Podcasts about Melanoma

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Please visit answersincme.com/XWB860 to participate, download slides and supporting materials, complete the post test, and obtain credit. In this activity, an expert in melanoma discusses combination anti–programmed cell death protein 1 (PD-1) plus anti–lymphocyte-activation gene 3 (LAG-3) therapy. Upon completion of this activity, participants should be better able to: Review the latest clinical evidence supporting use of combination anti–PD-1 plus anti-LAG-3 therapy in the first-line setting for patients with unresectable, advanced melanoma; Identify eligible patients with unresectable, advanced melanoma who can benefit from the use of combination anti–PD-1 plus anti–LAG-3 therapy in the first-line setting; and Outline strategies for managing adverse events associated with combination anti–PD-1 plus anti–LAG-3 therapy.

Luis Herrero entrevista a Ángeles Flórez, jefa del servicio de Dermatología en el Hospital Clínico Universitario de Santiago de Compostela.

“Vax to the Future: Cancer Immunity Revolution

In today's episode, supported by Immatics, we had the pleasure of speaking with Justin Moser, MD, about the ongoing phase 3 SUPRAME trial investigating the PRAME-directed T-cell receptor T-cell therapy IMA203 vs treatment of physician's choice in patients with previously treated, unresectable or metastatic cutaneous melanoma. Dr Moser is an associate clinical investigator, a melanoma and cutaneous oncology specialist, and a phase 1 trialist at HonorHealth Research Institute in Scottsdale, Arizona; as well as a research associate professor at the Arizona State University School of Medicine and Advanced Medical Engineering. In our exclusive interview, Dr Moser discussed the unique mechanism of action of IMA203, previously reported phase 1 data with this agent in patients with melanoma, and the design and potential future implications of SUPRAME. 

