, and topics that you'd like to hear us cover in the future. That's it for CancerCast, conversations about new developments in medicine, cancer care and research. I'm Dr. Manish Shah. Thanks for listening.

Promo: Listen now to On the Mind, the new podcast from Weill Cornell Medicine, discussing the latest hot topics in psychiatry, psychology, and mental health. Join Dr. Daniel Knoepflmacher as he explores recent research in cutting-edge clinical care with leading scientists and providers. Learn new initiatives in community wellness and how to process your mental health journey while exploring everything on the mind. Subscribe wherever you listen to podcasts.

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Participants may have consulting, equity, board membership, or other relationships with pharmaceutical, biotech, or device companies unrelated to their role in this podcast. No payments have been made by any company to endorse any treatments, devices, or procedures. And Weill Cornell Medicine does not endorse, approve, or recommend any product, service, or entity mentioned in this podcast.

Opinions expressed in this podcast are those of the speaker and do not represent the perspectives of Weill Cornell Medicine as an institution.