Dr. Diwakar Davar and Dr. Jason Luke discuss novel agents in melanoma and other promising new data in the field of immunotherapy that were presented at the 2025 ASCO Annual Meeting. TRANSCRIPT Dr. Diwakar Davar: Hello. My name is Diwakar Davar, and I am welcoming you to the ASCO Daily News Podcast. I'm an associate professor of medicine and the clinical director of the Melanoma and Skin Cancer Program at the University of Pittsburgh's Hillman Cancer Center. Today, I'm joined by my colleague and good friend, Dr. Jason Luke. Dr. Luke is a professor of medicine. He is also the associate director of clinical research and the director of the Phase 1 IDDC Program at the University of Pittsburgh's Hillman Cancer Center. He and I are going to be discussing some key advancements in melanoma and skin cancers that were presented at the 2025 ASCO Annual Meeting. Our full disclosures are available in the transcript of this episode.  Jason, it is great to have you back on the podcast. Dr. Jason Luke: Thanks again so much for the opportunity, and I'm really looking forward to it. Dr. Diwakar Davar: Perfect. So we will go ahead and start talking a little bit about a couple of key abstracts in both the drug development immunotherapy space and the melanoma space. The first couple of abstracts, the first two, will cover melanoma. So, the first is LBA9500, which was essentially the primary results of RELATIVITY-098. RELATIVITY-098 was a phase 3 trial that compared nivolumab plus relatlimab in a fixed-dose combination against nivolumab alone for the adjuvant treatment of resected high-risk disease. Jason, do you want to maybe give us a brief context of what this is? Dr. Jason Luke: Yeah, it's great, thanks. So as almost all listeners, of course, will be aware, the use of anti–PD-1 immunotherapies really revolutionized melanoma oncology over the last 10 to 15 years. And it has become a standard of care in the adjuvant setting as well. But to review, in patients with stage III melanoma, treatment can be targeted towards BRAF with BRAF and MEK combination therapy, where that's relevant, or anti–PD-1 with nivolumab or pembrolizumab are a standard of care. And more recently, we've had the development of neoadjuvant approaches for palpable stage III disease. And in that space, if patients present, based on two different studies, either pembrolizumab or nivolumab plus ipilimumab can be given prior to surgery for somewhere in the 6- to 9-week range. And so all of these therapies have improved time-to-event endpoints, such as relapse-free or event-free survival. It's worth noting, however, that despite those advances, we've had a couple different trials now that have actually failed in this adjuvant setting, most high profile being the CheckMate-915 study, which looked at nivolumab plus ipilimumab and unfortunately was a negative study. So, with RELATIVITY-047, which was the trial of nivolumab plus relatlimab that showed an improvement in progression-free survival for metastatic disease, there's a lot of interest, and we've been awaiting these data for a long time for RELATIVITY-098, which, of course, is this adjuvant trial of LAG-3 blockade with relatlimab plus nivolumab. Dr. Diwakar Davar: Great. So with that, let's briefly discuss the trial design and the results. So this was a randomized, phase 3, blinded study, so double-blinded, so neither the investigators knew what the patients were getting, nor did the patients know what they were getting. The treatment investigational arm was nivolumab plus relatlimab in the fixed-dose combination. So that's the nivolumab standard fixed dose with relatlimab that was FDA approved in RELATIVITY-047. And the control arm was nivolumab by itself. The duration of treatment was 1 year. The patient population consisted of resected high-risk stage III or IV patients. The primary endpoint was investigator-assessed RFS. Stage and geography were the standard stratifying factors, and they were included, and most of the criteria were balanced across both arms. What we know at this point is that the 2-year RFS rate was 64% and 62% in the nivolumab and nivolumab-combination arms, respectively. The 2-year DMFS rate was similarly equivalent: 76% with nivolumab monotherapy, 73% with the combination. And similar to what you had talked about with CheckMate 915, unfortunately, the addition of LAG-3 did not appear to improve the RFS or DMFS compared to control in this patient population. So, tell us a little bit about your take on this and what do you think might be the reasons why this trial was negative? Dr. Jason Luke: It's really unfortunate that we have this negative phase 3 trial. There had been a lot of hope that the combination of nivolumab with relatlimab would be a better tolerated combination that increased the efficacy. So in the metastatic setting, we do have 047, the study that demonstrated nivolumab plus relatlimab, but now we have this negative trial in the adjuvant setting. And so as to why exactly, I think is a complicated scenario. You know, when we look at the hazard ratios for relapse-free survival, the primary endpoint, as well as the secondary endpoints for distant metastasis-free survival, we see that the hazard ratio is approximately 1. So there's basically no difference. And that really suggests that relatlimab in this setting had no impact whatsoever on therapeutic outcomes in terms of efficacy. Now, it's worth noting that there was a biomarker subanalysis that was presented in conjunction with these data that looked at some immunophenotyping, both from circulating T cells, CD8 T cells, as well as from the tumor microenvironment from patients who were treated, both in the previous metastatic trial, the RELATIVITY-047 study, and now in this adjuvant study in the RELATIVITY-098 study. And to briefly summarize those, what was identified was that T cells in advanced melanoma seemed to have higher expression levels of LAG-3 relative to T cells that are circulating in patients that are in the adjuvant setting. In addition to that, there was a suggestion that the magnitude of increase is greater in the advanced setting versus adjuvant. And the overall summary of this is that the suggested rationale for why this was a negative trial may have been that the target of LAG-3 is not expressed as highly in the adjuvant setting as it is in the metastatic setting. And so while the data that were presented, I think, support this kind of an idea, I am a little bit cautious that this is actually the reason for why the trial was negative, however. I would say we're not really sure yet as to why the trial was negative, but the fact that the hazard ratios for the major endpoints were essentially 1 suggests that there was no impact whatsoever from relatlimab. And this really makes one wonder whether or not building on anti–PD-1 in the adjuvant setting is feasible because anti–PD-1 works so well. You would think that even if the levels of LAG-3 expression were slightly different, you would have seen a trend in one direction or another by adding a second drug, relatlimab, in this scenario. So overall, I think it's an unfortunate circumstance that the trial is negative. Clearly there's going to be no role for relatlimab in the adjuvant setting. I think this really makes one wonder about the utility of LAG-3 blockade and how powerful it really can be. I think it's probably worth pointing out there's another adjuvant trial ongoing now of a different PD-1 and LAG-3 combination, and that's cemiplimab plus fianlimab, a LAG-3 antibody that's being dosed from another trial sponsor at a much higher dose, and perhaps that may make some level of difference. But certainly, these are unfortunate results that will not advance the field beyond where we were at already. Dr. Diwakar Davar: And to your point about third-generation checkpoint factors that were negative, I guess it's probably worth noting that a trial that you were involved with, KeyVibe-010, that evaluated the PD-1 TIGIT co-formulation of vibostolimab, MK-4280A, was also, unfortunately, similarly negative. So, to your point, it's not clear that all these third-generation receptors are necessarily going to have the same impact in the adjuvant setting, even if they, you know, for example, like TIGIT, and they sometimes may not even have an effect at all in the advanced cancer setting. So, we'll see what the HARMONY phase 3 trial, that's the Regeneron cemiplimab/fianlimab versus pembrolizumab control with cemiplimab with fianlimab at two different doses, we'll see how that reads out. But certainly, as you've said, LAG-3 does not, unfortunately, appear to have an impact in the adjuvant setting. So let's move on to LBA9501. This is the primary analysis of EORTC-2139-MG or the Columbus-AD trial. This was a randomized trial of encorafenib and binimetinib, which we will abbreviate as enco-bini going forward, compared to placebo in high-risk stage II setting in melanoma in patients with BRAF V600E or K mutant disease. So Jason, you know, you happen to know one or two things about the resected stage II setting, so maybe contextualize the stage II setting for us based on the trials that you've led, KEYNOTE-716, as well as CheckMate-76K, set us up to talk about Columbus-AD. Dr. Jason Luke: Thanks for that introduction, and certainly stage II disease has been something I've worked a lot on. The rationale for that has been that building off of the activity of anti–PD-1 in metastatic melanoma and then seeing the activity in stage III, like we just talked about, it was a curious circumstance that dating back about 7 to 8 years ago, there was no availability to use anti–PD-1 for high-risk stage II patients, even though the risk of recurrence and death from melanoma in the context of stage IIB and IIC melanoma is in fact similar or actually higher than in stage IIIA or IIIB, where anti–PD-1 was approved. And in that context, a couple of different trials that you alluded to, the Keynote-716 study that I led, as well as the CheckMate 76K trial, evaluated pembrolizumab and nivolumab, respectively, showing an improvement in relapse-free and distant metastasis-free survival, and both of those agents have subsequently been approved for use in the adjuvant setting by the US FDA as well as the European Medicines Agency.  So bringing then to this abstract, throughout melanoma oncology, we've seen that the impact of anti–PD-1 immunotherapy versus BRAF and MEK-targeted therapy have had very similar outcomes on a sort of comparison basis, both in frontline metastatic and then in adjuvant setting. So it was a totally reasonable question to ask: Could we use adjuvant BRAF and MEK inhibitor therapy? And I think all of us expected the answer would be yes. As we get into the discussion of the trial, I think the unfortunate circumstance was that the timing of this clinical trial being delayed somewhat, unfortunately, made it very difficult to accrue the trial, and so we're going to have to try to read through the tea leaves sort of, based on only a partially complete data set. Dr. Diwakar Davar: So, in terms of the results, they wanted to enroll 815 patients, they only enrolled 110. The RFS and DMFS were marginally improved in the treatment arm but certainly not significantly, which is not surprising because the trial had only accrued 16% to 18% of its complete accrual. As such, we really can't abstract from the stage III COMBI-AD data to stage II patients. And certainly in this setting, one would argue that the primary treatment options certainly remain either anti–PD-1 monotherapy, either with pembrolizumab or nivolumab, based on 716 or 76K, or potentially active surveillance for the patients who are not inclined to get treated.  Can you tell us a little bit about how you foresee drug development going forward in this space because, you know, for example, with HARMONY, certainly IIC disease is a part of HARMONY. We will know at least a little bit about that in this space. So what do you think about the stage IIB/C patient population? Is this a patient population in which future combinations are going to be helpful, and how would you think about where we can go forward from here? Dr. Jason Luke: It is an unfortunate circumstance that this trial could not be accrued at the pace that was necessary. I think all of us believe that the results would have been positive if they'd been able to accrue the trial. In the preliminary data set that they did disclose of that 110 patients, you know, it's clear there is a difference at a, you know, a landmark at a year. They showed a 16% difference, and that would be in line with what has been seen in stage III. And so, you know, I think it's really kind of too bad. There's really going to be no regulatory approach for this consideration. So using BRAF and MEK inhibition in stage II is not going to be part of standard practice moving into the future. To your point, though, about where will the field go? I think what we're already realizing is that in the adjuvant setting, we're really overtreating the total population. And so beyond merely staging by AJCC criteria, we need to move to biomarker selection to help inform which patients truly need the treatment. And in that regard, I don't think we've crystallized together as a field as yet, but the kinds of things that people are thinking about are the integration of molecular biomarkers like ctDNA. When it's positive, it can be very helpful, but in melanoma, we found that, unfortunately, the rates are quite low, you know, in the 10% to 15% range in the adjuvant setting. So then another consideration would be factors in the primary tumor, such as gene expression profiling or other considerations.  And so I think the future of adjuvant clinical trials will be an integration of both the standard AJCC staging system as well as some kind of overlaid molecular biomarker that helps to enrich for a higher-risk population of patients because on a high level, when you abstract out, it's just clearly the case that we're rather substantially overtreating the totality of the population, especially given that in all of our adjuvant studies to date for anti–PD-1, we have not yet shown that there's an overall survival advantage. And so some are even arguing perhaps we should even reserve treatment until patients progress. I think that's a complicated subject, and standard of care at this point is to offer adjuvant therapy, but certainly a lot more to do because many patients, you know, unfortunately, still do progress and move on to metastatic disease. Dr. Diwakar Davar: Let's transition to Abstract 2508. So we're moving on from the melanoma to the novel immunotherapy abstracts. And this is a very, very, very fascinating drug. It's IMA203. So Abstract 2508 is a phase 1 clinical update of IMA203. IMA203 is an autologous TCR-T construct targeting PRAME in patients with heavily pretreated PD-1-refractory metastatic melanoma. So Jason, in the PD-1 and CTLA-4-refractory settings, treatment options are either autologous TIL, response rate, you know, ballpark 29% to 31%, oncolytic viral therapy, RP1 with nivolumab, ORR about 30-ish percent. So new options are needed. Can you tell us a little bit about IMA203? Perhaps tell us for the audience, what is the difference between a TCR-T and traditional autologous TIL? And a little bit about this drug, IMA203, and how it distinguishes itself from the competing TIL products in the landscape. Dr. Jason Luke: I'm extremely enthusiastic about IMA203. I think that it really has transformative potential based on these results and hopefully from the phase 3 trial that's open to accrual now. So, what is IMA203? We said it's a TCR-T cell product. So what that means is that T cells are removed from a patient, and then they can be transduced through various technologies, but inserted into those T cells, we can then add a T-cell receptor that's very specific to a single antigen, and in this case, it's PRAME. So that then is contrasted quite a bit from the TIL process, which includes a surgical resection of a tumor where T cells are removed, but they're not specific necessarily to the cancer, and they're grown up in the lab and then given to the patient. They're both adoptive cell transfer products, but they're very different. One is genetically modified, and the other one is not. And so the process for generating a TCR-T cell is that patients are required to have a new biomarker that some may not be familiar with, which is HLA profiling. So the T-cell receptor requires matching to the concomitant HLA for which the peptide is bound in. And so the classic one that is used in most oncology practices is A*02:01 because approximately 48% of Caucasians have A*02:01, and the frequency of HLA in other ethnicities starts to become highly variable. But in patients who are identified to have A*02:01 genotype, we can then remove blood via leukapheresis or an apheresis product, and then insert via lentiviral transduction this T-cell receptor targeting PRAME. Patients are then brought back to the hospital where they can receive lymphodepleting chemotherapy and then receive the reinfusion of the TCR-T cells. Again, in contrast with the TIL process, however, these T cells are extremely potent, and we do not need to give high-dose interleukin-2, which is administered in the context of TIL. Given that process, we have this clinical trial in front of us now, and at ASCO, the update was from the phase 1 study, which was looking at IMA203 in an efficacy population of melanoma patients who were refractory at checkpoint blockade and actually multiple lines of therapy. So here, there were 33 patients and a response rate of approximately 50% was observed in this population of patients, notably with a duration of response approximately a year in that treatment group. And I realize that these were heavily pretreated patients who had a range of very high-risk features. And approximately half the population had uveal melanoma, which people may be aware is a generally speaking more difficult-to-treat subtype of melanoma that metastasizes to the liver, which again has been a site of resistance to cancer immunotherapy. So these results are extremely promising. To summarize them from what I said, it's easier to make TCR-T cells because we can remove blood from the patient to transduce the T cells, and we don't have to put them through surgery. We can then infuse them, and based on these results, it looks like the response rate to IMA203 is a little bit more than double what we expect from lifileucel. And then, whereas with lifileucel or TILs, we have to give high-dose IL-2, here we do not have to give high-dose IL-2. And so that's pretty promising. And a clinical trial is ongoing now called the SUPREME phase 3 clinical trial, which is hoping to validate these results in a randomized global study. Dr. Diwakar Davar: Now, one thing that I wanted to go over with you, because you know this trial particularly well, is what you think of the likelihood of success, and then we'll talk a little bit about the trial design. But in your mind, do you think that this is a trial that has got a reasonable likelihood of success, maybe even a high likelihood of success? And maybe let's contextualize that to say an alternative trial, such as, for example, the TebeAM trial, which is essentially a T-cell bispecific targeting GP100. It's being compared against SOC, investigator's choice control, also in a similarly heavily pretreated patient population. Dr. Jason Luke: So both trials, I think, have a strong chance of success. They are very different kinds of agents. And so the CD3 bispecific that you referred to, tebentafusp, likely has an effect of delaying progression, which in patients with advanced disease could have a value that might manifest as overall survival. With TCR-T cells, by contrast, we see a very high response rate with some of the patients going into very durable long-term benefit. And so I do think that the SUPREME clinical trial has a very high chance of success. It will be the first clinical trial in solid tumor oncology randomizing patients to receive a cell therapy as compared with a standard of care. And within that standard of care control arm, TILs are allowed as a treatment. And so it will also be the first study that will compare TCR-T cells against TILs in a randomized phase 3. But going back to the data that we've seen in the phase 1 trial, what we observe is that the duration of response is really connected to the quality of the response, meaning if you have more than a 50% tumor shrinkage, those patients do very, very well. But even in patients who have less than 50% tumor shrinkage, the median progression-free survival right now is about 4.5 months. And again, as we think about trial design, standard of care options for patients who are in this situation are unfortunately very bad. And the progression-free survival in that population is probably more like 2 months. So this is a trial that has a very high likelihood of being positive because the possibility of long-term response is there, but even for patients who don't get a durable response, they're likely going to benefit more than they would have based on standard chemotherapy or retreatment with an anti–PD-1 agent. Dr. Diwakar Davar: Really, a very important trial to enroll, a trial that is first in many ways. First of a new generation of TCR-T agents, first trial to look at cell therapy in the control arm, a new standard of efficacy, but potentially also if this trial is successful, it will also be a new standard of trial conduct, a new kind of trial, of a set of trials that will be done in the second-line immunotherapy-refractory space. So let's pivot to the last trial that we were going to discuss, which was Abstract 2501. Abstract 2501 is a first-in-human phase 1/2 trial evaluating BNT142, which is the first-in-class mRNA-encoded bispecific targeting Claudin-6 and CD3 in patients with Claudin-positive tumors. We'll talk a little bit about this, but maybe let's start by talking a little bit about Claudin-6. So Claudin-6 is a very interesting new target. It's a target that's highly expressed in GI and ovarian tumors. There are a whole plethora of Claudin-6-targeting agents, including T-cell bispecifics and Claudin-6-directed CAR-Ts that are being developed. But BNT142 is novel. It's a novel lipid nanoparticle LNP-encapsulated mRNA. The mRNA encodes an anti–Claudin-6 CD3 bispecific termed RiboMAB-021. And it then is administered to the patient. The BNT142-encoding mRNA LNPs are taken up by the liver and translated into the active drug. So Jason, tell us a little bit about this agent. Why you think it's novel, if you think it's novel, and let's talk a little bit then about the results. Dr. Jason Luke: So I certainly think this is a novel agent, and I think this is just the first of what will probably become a new paradigm in oncology drug development. And so you alluded to this, but just to rehash it quickly, the drug is encoded as genetic information that's placed in the lipid nanoparticle and then is infused into the patient. And after the lipid nanoparticles are taken up by the liver, which is the most common place that LNPs are usually taken up, that genetic material in the mRNA starts to be translated into the actual protein, and that protein is the drug. So this is in vivo generation, so the patient is making their own drug inside their body. I think it's a really, really interesting approach. So for any drug that could be encoded as a genetic sequence, and in this case, it's a bispecific, as you mentioned, CD3-Claudin-6 engager, this could have a tremendous impact on how we think about pharmacology and novel drug development moving into the future in oncology. So I think it's an extremely interesting drug, the like of which we'll probably see only more moving forward. Dr. Diwakar Davar: Let's maybe briefly talk about the results. You know, the patient population was heavily pretreated, 65 or so patients, mostly ovarian cancer. Two-thirds of the patients were ovarian cancer, the rest were germ cell and lung cancer patients. But let's talk a little bit about the efficacy. The disease control rate was about 58% in the phase 1 population as a whole, but 75% in the ovarian patient population. Now tell us a little bit about the interesting things about the drug in terms of the pharmacokinetics, and also then maybe we can pivot to the clinical activity by dose level. Dr. Jason Luke: Well, so they did present in their presentation at ASCO a proportionality showing that as higher doses were administered, that greater amounts of the drug were being made inside the patient. And so that's an interesting observation, and it's an important one, right? Suggesting that the pharmacology that we classically think of by administering drugs by IV, for example, would still be in play. And that did translate into some level of efficacy, particularly at the higher dose levels. Now, the caveat that I'll make a note of is that disease control rate is an endpoint that I think we have to be careful about because what that really means is sometimes a little bit unclear. Sometimes patients have slowly growing tumors and so on and so forth. And the clinical relevance of disease control, if it doesn't last at least 6 months, I think is probably pretty questionable. So I think these are extremely interesting data, and there's some preliminary sense that getting the dose up is going to matter because the treatment responses were mostly observed at the highest dose levels. There's also a caveat, however, that across the field of CD3 bispecific molecules like this, there's been quite a bit of heterogeneity in terms of the response rate, with some of them only really generating stable disease responses and other ones having more robust responses. And so I think this is a really interesting initial foray into this space. My best understanding is this molecule is not moving forward further after this, but I think that this really does set it up to be able to chase after multiple different drug targets on a CD3 bispecific backbone, both in ovarian cancer, but then basically across all of oncology. Dr. Diwakar Davar: Perfect. This is a very new sort of exciting arena where we're going to be looking at, in many ways, these programmable constructs, whether we're looking at in vivo-generated, in this case, a T-cell bispecific, but we've also got newer drugs where we are essentially giving drugs where people are generating in vivo CAR T, and also potentially even in vivo TCR-T. But certainly lots of new excitement around this entire class of drugs. And so, what we'd like to do at this point in time is switch to essentially the fact that we've got a very, very exciting set of data at ASCO 2025. You've heard from Dr. Luke regarding the advances in both early drug development but also in advanced cutaneous melanoma. And Jason, as always, thank you so much for sharing your very valuable and great, fantastic insights with us on the ASCO Daily News Podcast. Dr. Jason Luke: Well, thanks again for the opportunity. Dr. Diwakar Davar: And thank you to our listeners for taking your time to listen today. You will find the links to the abstracts that we discussed today in the transcript of this episode. And finally, if you value the insights that you hear on the ASCO Daily News Podcast, please take a moment to rate, review, and subscribe wherever you get your podcasts. Disclaimer: The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement. Follow today's speakers:    Dr. Diwakar Davar    @diwakardavar    Dr. Jason Luke @jasonlukemd Follow ASCO on social media:     @ASCO on Twitter       ASCO on Bluesky   ASCO on Facebook       ASCO on LinkedIn   Disclosures:     Dr. Diwakar Davar:      Honoraria: Merck, Tesaro, Array BioPharma, Immunocore, Instil Bio, Vedanta Biosciences     Consulting or Advisory Role: Instil Bio, Vedanta Biosciences     Consulting or Advisory Role (Immediate family member): Shionogi     Research Funding: Merck, Checkmate Pharmaceuticals, CellSight Technologies, GSK, Merck, Arvus Biosciences, Arcus Biosciences     Research Funding (Inst.): Zucero Therapeutics     Patents, Royalties, Other Intellectual Property: Application No.: 63/124,231 Title: COMPOSITIONS AND METHODS FOR TREATING CANCER Applicant: University of Pittsburgh–Of the Commonwealth System of Higher Education Inventors: Diwakar Davar Filing Date: December 11, 2020 Country: United States MCC Reference: 10504-059PV1 Your Reference: 05545; and Application No.: 63/208,719 Enteric Microbiotype Signatures of Immune-related Adverse Events and Response in Relation to Anti-PD-1 Immunotherapy     Dr. Jason Luke:     Stock and Other Ownership Interests: Actym Therapeutics, Mavu Pharmaceutical, Pyxis, Alphamab Oncology, Tempest Therapeutics, Kanaph Therapeutics, Onc.AI, Arch Oncology, Stipe, NeoTX     Consulting or Advisory Role: Bristol-Myers Squibb, Merck, EMD Serono, Novartis, 7 Hills Pharma, Janssen, Reflexion Medical, Tempest Therapeutics, Alphamab Oncology, Spring Bank, Abbvie, Astellas Pharma, Bayer, Incyte, Mersana, Partner Therapeutics, Synlogic, Eisai, Werewolf, Ribon Therapeutics, Checkmate Pharmaceuticals, CStone Pharmaceuticals, Nektar, Regeneron, Rubius, Tesaro, Xilio, Xencor, Alnylam, Crown Bioscience, Flame Biosciences, Genentech, Kadmon, KSQ Therapeutics, Immunocore, Inzen, Pfizer, Silicon Therapeutics, TRex Bio, Bright Peak, Onc.AI, STipe, Codiak Biosciences, Day One Therapeutics, Endeavor, Gilead Sciences, Hotspot Therapeutics, SERVIER, STINGthera, Synthekine     Research Funding (Inst.): Merck , Bristol-Myers Squibb, Incyte, Corvus Pharmaceuticals, Abbvie, Macrogenics, Xencor, Array BioPharma, Agios, Astellas Pharma , EMD Serono, Immatics, Kadmon, Moderna Therapeutics, Nektar, Spring bank, Trishula, KAHR Medical, Fstar, Genmab, Ikena Oncology, Numab, Replimmune, Rubius Therapeutics, Synlogic, Takeda, Tizona Therapeutics, Inc., BioNTech AG, Scholar Rock, Next Cure     Patents, Royalties, Other Intellectual Property: Serial #15/612,657 (Cancer Immunotherapy), and Serial #PCT/US18/36052 (Microbiome Biomarkers for Anti-PD-1/PD-L1 Responsiveness: Diagnostic, Prognostic and Therapeutic Uses Thereof)     Travel, Accommodations, Expenses: Bristol-Myers Squibb, Array BioPharma, EMD Serono, Janssen, Merck, Novartis, Reflexion Medical, Mersana, Pyxis, Xilio

With the hottest summer months still ahead, there's lots of time for fun in the sun. But it's important to protect your skin. Studies show that melanoma, a form of skin cancer, is on the rise, and youth are becoming more susceptible. Dr. Krista Rubin, nurse practitioner at the Massachusetts General Hospital Center for Melanoma, joins Brent Loucks with her tips on how to protect your skin not only now, but for the future.

El Dr. Jerónimo Rodríguez Cid, oncólogo médico del Instituto Nacional de Enfermedades Respiratorias en la Ciudad de México, comparte su análisis de los estudios más relevantes en melanoma presentados durante la Reunión Anual 2025 de la Sociedad Americana de Oncología Clínica, celebrada en Chicago. Su revisión aborda los avances más destacados en estrategias neoadyuvantes y adyuvantes, así como en enfermedad metastásica, incluyendo metástasis cerebrales y subtipos raros como el melanoma mucoso, acral y uveal, con base en la información disponible al momento de esta grabación.Neoadyuvancia y adyuvanciaAbstract #e21543Columbus-AD (abstract #LBA9501)RELATIVITY-098 (abstract #LBA9500)NeoACTIVATE arm C (abstract #9503)Abstract #9502Melanoma avanzado y metastásicoAbstract #9543RELATIVITY-020 (abstract #9525)SWOG S2000 (abstract #LBA9507)Melanomas raros: acral, mucoso y uvealAbstract #2502Abstract #9555Abstract #9509Material exclusivo para profesionales de la salud.Este material ha sido desarrollado únicamente con fines educativos e informativos y no tiene la intención de sustituir el juicio clínico de los profesionales de la salud.Las opiniones y declaraciones presentadas en este contenido son responsabilidad exclusiva de los ponentes y no reflejan necesariamente la postura institucional de ScienceLink ni de terceros mencionados.La información presentada se basa en el conocimiento y la experiencia profesional de los ponentes. La veracidad, exactitud y actualidad científica de los datos son de su exclusiva responsabilidad. Así mismo garantizan que el contenido utilizado no infringe derechos de autor de terceros y asumen toda responsabilidad por su uso.Se deberán de revisar las indicaciones aprobadas en el país con estricto apego al marco regulatorio aplicable para cada uno de los tratamientos y medicamentos comentados.ASCO® es una marca registrada de la American Society of Clinical Oncology. Este material ha sido producido de manera independiente y no está autorizado, patrocinado ni avalado por dicha organización.

I'm joined by Susanna Daniels, CEO of Melanoma Focus, and horticulturists Rachel Reynolds, Paul Kimberley and Jenny Warner, who share their personal experiences with skin cancer. With temperatures on the rise, we explore why sun safety is essential for anyone working outdoors, how to protect yourself effectively, and the serious risks of not taking the sun seriously. Links Melanoma Focus is a national charity dedicated to providing help and support to melanoma patients and healthcare professionals as well as raising awareness of melanoma, the 5th most common cancer in the UK.  As nearly 9 in 10 melanomas are preventable, awareness and advocacy work is key element of the work.  Melanoma awareness posters and a comms toolkit (including a specific farming and horticultural comms toolkit) is available via our melanoma awareness page. Some other useful pages: What is melanoma  Sun safety Signs and symptoms of melanoma  How to check your skin and nails How a melanoma is diagnosed The Melanoma Helpline – expert skin cancer nurses are available for anyone with a worry about melanoma from diagnosis to treatment and beyond Melanoma Stages and Treatment – Patient Guide    Please support the podcast on Patreon

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/AAPA/IPCE information, and to apply for credit, please visit us at PeerView.com/CMF865. CME/MOC/AAPA/IPCE credit will be available until June 30, 2026.Moving the Efficacy NeedleWith Immunotherapy in Melanoma: Modern Standards and Next-Gen Strategies in Resectable and Unresectable Disease In support of improving patient care, this activity has been planned and implemented by PVI, PeerView Institute for Medical Education, and AIM at Melanoma Foundation. PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported through educational grants from Bristol Myers Squibb and Iovance Biotherapeutics.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/AAPA/IPCE information, and to apply for credit, please visit us at PeerView.com/CMF865. CME/MOC/AAPA/IPCE credit will be available until June 30, 2026.Moving the Efficacy NeedleWith Immunotherapy in Melanoma: Modern Standards and Next-Gen Strategies in Resectable and Unresectable Disease In support of improving patient care, this activity has been planned and implemented by PVI, PeerView Institute for Medical Education, and AIM at Melanoma Foundation. PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported through educational grants from Bristol Myers Squibb and Iovance Biotherapeutics.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/AAPA/IPCE information, and to apply for credit, please visit us at PeerView.com/CMF865. CME/MOC/AAPA/IPCE credit will be available until June 30, 2026.Moving the Efficacy NeedleWith Immunotherapy in Melanoma: Modern Standards and Next-Gen Strategies in Resectable and Unresectable Disease In support of improving patient care, this activity has been planned and implemented by PVI, PeerView Institute for Medical Education, and AIM at Melanoma Foundation. PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported through educational grants from Bristol Myers Squibb and Iovance Biotherapeutics.Disclosure information is available at the beginning of the video presentation.

Prema novom izvještaju organizacije za zaštitu potrošača CHOICE, samo četiri od 20 popularnih krema za sunčanje zaista pružaju deklariranu razinu zaštite. Rezultati su zabrinuli mnoge potrošače. Međutim, stručnjaci i zagovornici prevencije ističu kako je primjena kreme za sunčanje i dalje od velike važnosti u zaštiti od raka kože.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/AAPA/IPCE information, and to apply for credit, please visit us at PeerView.com/CMF865. CME/MOC/AAPA/IPCE credit will be available until June 30, 2026.Moving the Efficacy NeedleWith Immunotherapy in Melanoma: Modern Standards and Next-Gen Strategies in Resectable and Unresectable Disease In support of improving patient care, this activity has been planned and implemented by PVI, PeerView Institute for Medical Education, and AIM at Melanoma Foundation. PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported through educational grants from Bristol Myers Squibb and Iovance Biotherapeutics.Disclosure information is available at the beginning of the video presentation.

Sona Nanotech CEO David Regan joined Steve Darling from Proactive at a key BioTech conference in Boston to announce a significant milestone for the company in the development of its innovative cancer treatment technology. Sona has officially entered into a clinical trial agreement with Bradford Hill in Chile to conduct an early feasibility study of its Targeted Hyperthermia Therapy, focusing on patients with advanced melanoma. The study will enroll up to ten patients who have previously been treated with, but failed to respond to, standard immunotherapy protocols. The trial is designed to assess the safety, tolerability, and preliminary efficacy of Sona's THT approach. Each participant will receive two treatments spaced one week apart, applying Sona's novel photothermal therapy to hard-to-treat tumors. Pending final ethics committee approval, patient enrollment is expected to begin by the end of June, with interim results anticipated later this summer and final results projected for fall 2025. Regan emphasized that this feasibility study will play a crucial role in advancing the clinical development of THT, providing the first in-human data to support its future application across broader patient populations and cancer types. Sona's Targeted Hyperthermia Therapy is a cutting-edge photothermal cancer treatment that uses gold nanorods to deliver heat directly to solid tumors. These nanorods are introduced into the tumor site, where they absorb infrared light, converting it into localized therapeutic heat that can help destroy cancerous tissue without harming surrounding healthy cells. Regan noted that the company is optimistic about the study's outcomes and sees this trial as a potential catalyst for broader clinical adoption, strategic partnerships, and future regulatory submissions. With early results expected in just a few months, Sona Nanotech is well-positioned to advance its mission of transforming cancer treatment through targeted nanotechnology-driven therapies. #proactiveinvestors #sonananotechinc #cse #sona #otcqb #snanf #CancerTherapy #GoldNanorods #FDAApproval #BiotechNews #Immunotherapy #ClinicalTrials #Nanomedicine #DrugSafety #CancerTherapy #TargetedHyperthermia #ClinicalTrials #MelanomaTreatment #BiotechNews #MedicalDevices #Immunotherapy #HealthcareInnovation #ProactiveInvestors

The detection of melanoma and a range of other skin diseases could become faster and more accurate with a new AI powered tool 

Today's witnesses are from Matthew West's website, called popwe.org. If you don't know who Matthew West is, he is a singer, songwriter, and storyteller. This website is for the non-profit that he has with his father, a pastor. Matthew and his father encourage people to share their stories. They have various categories of stories. Today, I chose three testimonies from the God Stories Category. Often, we can hear our own story in someone else's story. When we listen to others tell their story, it helps us see that we are not alone. Hearing how God worked in their situation gives us hope that He will work in ours, too! I pray that when you hear this testimony, you get the faith and hope to believe that miracles can happen in your situation, too. I pray you know that God is there with you, and if you invite Him into your situation, He can help. I hope you enjoy these testimonies.First is Diane: I run a Christian camp for people who have developmental and physical disabilities, or as I like to say, “diversabilities.” Because isn't that who we all are? We experienced great tragedy in September of 2020 when we lost many of our physical buildings, including our activity spaces, bunkhouses, and gymnasium, in a fire. Many of which had been built in the 1940s.Our campers were devastated. Many have been coming to camp for over 40 years, but without indoor facilities and bunkhouses to serve and host our campers, the future looked bleak. That said, we dutifully signed up for FEMA support to rebuild and began the process of determining eligibility in early 2021.After much prayer and consideration, we made a commitment to continue serving campers someway, somehow. And we were overwhelmed by the blessing of grants, private donations and many volunteers. We cleared our 18-acre property of fire debris, established and activity meadow, purchased 18 beautiful bell tents and opened our gates to 10 campers a week for 6 weeks. We had only a few doors left after the fires and that first year, all activities and meals were outside. Before the fires and COVID we were serving 25 campers a week, but we promised we would do what we could, and God provided everything we needed!Fast forward 4 ½ years and here we are, still providing camp with temporary facilities. We continue to work with FEMA and have only just begun to receive money to begin the process of rebuilding.We were gifted a master plan through the assistance of the Christian Camp and Conference Association (CCCA) in 2021, and now we are working with an incredible architecture and design firm of which 90% is being paid for through FEMA funds. For us 10% is a significant funding gap, but we trust our Father in heaven to pave a way for us to continue moving forward with rebuilding. If all goes well, we anticipate breaking ground on our new buildings later this year.And finally, to the reason for this long explanation. Our campers love those VBS songs you mention in some of your devos, and I like to re-introduce a few of them every year, so when I read your post this morning, I knew it was time to bring this old chestnut back to our campfire songs, “This little light of mine.” As we rebuild Upward Bound Camp we stand on the firm foundation of our Lord and Savior Jesus Christ, sharing and rejoicing in His love for all of us!Second is Heather: My story is about meeting my husband at the warehouse we where we worked, marrying him and then losing him to cancer after twelve life changing years of marriage and seven kids later.He came to me one day asking, “is this a pimple?” I said,” No love, you should get that checked.” He wasted no time, and the test came back as Melanoma. Within a year of that diagnosis, he went to be with Jesus.He fought really hard and had a heart of gold the whole way through. He said these words to me towards the end” I am at peace with this.”Those words will stay in my heart always. He loved Jesus so much and trusted him. I believed before I met Doug, but I honestly believe that he was put on this earth to prepare me and the kids spiritually for what was ahead. For things we did not know were going to happen.He served God in many ways, but if not for him I believe our lives would have taken a much different path. With him rooting me in the Catholic faith and me coming to truly believe it, allowed me to have the strength to carry on and keep the kids rooted in their faith.He was an amazing man. I thank you God for blessing us with him if even for a short time. We love you Daddy/ Douglas.Third is Roy: Last night, my family and I were at your concert here in Lincoln. What a beautiful evening of worship! Seeing my family laugh, sing, and worship together was a powerful reminder of God's faithfulness and goodness.Matthew, we met about 15 years ago at a Parenting Simulcast. I was the parenting manager running point that day. It was such a joy to work with you during that event, and I still treasure the memories of that experience.I'm reaching out to tell you how deeply your song, The God Who Stays, has impacted my life. It became an Ebenezer for me during one of the most broken seasons I've ever experienced.In 2014, I left that organization due to downsizing and took over a struggling Bible and youth camp in New England. After six difficult years of ministry, the camp had to close during COVID, and the board dissolved it. I was devastated.It felt like I had failed everyone—including God. After closing the doors and letting the staff go, my wife took our kids away for a weekend and told me, “You need to do business with God.”I went to a place we called “One Tree Hill,” a beautiful hillside at the base of Mount Monadnock, and I listened to The God Who Stays on repeat. I cried like I've never cried before. It was there, in my brokenness, that I encountered Christ in such a profound way.I felt His warmth and embrace, even in the midst of my pain and failure. I was ready to give up leadership entirely, but in that moment, Christ whispered to me: I am not done with you yet. I have been preparing you for what's next.Within 48 hours of that encounter, I connected with the ministry I serve today.  This January, I will celebrate four years stewarding this organization, which serves vulnerable families through foster care, family preservation, and ministry to families impacted by incarceration.These last four years have brought so much healing and restoration. Not only in my ministry but in my marriage and family. My wife and kids (25, 21, and 17) have endured so much over the past 15 years, through four major moves and countless challenges. But God has been faithful. To sit together last night in worship reminded me how far He has carried us. Thank you, Matthew, for allowing God to use your music to minister to so many, including me. The God Who Stays will forever be a reminder of His steadfast love and presence in my life.Thank you all so much for being brave enough to share your stories. I know these stories are going to touch the lives of so many people. www.findingtruenorthcoaching.comCLICK HERE TO DONATECLICK HERE to sign up for Mentoring CLICK HERE to sign up for Daily "Word from the Lord" emailsCLICK HERE to sign up for my newsletter & receive a free audio training about inviting Jesus into your daily lifeCLICK HERE to buy my book Total Trust in God's Safe Embrace

What happens when you're forced to stop doing what you love—and rebuild your life from the inside out? In this deeply moving episode of All Talk Oncology, host Kenny Perkins sits down with Leah Adams, a melanoma survivor, passionate runner, and daughter of a stage four cancer fighter. Diagnosed at just 26 years old with Stage 1A melanoma, Leah shares how cancer interrupted her daily running routine—and how she eventually turned pain into power. From being unable to run post-surgery, to completing multiple marathons, Leah's story is a powerful testament to the strength of the human spirit and the power of reframing your mindset. Whether it's her honesty about guilt, body image, or mental recovery—this conversation is full of hard truths, healing lessons, and undeniable hope. Key points discussed: Leah's diagnosis at age 26 and her emotional reaction to stopping running The surgeries she underwent and how melanoma impacted her body and mindset Why she believed she gave herself cancer—and how she forgave herself How running became both her therapy and her triumph The shift in self-talk and mindset that changed her emotional healing Her public vulnerability through social media and how it helped others Her journey through frequent skin checks, biopsies, and long-term follow-ups Crossing the five-year cancer-free mark and what that milestone meant Why she now advocates for skin checks and sun protection Her mission to use her story to spread awareness and hope   Immortalize your voice by being an ALL TALK ONCOLOGY GUEST! Just fill-out this FORM.   SOCIAL MEDIA LINKS: All Talk Oncology: Instagram & Facebook JOIN OUR FREE COMMUNITY: Facebook Community WEBSITE: https://www.alltalkoncology.com

A new report from consumer advocacy group CHOICE has found only four out of 20 popular sunscreen products actually meet their claims of sun protection. The findings have sparked concerns among consumers. But experts and advocates say putting on sunscreen is still important for skin cancer prevention. - صارفین کے حقوق کے گروپ CHOICE کی ایک نئی رپورٹ میں پتہ چلا ہے کہ 20 مشہور سن اسکرین مصنوعات میں سے صرف چار ہی اپنے دعوے کے مطابق سورج سے درج شدہ لیول کا تحفظ فراہم کرتی ہیں۔ اس تحقیق کے نتائج نے صارفین میں تشویش پیدا کر دی ہے۔ تاہم، ماہرین اور جلد کی صحت کے حامی کہتے ہیں کہ سن اسکرین کی مبالغہ آمیز لیبیلنگ کے باوجود جلد کےکینسر کی روک تھام کے لیے سن اسکرین لگانا اب بھی انتہائی اہم ہے۔

A new report from consumer advocacy group CHOICE has found only four out of 20 popular sunscreen products actually meet their claims of sun protection. The findings have sparked concerns among consumers. But experts and advocates say putting on sunscreen is still important for skin cancer prevention. - В новом отчете группы по защите прав потребителей CHOICE было обнаружено, что только четыре из 20 популярных солнцезащитных средств действительно соответствуют заявленным характеристикам защиты от солнца. Результаты вызвали беспокойство у потребителей. Однако эксперты и защитники говорят, что нанесение солнцезащитного крема по-прежнему важно для профилактики рака кожи.

A new report from consumer advocacy group CHOICE has found only four out of 20 popular sunscreen products actually meet their claims of sun protection. The findings have sparked concerns among consumers. But experts and advocates say putting on sunscreen is still important for skin cancer prevention.

Cancer-fighting implant shows promise in treating melanoma, pancreatic and colorectal tumors. Rice-led study serves as foundation for FDA investigational new drug application and emerging new company to launch from RBL LLC. Veiseh's team at Rice University has created an implant that functions like a “cytokine factory,” delivering IL-12 — a powerful immune-stimulating molecule — directly into the tumor environment. This approach boosts the body's ability to fight cancer while avoiding the severe side effects usually associated with systemic IL-12 therapy.

Interview with Jade Homsi, MD

Melanoma is on the rise in Canada, a recent study found the number of new cases increased 17 per cent last year. We hear about the questions you have about sunscreen and other ways to project yourself from skin cancer and we speak with Dr. Cheryl Rosen, head of dermatology with the University Health Network.

Dr. John Sweetenham shares highlights from Day 5 of the 2025 ASCO Annual Meeting, including data from large trials in advanced malignant melanoma and mCSPC plus a new approach to first-line treatment for patients with multiple myeloma who are not transplant eligible. Transcript Hello, I'm Dr. John Sweetenham, the host of the ASCO Daily News Podcast, with my takeaways on selected abstracts from Day 5 of the 2025 ASCO Annual Meeting. My disclosures are available in the transcript of this episode. The selected abstracts from this final day of ASCO25 include important new data from large, randomized trials in patients with advanced malignant melanoma and patients with metastatic castration-sensitive prostate cancer, as well as a new approach to the first-line treatment of patients with multiple myeloma who are not transplant eligible.  Starting with LBA9500, this study was conducted in patients with completely resected stage III or IV malignant melanoma and compared the combination of relatlimab plus nivolumab versus nivolumab alone in this population. The study, named the RELATIVITY-098 trial, was presented by Dr. Georgina Long from the University of Sydney, Australia. In her introduction to the study, Dr. Long explained that the current standard of care for adjuvant therapy of resected stage III/IV melanoma is with PD-1 monotherapy with nivolumab, but that about 50% of patients will suffer from a subsequent relapse. In the first-line setting in patients with advanced or unresectable melanoma, the combination of nivolumab with the LAG-3 inhibitor, relatlimab, has been previously shown to improve progression-free survival in the RELATIVITY-047 trial. The current study evaluated this same combination in the adjuvant setting. More than 1,000 patients from 24 countries were randomized to receive either nivolumab alone (546 patients) or the combination of nivolumab with relatlimab (547 patients). Both treatments were given for a maximum of 1 year or until progression of disease, unacceptable toxicity, withdrawal, or death. Various biomarker studies were also undertaken including LAG-3 and PD-1 expression on CD8-positive T cells. The primary endpoint of the study was relapse-free survival, and Dr. Long reported that this was the same in both arms of the study. For example, at 24 months, the relapse-free survival was 64% in the monotherapy arm compared with 62% in the combination arm. The hazard ratio was 1.01 and the P value was 0.928. Metastasis-free survival was also identical in both arms. No benefit was observed for the combination in any of the prespecified subgroups. No new toxicity signals emerged compared with the RELATIVITY-047 trial. Interestingly, the baseline surface expression of LAG-3 and co-expression of LAG-3 and PD-1 on CD8 T cells in the 098 adjuvant trial were lower than in the 047 advanced disease trial, perhaps explaining why the combination did not confer benefit over nivo alone in the adjuvant setting. This is an important result, demonstrating that results from one clinical setting cannot always be extrapolated to another. Although the combination has gained some use in the adjuvant setting, this study clearly demonstrates that more drug in this situation is no better and that monotherapy remains the current standard of care. Results from the AMPLITUDE trial for patients with metastatic castration-sensitive prostate cancer with alterations in homologous recombination repair (HRR) genes, in LBA5006, were presented today by Dr. Gerhardt Attard from University College London, UK. This international, multicenter study evaluated the combination of the selective PARP inhibitor, niraparib, in combination with abiraterone acetate and prednisone. The same combination has been previously shown to improve outcomes in castration-resistant metastatic prostate cancer harboring BRCA mutations in the MAGNITUDE study. The current trial included patients with castration-sensitive disease with HRR mutations including BRCA1/2. Six hundred and ninety-six patients were randomized between niraparib, abiraterone, and prednisone plus androgen deprivation therapy, or the same combination with placebo instead of niraparib. Permitted prior therapies included no more than 6 months of prior androgen deprivation therapy and the use of docetaxel, or prior palliative radiation therapy. The primary endpoint of the study was radiographic relapse-free survival. Dr. Attard reported that the risk for radiographic progression-free survival in the whole population was significantly reduced by 37% with niraparib and abiraterone acetate plus prednisone compared with the placebo arm. The radiographic progression-free survival risk reduction with niraparib in the prespecified BRCA1/2 subgroup was 48% and reached statistical significance compared with the placebo arm. The secondary endpoint of time to symptomatic progression was also improved with niraparib in the HRR population and the BRCA1/2 subgroup. There was a trend for overall survival favoring the niraparib combination. However, the overall survival data were immature at this first interim analysis and did not yet reach statistical significance. No new safety concerns emerged with the toxicity data consistent with the MAGNITUDE study. Less than 5% more of the patients on the experimental arm discontinued treatment in comparison to the control arm. The authors conclude that the AMPLITUDE study results support the use of niraparib, abiraterone, and prednisone as a new treatment option for patients with metastatic castration- sensitive prostate cancer and BRCA and homologous recombination repair gene alterations. The results certainly support this conclusion and are potentially practice-changing. Turning to hematologic malignancies, my final selection from today's presentations is Abstract 7504, presented by Dr. Hang Quach from St Vincent's Hospital, Melbourne, Australia, and describes a novel combination of elranatamab, daratumumab, and lenalidomide in patients with newly diagnosed multiple myeloma who are not transplant-eligible – the so-called MagnetisMM-6 trial part 1. Elranatamab is a novel bispecific T-cell engaging antibody directed against BCMA and CD3, which has previously been approved for certain patients with relapsed and refractory multiple myeloma. In the present study, this was combined with lenalidomide and daratumumab in newly diagnosed patients. The report today describes the dose-finding phase of this study, which was part 1, specifically addressing so-called dose level ‘G', comprising elranatamab 76mg subcutaneously every 4 weeks plus daratumumab 1800mg subcutaneously and lenalidomide 25mg given orally. Thirty-seven patients were entered at this dose level, of whom 32 were on treatment at the time of analysis. Early response data show an overall response rate of 97.3%. With median follow up of 7.9 months, the current CR rate is 27% with a VGPR rate of almost 68%. The most frequent toxicities were hematologic, with neutropenia observed in 75%. Some cytokine release syndrome was observed in about 60% of patients, but none was greater than grade 2. The authors conclude that this combination is active in untreated multiple myeloma, with manageable toxicity and evidence of responses which appear to deepen over time. The dose-finding component of this trial is continuing and will subsequently progress into a phase 3 trial based on the data from the current study. This will compare daratumumab plus lenalidomide with the same combination plus elranatamab in previously untreated patients. That concludes our special coverage from the 2025 ASCO Annual Meeting. Thanks for listening and we hope you have enjoyed listening to our top takeaways from ASCO25. If you value the insights that you hear on the ASCO Daily News Podcast, please remember to rate, review, and subscribe wherever you get your podcasts. Disclaimer:  The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement.  Find out more about today's speaker:    Dr. John Sweetenham    Follow ASCO on social media:     @ASCO on Twitter    @ASCO on Bluesky    ASCO on Facebook    ASCO on LinkedIn     Disclosures:   Dr. John Sweetenham:    No relationships to disclose

Ray is joined by three women taking part in the campaign. Kelsey O'Donnell is a Skin Cancer Clinical Nurse Specialist at the Mater Hospital, Noelle O'Connor who has conducted research into attitudes towards suncare in Ireland, and Lydia O'Toole who was diagnosed with Stage 4 Melanoma in 2022.

- Overview of Metastatic Melanoma, Including Diagnosing & Staging - New Treatment Approaches - Targeted Therapy & the Role of Precision Medicine - The Role of Immunotherapy - Clinical Trial Updates - Follow-Up Care - Tips for Caring for Your Skin During Cancer Treatments, Including Sun & Wind Safety Recommendations - Controlling Side Effects, Symptoms, Discomfort & Pain - Key Questions to Ask When Communicating with Your Health Care Team - Guidelines to Prepare for Telehealth/Telemedicine Appointments, Including Technology, Prepared List of Questions, and Discussion of OpenNotes - Questions for Our Panel of Experts

- Overview of Metastatic Melanoma, Including Diagnosing & Staging - New Treatment Approaches - Targeted Therapy & the Role of Precision Medicine - The Role of Immunotherapy - Clinical Trial Updates - Follow-Up Care - Tips for Caring for Your Skin During Cancer Treatments, Including Sun & Wind Safety Recommendations - Controlling Side Effects, Symptoms, Discomfort & Pain - Key Questions to Ask When Communicating with Your Health Care Team - Guidelines to Prepare for Telehealth/Telemedicine Appointments, Including Technology, Prepared List of Questions, and Discussion of OpenNotes - Questions for Our Panel of Experts

This Oncology PER®Spectives™ podcast examines the recent advancements in the treatment landscape for advanced melanoma.In this activity, expertsYana Najjar, MD; Rahul A. Sheth, MD, FSIR; and Douglas Johnson, MD, MSCI, discuss the challenges of immune checkpoint inhibitor resistance and the practical strategies for overcoming this by using direct intratumoral injections of oncolytic viral immunotherapies, which rely on close interdisciplinary collaboration between medical oncologists and interventional radiologists.

Megan Williams sy'n sgwrsio gyda'r meddyg teulu o Sir Gaerfyrddin, Dr Sioned Rowlands.

Dr Bill Nelson talks with Dr Ashani Weeraratna about her work in melanoma research, the progress that has been made in treating patients with melanoma, and the importance of federal research funding in finding advancements in treatment for this disease.

Dr. Justin McLawhorn discusses Melanoma and the importance of sunscreen usage, especially during the summer months.

In this JCO Precision Oncology Article Insights episode, Jiasen He summarizes "Predictive Impact of Tumor Mutational Burden on Real-World Outcomes of First-Line Immune Checkpoint Inhibition in Metastatic Melanoma” by Dr. Miles C. Andrews, et al. published on June 07, 2024. Transcript The guest on this podcast episode has no disclosures to declare. Jiasen He: Hello and welcome to the JCO Precision Oncology Article Insights. I'm your host, Jiasen, and today we'll be discussing the JCO Precision Oncology article, "Predictive Impact of Tumor Mutational Burden on Real-World Outcomes of First-Line Immune Checkpoint Inhibition in Metastatic Melanoma," by Dr. Miles C. Andrews and colleagues. This study was supported by Foundation Medicine, a for-profit company that conducts FDA-regulated molecular diagnostics, including assays used to measure tumor mutational burdens, or TMB, as described in this article. Immune checkpoint inhibitor (ICI) therapy has become a cornerstone in the treatment of metastatic melanoma. They work by activating the patient's own immune system, representing a fundamentally different approach from traditional chemotherapy. Several biomarkers have emerged as promising tools to predict ICI therapy response, and TMB is one of the most extensively studied. TMB is defined as the number of somatic mutations per megabase of an interrogated genome sequence. In the KEYNOTE-158 study, patients with high TMB showed better response rates and longer progression-free survival compared to those with low TMB, which led to the FDA tumor-agnostic approval of TMB as a biomarker to guide ICI therapy. In this manuscript, Dr. Andrews and colleagues set out to answer an important question: does TMB predict outcomes of ICI therapy in real-world patients with advanced melanoma? To explore this, they analyzed de-identified data from the nationwide Flatiron Health-Foundation Medicine Clinico-Genomic Database (CGDB). To be included, patients needed to have had at least two visits to a Flatiron Health clinic and a Foundation Medicine Comprehensive Genomic Profiling report. Eligible patients had received first-line treatment with either monotherapy (nivolumab or pembrolizumab) or dual therapy with the combination of ipilimumab and nivolumab for metastatic melanoma. They also needed a tissue-based TMB score from either the FoundationOne or FoundationOne CDx genomic test. For this study, TMB less than 10 mutations per megabase was considered low TMB; TMB equal to or more than 10 mutations per megabase was considered high TMB; and TMB equal to or more than 20 mutations per megabase was considered very high TMB. Of the 497 patients in the final cohort, 29% had low TMB, while 71% had high TMB, and 50% had very high TMB. The authors observed that patients with very high TMB were more often male, had BRAF wild-type tumors, and were more likely to receive anti-PD-1 monotherapy. This group also had tumors more commonly sampled from brain and lung metastases. Patients with high TMB but not very high TMB were more likely to carry the BRAF V600K mutation and were least likely to have lung metastases. Meanwhile, those with low TMB tended to be younger and had disease limited to non-visceral sites. As expected, the presence of ultraviolet mutation signatures, a known driver of melanoma, was strongly associated with TMB. UV signatures were found in just 18% of the low TMB group, but in 89% of the high TMB and 93% of the very high TMB group. High TMB was found to be prognostic of improved real-world progression-free survival (PFS) and overall survival (OS) in patients receiving both monotherapy and dual immune checkpoint inhibitors, even after adjusting for other established prognostic factors. Interestingly, in the low TMB group, overall survival was likely confounded by the availability of effective second-line targeted therapy, particularly for BRAF-mutant patients. These patients had better outcomes compared to their BRAF wild-type counterparts, likely reflecting a greater reliance on salvage therapy in low TMB patients who derived less benefit from first-line immunotherapy. The authors then further examined the ICI outcomes using stepwise TMB thresholds, with TMB less than 10 as low, 10 to 19 as high, and equal to or more than 20 as very high. For those receiving ICI monotherapy, both PFS and OS were highest in the very high TMB group, followed by the high TMB group, and lowest in the low TMB group. However, in patients treated with dual ICI therapy, the results diverged. While low TMB patients still had the poorest outcomes, those with high TMB (mutations 10 to 19 per megabase) had better PFS and overall survival than those with very high TMB (mutations equal to or more than 20 per megabase). The authors then conducted exploratory multivariable modeling, showing that among very high TMB patients with BRAF mutations, dual ICI therapy was associated with a significantly higher hazard ratio compared to monotherapy. They concluded that dual ICI may not benefit, and could even harm, patients with very high TMB, whereas those with TMB between 10 and 20 mutations per megabase may get more from the intensified regimen. Importantly, as the authors stated in the manuscript, we need to note that in this cohort, very high TMB patients were more likely to have brain metastases at treatment initiation, be male, and lack BRAF V600E/K mutations—all factors associated with poorer prognosis. This might partially explain inferior outcomes to dual ICI in very high TMB patients, as patients were not randomly assigned to therapy in this retrospective, real-world study. As such, these findings should be interpreted with caution and validated in future studies. In summary, this study showed that in a real-world setting, high tumor mutational burden predicts better outcomes with immune checkpoint inhibitor therapy in patients with advanced melanoma. Interestingly, the authors found that dual ICI therapy may offer no added benefit for patients with very high TMB compared to ICI monotherapy. However, this was a retrospective, non-randomized study, and the cohorts were imbalanced for some known risk factors, which could confound outcomes. As a result, these findings should be interpreted with caution and will need to be validated in future prospective studies. Thank you for tuning into JCO Precision Oncology Article Insights. Don't forget to subscribe and join us next time as we explore more groundbreaking research shaping the future of oncology. Until then, stay informed and stay inspired. The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement.

Smriti Patodia, Senior Editor of The Lancet Oncology, is joined by Professor Caroline Robert from Gustave Roussy Cancer Campus, France to discuss the EBIN trial. EBIN was an open-label, randomised, controlled, phase 2 trial conducted at 37 centres in eight European countries, and aimed to investigate the use of a targeted-therapy induction regimen before treatment with immune checkpoint inhibitors in patients with metastatic melanoma with BRAFV600E or BRAFV600K mutations. They discuss the disease burden of advanced melanoma with BRAF mutations, the key findings from the EBIN trial, and the future implications of the study findings, especially for a select sub-population of patients with advanced melanoma.Read the full article:https://www.thelancet.com/journals/lanonc/article/PIIS1470-2045(25)00133-0/fulltext?dgcid=buzzsprout_icw_podcast_May_25_lanoncTell us what you thought about this episodeContinue this conversation on social!Follow us today at...https://thelancet.bsky.social/https://instagram.com/thelancetgrouphttps://facebook.com/thelancetmedicaljournalhttps://linkedIn.com/company/the-lancethttps://youtube.com/thelancettv

May is Melanoma Awareness month and yet so many men don't use sunscreen. So what can be done to encourage them to start using sunscreen and just how damaging can the sun be to our skin?

Making strides against melanoma: how can medical oncologists and interventional oncologists join forces to deliver smarter, patient-centered care? In this episode of BackTable, Dr. Tyler Sandow, hosts Dr. Sunandana Chandra, medical oncologist at Northwestern, and Dr. Riad Salem, interventional oncologist at Northwestern to discuss the evolving management of advanced melanoma. --- This podcast is supported by an educational grant from Replimune. --- SYNPOSIS The doctors open the episode with an overview of melanoma and recent advances in its treatment, highlighting key trials such as DREAMseq and CheckMate 067. The discussion explores the shift from medical oncologist as solo primary providers to a dynamic, multidisciplinary approach to advanced cancer care—emphasizing cutting-edge treatments like immunotherapy and intratumoral oncolytic viruses. Dr. Salem shares practical insights on the procedural techniques of administering intratumoral oncolytics like Replimune, emphasizing the importance of thorough documentation and patient-centered care. The doctors also provide an overview of the ongoing IGNYTE-3 Trial, a Phase 3 study assessing the safety and efficacy of the oncolytic immunotherapy RP1 in combination with nivolumab for the treatment of advanced melanoma. The episode underscores the transformative potential of innovative melanoma treatments and the crucial role of integrated, team-based approaches in improving cancer patient outcomes. --- TIMESTAMPS 00:00 - Introduction03:48 - The Evolution of Melanoma Treatment: From Chemotherapy to Immunotherapy14:05 - The Role of Oncolytic Viruses in Melanoma Treatment20:14 - Interventional Radiology's Role in Cancer Treatment27:00 - Collaborative Approach to Cancer Care32:53 - Hyper Documentation and Communication Efficiency44:47 - Future of Intratumoral Oncolytics48:10 - Multidisciplinary Approach in Advanced Cancer Management51:46 - Conclusion and Final Thoughts --- RESOURCES DREAMseq Trial: Atkins MB, Lee SJ, Chmielowski B, et al. Combination Dabrafenib and Trametinib Versus Combination Nivolumab and Ipilimumab for Patients With Advanced BRAF-Mutant Melanoma: The DREAMseq Trial-ECOG-ACRIN EA6134. J Clin Oncol. 2023;41(2):186-197. doi:10.1200/JCO.22.01763 CheckMate 067 trial: Wolchok JD, Chiarion-Sileni V, Rutkowski P, et al. Final, 10-Year Outcomes with Nivolumab plus Ipilimumab in Advanced Melanoma. N Engl J Med. 2025;392(1):11-22. doi:10.1056/NEJMoa2407417

In this episode of SHE MD, Dr. Thaïs Aliabadi and Mary Alice Haney welcome melanoma specialist Dr. Omid Hamid. They explore the rising incidence of melanoma in young people, debunk common misconceptions, and discuss groundbreaking treatments. Dr. Hamid explains the different stages of melanoma and the revolutionary immunotherapy treatments that are changing patient outcomes. The hosts and guest discuss real-life cases, including those of celebrities Khloe Kardashian and Teddy Mellencamp, to illustrate the importance of awareness and regular skin checks. The conversation also touches on melanoma during pregnancy and genetic predisposition to the disease - learn why genetic testing is crucial, even without family history.Access more information about the podcast and additional expert health tips by visiting SHE MD Podcast and Ovii. Sponsors: Myriad: Knowing your family's history of cancer is the first step to understanding your own cancer risk and may qualify you for the MyRisk Hereditary Cancer Test with RiskScore hereditary cancer test. It's easy, accurate and covered by most insurers. Learn more at GetMyRisk.comCymbiotika: Go to Cymbiotikia.com/SHEMD for 20% off your order + free shipping today.Purely Elizabeth: Visit purelyelizabeth.com and use code SHEMD at checkout for 20% off. Purely Elizabeth. Taste the ObsessionEquip: To learn more about Equip treatment, visit equip.health/sobermomlife.Strivektin: Discover the Science Behind Great SkinDavid's Protein: David is giving my listeners an exclusive offer – buy four cartons and get the fifth free at davidprotein.com/shemdCure Hydration: Cure is offering 20% off your first order! Stay hydrated and feel your best by visiting curehydration.com/SHEMD and using promo code SHEMD at checkout. Dr. Omid Hamid's Key Takeaways:1. Reduce Sun Exposure: Limit time spent in direct sunlight, especially during peak hours. Use protective clothing, hats, and sunglasses to shield your skin from harmful UV rays.2. Schedule Regular Skin Checks: Schedule routine visits with a dermatologist for comprehensive skin examinations. Self-examine your skin monthly for any new or changing moles or lesions.3. Use Effective Sunscreen: Apply broad-spectrum sunscreen with at least SPF 30 daily, even on cloudy days. Reapply every two hours when outdoors, and after swimming or sweating.4. Get Genetic Testing Done: If you have a family history of melanoma or other cancers, consider genetic testing to assess your risk. Tests like the MYRIS can identify melanoma-related gene mutations.5. Avoid Tanning Beds: Steer clear of tanning beds, as they significantly increase the risk of developing melanoma and other skin cancers.6. Be Your Own Health Advocate: Stay informed about your health, ask questions, and seek second opinions if necessary. Advocate for yourself and your loved ones by being proactive about potential health concerns.In This Episode: (00:00) Intro: Melanoma Awareness Month(02:40) Dr. Omid Hamid: Melanoma specialist introduction(6:58) Surgery for melanoma explained(10:49) Immunotherapy revolutionizes melanoma treatment(14:57) Genetic testing for melanoma risk(23:25) Importance of advocating for yourself(32:22) Teddy Mellencamp's stage 4 melanoma journey(50:51) Hormonal changes and melanoma risk(57:00) Two key melanoma prevention tipsRESOURCES:Melanoma Research Alliance: https://www.curemelanoma.org/blog/omid-hamid-mdMelanoma Research Foundation https://melanoma.org/Myriad Genetics: https://myriad.com/ GUEST BIOGRAPHY:Omid Hamid, MD, is the Chief of the Translational Research and Immuno-Oncology Department at The Angeles Clinic and Research Institute and serves as the Co-Director of the Melanoma and Phase I Programs. Academic Title as Professor, Department of Medicine at Cedars-Sinai Medical Center. His areas of expertise include immunotherapy and Phase I drug development.Dr. Hamid has published extensively and has been at the forefront of the development of paradigm-shifting breakthroughs including BRAF/MEK targeted agents, AntiCTL4A, antiPD1, and PDL1 therapies. His current interests include new immunotherapeutic options for patients including bi-specific antibodies, Adoptive T-cell Therapy, and oncolytic therapies with a focus on combinatorial approaches resulting in potentially great patient benefit.See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

Hello Sunday is a skincare brand on a mission to make SPF a daily essential, not just a beach-day afterthought. Founded by Amy Ford after spending years under the intense Australian sun, the brand was born from her realization that sun protection is crucial year-round—even on cloudy days in the UK. Amy returned home with a clear vision: to create affordable, effective SPF products that combine skincare benefits with broad-spectrum protection. She teamed up with a dedicated group of skincare lovers and formulation experts to bring that vision to life. Hello Sunday's formulas are designed to fit seamlessly into any routine, promoting healthy, protected skin every day because every day is a SUN day.In this episode, Amy also discusses:The risk of exposure to UV rays even at low levelsBeing new and different merging skincare and sun careExpensive doesn't mean betterWhy using SPF is the #1 thing you can do for your skin to age healthily Entering in the US in Sephora and growing in this marketWe hope you enjoy this episode and gain valuable insights into Amy's journey and the growth of www.us.hellosundayspf.com. Don't forget to subscribe to the Glam & Grow podcast for more in-depth conversations with the most incredible brands, founders, and more.Be sure to check out Hello Sunday at www.us.hellosundayspf.com and on Instagram at @hellosundayspfRated #1 Best Beauty Business Podcast on FeedPostThis episode is brought to you by WavebreakLeading direct-to-consumer brands hire Wavebreak to turn email marketing into a top revenue driver.Most eCommerce brands don't email right... and it costs them. At Wavebreak, our eCommerce email marketing agency helps qualified brands recapture 7+ figures of lost revenue each year.From abandoned cart emails to Black Friday campaigns, our best-in-class team manage the entire process: strategy, design, copywriting, coding, and testing. All aimed at driving growth, profit, brand recognition, and most importantly, ROI.Curious if Wavebreak is right for you? Reach out at Wavebreak.co

Episodio número 26 de Cuéntame Más Ciencia con la Dra. Marisol Soengas, jefa de grupo de Melanoma en el Centro Nacional de Investigaciones Oncológicas (CNIO).Marisol realizó su tesis con la celebérrima Margarita Salas y, más adelante, formó parte del grupo de Scott Lowe en Nueva York. Dos experiencias científicas que marcaron profundamente su desarrollo como investigadora y como persona. Actualmente, dirige en el CNIO el grupo de investigación en melanoma, desde donde ha realizado importantes descubrimientos que han contribuido a entender mejor las metástasis y a desarrollar nuevas aproximaciones terapéuticas.Ha sido también presidenta de ASEICA (Asociación Española de Investigación sobre el Cáncer) y participa activamente en iniciativas para visibilizar y combatir las desigualdades de género en la Ciencia. Desde hace un año, Marisol afronta el cáncer desde una nueva perspectiva: la personal. Fue diagnosticada con cáncer de mama, una situación que encara con valentía, convirtiéndose en una voz comprometida en defensa de todas las personas que viven con esta enfermedad.Episodio grabado por ⁠⁠⁠⁠Fernando de Miguel⁠⁠⁠⁠.Cuéntame Más Ciencia es un podcast financiado por la Fundación Ramón Areces y elaborado por el programa E-Visibility de la Comisión de Comunicación de ECUSA. Visita nuestra web ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠www.ecusa.es⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ y síguenos en las redes sociales⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠.Las opiniones y declaraciones expresadas en Cuéntame Más Ciencia representan el punto de vista de cada participante y no de ECUSA como asociación, ni de cualquier otra institución.

Federico, Isabel González y Teresa de la Cierva hablan del melanoma con las dermatólogas María Vitale y Natividad Cano.

In this episode of Feel Better, Feel Great, Dr. Andrea McSwain explores the deeper layers of skin cancer, toxic burden, and the powerful connection between your internal health and skin. Learn how to identify the three main types of skin cancer—basal cell, squamous cell, and melanoma—while discovering how detox pathways, inflammation, oxidative stress, and conventional skincare products contribute to skin damage. Packed with holistic prevention strategies like clean beauty swaps, anti-inflammatory nutrition, natural sun protection, and daily detox support, this episode empowers you to protect your skin from the inside out. Tune in to decode your body's signals, reduce your toxic load, and embrace radiant, resilient skin. #skincancerawareness #HolisticSkincare #DetoxYourSkin #FunctionalMedicine #NaturalHealth #OxidativeStress #ToxicBurden #CleanBeauty #AntiInflammatoryLifestyle

JCO PO author Dr. Dean A. Regier at the Academy of Translational Medicine, University of British Columbia (UBC), and the School of Population and Public Health, BC Cancer Research Institute shares insights into his JCO PO article, “Clinical Effectiveness and Cost-Effectiveness of Multigene Panel Sequencing in Advanced Melanoma: A Population-Level Real-World Target Trial Emulation.” Host Dr. Rafeh Naqash and Dr. Regier discuss the real-world clinical effectiveness and cost-effectiveness of multigene panels compared with single-gene BRAF testing to guide therapeutic decisions in advanced melanoma. Transcript Dr. Rafeh Naqash:Hello and welcome to JCO Precision Oncology Conversations, where we bring you engaging conversations with authors of clinically relevant and highly significant JCO PO articles. I'm your host, Dr. Rafeh Naqash, Podcast Editor for JCO Precision Oncology and Assistant Professor at the OU Health Stephenson Cancer Center in the University of Oklahoma. Today, we are excited to be joined by Dr. Dean A. Regier, Director at the Academy of Translational Medicine, Associate Professor at the School of Population and Public Health, UBC Senior Scientist at the British Columbia Cancer Research Institute, and also the senior author of the JCO Precision Oncology article entitled "Clinical Effectiveness and Cost-Effectiveness of Multigene Panel Sequencing in Advanced Melanoma: A Population-Level Real-World Target Trial Emulation." At the time of this recording, our guest's disclosures will be linked in the transcript. Dean, welcome to our podcast and thank you for joining us today. Dr. Dean Regier:Thank you. I'm delighted to be here. Dr. Rafeh Naqash:So, obviously, you are from Canada, and medicine, or approvals of drugs to some extent, and in fact approvals of gene testing to some extent is slightly different, which we'll come to learn about more today, compared to what we do in the US—and in fact, similarly, Europe versus North America to a large extent as well. Most of the time, we end up talking about gene testing in lung cancer. There is a lot of data, a lot of papers around single-gene panel testing in non-small cell lung cancer versus multigene testing. In fact, a couple of those papers have been published in JCO PO, and it has shown significant cost-effectiveness and benefit and outcomes benefit in terms of multigene testing. So this is slightly, you know, on a similar approach, but in a different tumor type. So, could you tell us first why you wanted to investigate this question? What was the background to investigating this question? And given your expertise in health economics and policy, what are some of the aspects that one tends or should tend to understand in terms of cost-effectiveness before we go into the results for this very interesting manuscript? Dr. Dean Regier:Yeah, of course, delighted to. So, one of the reasons why we're deeply interested in looking at comparative outcomes with respect to single- versus multigene testing— whether that's in a public payer system like Canada or an insurer system, a private system in the United States— is that the question around does multigene versus single-gene testing work, has not typically tested in randomized controlled trials. You don't have people randomized to multigene versus single-gene testing. And what that does, it makes the resulting evidence base, whether it's efficacy, safety, or comparative cost-effectiveness, highly uncertain. So, the consequence of that has been uneven uptake around the world of next-generation sequencing panels. And so if we believe that next-gen sequencing panels are indeed effective for our patients, we really need to generate that comparative evidence around effectiveness and cost-effectiveness. So we can go to payers, whether it be single payer or a private insurer, to say, "Here are the comparative outcomes." And when I say that uptake has been uneven, uptake there's been actually plenty, as you know, publications around that uneven uptake, whether it be in Europe, in the United States, in Canada. And so we're really interested in trying to produce that evidence to create the type of deliberations that are needed to have these types of technologies accessible to patients. And part of those deliberations, of course, is the clinical, but also in some contexts, cost-effectiveness. And so, we really start from the perspective of, can we use our healthcare system data, our learning healthcare system, to generate that evidence in a way that emulates a randomized controlled trial? We won't be able to do these randomized controlled trials for various, like really important and and reasons that make sense, quite frankly. So how can we mimic or emulate randomized controlled trials in a way that allows us to make inference around those outcomes? And for my research lab, we usually think through how do we do causal inference to address some of those biases that are inherent in observational data. So in terms of advanced melanoma, we were really interested in this question because first of all, there have been no randomized controlled trials around next-gen sequencing versus single-gene testing. And secondly, these products, these ICIs, immune checkpoint inhibitors, and BRAF and MEK inhibitors, they are quite expensive. And so the question really becomes: are they effective? And if so, to what extent are they cost-effective? Do they provide a good reason to have information around value for money? Dr. Rafeh Naqash:So now going to the biology of melanoma, so we know that BRAF is one of the tumor-agnostic therapies, it has approvals for melanoma as well as several other tumor types. And in fact, I do trials with different RAF-RAS kinase inhibitors. Now, one of the things that I do know is, and I'm sure some of the listeners know, is the DREAMseq trial, which was a melanoma study that was an NCI Cooperative Group trial that was led by Dr. Mike Atkins from Georgetown a couple of years back, that did show survival benefit of first-line immunotherapy sequencing. It was a sequencing study of whether to do first-line BRAF in BRAF-mutant melanoma followed by checkpoint inhibitors, or vice versa. And the immune checkpoint inhibitors followed by BRAF was actually the one that showed benefit, and the trial had to stop early, was stopped early because of the significant benefit seen. So in that context, before we approach the question of single-gene versus multigene testing in melanoma, one would imagine that it's already established that upfront nivolumab plus ipilimumab, for that matter, doublet checkpoint inhibitor therapy is better for BRAF-mutant melanoma. And then there's no significant other approvals for melanoma for NRAS or KIT, you know, mucosal melanomas tend to have KIT mutations, for example, or uveal melanomas, for that matter, have GNAQ, and there's no targeted therapies. So, what is the actual need of doing a broader testing versus just testing for BRAF? So just trying to understand when you started looking into this question, I'm sure you kind of thought about some of these concepts before you delved into that. Dr. Dean Regier:I think that is an excellent question, and it is a question that we asked ourselves: did we really expect any differences in outcomes between the testing strategies? And what did the real-world implementation, physician-guided, physician-led implementation look like? And so, that was kind of one of the other reasons that we really were interested is, why would we go to expanded multigene panel sequencing at all? We didn't really expect or I didn't expect an overall survival a priori. But what we saw in our healthcare system, what happened in our healthcare system was the implementation in 2016 of this multigene panel. And this panel covered advanced melanoma, and this panel cost quite a bit more than what they were doing in terms of the single-gene BRAF testing. And so when you're a healthcare system, you have to ask yourself those questions of what is the additional value associated with that? And indeed, I think in a healthcare system, we have to be really aware that we do not actually follow to the ideal extent randomized controlled trials or trial settings. And so that's the other thing that we have to keep in mind is when these, whether it's an ICI or a BRAF MEK inhibitor, when these are implemented, they do not look like randomized controlled trials. And so, we really wanted to emulate not just a randomized controlled trial, but a pragmatic randomized controlled trial to really answer those real-world questions around implementation that are so important to decision making. Dr. Rafeh Naqash:Sure. And just to understand this a little better: for us in the United States, when we talk about multigene testing, we generally refer to, these days, whole-exome sequencing with whole-transcriptome sequencing, which is like the nuclear option of of the testings, which is not necessarily cheap. So, when you talk about multigene testing in your healthcare system, what does that look like? Is it a 16-gene panel? Is it a 52-gene panel? What is the actual makeup of that platform? Dr. Dean Regier:Excellent question. Yeah, so at the time that this study is looking at, it was 2016, when we, as BC Cancer—so British Columbia is a population right now of 5.7 million people, and we have data on all those individuals. We are one healthcare system providing health care to 5.7 million people. In 2016, we had what I call our "home-brew" multigene panel, which was a 53-gene panel that was reimbursed as standard of care across advanced cancers, one of them being advanced melanoma. We have evolved since then. I believe in 2022, we are using one of the Illumina panels, the Focus panel. And so things have changed; it's an evolving landscape. But we're specifically focused on the 53-gene panel. It was called OncoPanel. And that was produced in British Columbia through the Genome Sciences Centre, and it was validated in a single-arm trial mostly around validity, etc. Dr. Rafeh Naqash:Thank you for explaining that. So now, onto the actual meat and the science of this project. So, what are some of the metrics from a health economy standpoint that you did look at? And then, methodology-wise, I understand, in the United States, we have a fragmented healthcare system. I have data only from my institution, for that matter. So we have to reach out to outside collaborators and email them to get the data. And that is different for you where you have access to all the data under one umbrella. So could you speak to that a little bit and how that's an advantage for this kind of research especially? Dr. Dean Regier:Yeah. In health economics, we look at the comparative incremental costs against the incremental effectiveness. And when we think about incremental costs, we think not just about systemic therapy or whether you see a physician, but also about hospitalizations, about all the healthcare interactions related to oncology or not that a patient might experience during their time or interactions with the healthcare system. You can imagine with oncology, there are multiple interactions over a prolonged time period depending on survival. And so what we try to do is we try to—and the benefit of the single-payer healthcare system is what we do is we link all those resource utilization patterns that each patient encounters, and we know the price of that encounter. And we compare those incremental costs of, in this case, it's the multigene panel versus the single-gene panel. So it's not just the cost of the panel, not just the cost of systemic therapy, but hospitalizations, physician encounters, etc. And then similarly, we look at, in this case, we looked at overall survival - we can also look at progression-free survival - and ask the simple question, you know, what is the incremental cost per life-year gained? And in that way, we get a metric or an understanding of value for money. And how we evaluate that within a deliberative priority setting context is we look at safety and efficacy first. So a regulatory package that you might get from, in our case, Health Canada or the FDA, so we look at that package, and we deliberate on, okay, is it safe and is it effective? How many patients are affected, etc. And then separately, what is the cost-effectiveness? And at what price, if it's not cost-effective, at what price would it be cost-effective? Okay, so for example, we have this metric called the incremental cost-effectiveness ratio, which is incremental cost in the numerator, and in this case, life-years gained in the denominator. And if it is around $50,000 or $100,000 per life-year gained—so if it's in that range, this ratio—then we might say it's cost-effective. If it's above this range, which is common in oncology, especially when we talk about ICIs, etc., then you might want to negotiate a price. And indeed, when we negotiate that price, we use the economic evaluation, that incremental cost-effectiveness ratio, as a way to understand at what price should we negotiate to in order to get value for money for the healthcare system. Dr. Rafeh Naqash:Thank you for explaining those very interesting terminologies. Now, one question I have in the context of what you just mentioned is, you know, like the drug development space, you talked about efficacy and safety, but then on the safety side, we talk about all-grade adverse events or treatment-related adverse events—two different terminologies. From a healthcare utilization perspective, how do you untangle if a patient on a BRAF therapy got admitted for a hypoxic respiratory failure due to COPD, resulting in a hospitalization from the cost, overall cost utilization, or does it not matter? Dr. Dean Regier:We try to do as much digging into those questions as possible. And so, this is real-world data, right? Real-world data is not exactly as clean as you'd get from a well-conducted clinical trial. And so what we do is we look at potential adverse event, whether it's hospitalization, and the types of therapies around that hospitalization to try- and then engage with clinicians to try to understand or tease out the different grades of the adverse event. Whether it's successful or not, I think that is a real question that we grapple with in terms of are we accurate in delineating different levels of adverse events? But we try to take the data around the event to try to understand the context in which it happens. Dr. Rafeh Naqash:Thank you for explaining that, Dean. So, again to the results of this manuscript, could you go into the methodology briefly? Believe you had 147 patients, 147 patients in one arm, 147 in the other. How did you split that cohort, and what were some of the characteristics of this cohort? Dr. Dean Regier:So, the idea, of course, is that we have selection criteria, study inclusion criteria, which included in our case 364 patients. And these were patients who had advanced melanoma within our study time period. So that was 2016 to 2018. And we had one additional year follow. So we had three total years. And what we did is that we linked our data, our healthcare system data. During this time, because the policy change was in 2016, we had patients both go on the multigene panel and on the single-gene BRAF testing. So, the idea was to emulate a pragmatic randomized controlled trial where we looked at contemporaneous patients who had multigene panel testing versus single-gene BRAF testing. And then we did a matching procedure—we call it genetic matching. And that is a type of matching that allows us to balance covariates across the patient groups, across the multigene versus BRAF testing cohorts. The idea again is, as you get in a randomized controlled trial, you have these baseline characteristics that look the same. And then the hope is that you address any source selection or confounding biases that prohibit you to have a clean answer to the question: Is it effective or cost-effective? So you address all those biases that may prohibit you to find a signal if indeed a signal is there. And so, what we did is we created—we did this genetic matching to balance covariates across the two cohorts, and we matched them one-to-one. And so what we were able to do is we were able to find, of those 364 patients in our pool, 147 in the multigene versus 147 in the single-gene BRAF testing that were very, very similar. In fact, we created what's called a directed acyclic graph or a DAG, together with clinicians to say, “Hey, what biases would you expect to have in these two cohorts that might limit our ability to find a signal of effectiveness?” And so we worked with clinicians, with health economists, with epidemiologists to really understand those different biases at play. And the genetic matching was able to match the cohorts on the covariates of interest. Dr. Rafeh Naqash:And then could you speak on some of the highlights from the results? I know you did survival analysis, cost-effectiveness, could you explain that in terms of what you found? Dr. Dean Regier:We did two analyses. The intention-to-treat analysis is meant to emulate the pragmatic randomized controlled trial. And what that does is it answers the question, for all those eligible for multigene or single-gene testing: What is the cost-effectiveness in terms of incremental life-years gained and incremental cost per life-years gained? And the second one was around a protocol analysis, which really answered the question of: For those patients who were actually treated, what was the incremental effectiveness and cost-effectiveness? Now, they're different in two very important ways. For the intention-to-treat, it's around population questions. If we gave single-gene or multigene to the entire population of advanced melanoma patients, what is the cost-effectiveness? The per-protocol is really around that clinical question of those who actually received treatment, what was the incremental cost and effectiveness? So very different questions in terms of population versus clinical cost and effectiveness. So, for the intention-to-treat, what we found is that in terms of life-years gained is around 0.22, which is around 2.5 months of additional life that is afforded to patients who went through the multigene panel testing versus the single-gene testing. That was non-statistically significant from zero at the 5% level. But on average, you would expect this additional 2.5 months of life. The incremental costs were again non-statistically significant, but they're around $20,000. And so when we look at incremental cost-effectiveness, we can also look at the uncertainty around that question, meaning what percentage of incremental cost-effectiveness estimates are likely to be cost-effective at different willingness-to-pay thresholds? Okay? So if you are willing to pay $100,000 to get one gain of life-years, around 52.8% of our estimates, in terms of when we looked at the entire uncertainty, would be cost-effective. So actually that meets the threshold of implementation in our healthcare system. So it's quite uncertain, just over 50%. But what we see is that decision-makers actually have a high tolerance for uncertainty around cost-effectiveness. And so, while it is uncertain, we would say that, well, the cost-effectiveness is finely balanced. Now, when we looked at the population, the per-protocol population, those folks who just got treatment, we actually have a different story. We have all of a sudden around 4.5 or just under 5 months of life gained that is statistically significantly different from zero, meaning that this is a strong signal of benefit in terms of life-years gained. In terms of the changes in costs or the incremental costs, they are larger again, but statistically insignificant. So the question now is, to what extent is it cost-effective? What is the probability of it being cost-effective? And at the $100,000 per life-year gained willingness-to-pay, there was a 73% chance that multigene panel testing versus single-gene testing is cost-effective. Dr. Rafeh Naqash:So one of the questions I have here, this is a clarification both for myself and maybe the listeners also. So protocol treatment is basically if you had gene testing and you have a BRAF in the multigene panel, then the patient went on a BRAF treatment. Is that correct? Dr. Dean Regier:It's still physician choice. And I think that's important to say that. So typically what we saw in both in our pre- and post-matching data is that we saw around 50% of patients, irrespective of BRAF status, get an ICI, which is appropriate, right? And so the idea here is that you get physician-guided care, but if the patient no longer performs on the ICI, then it gives them a little bit more information on what to do next. Even during that time when we thought it wasn't going to be common to do an ICI, but it was actually quite common. Dr. Rafeh Naqash:Now, did you have any patients in this study who had the multigene testing done and had an NRAS or a KIT mutation and then went on to those therapies, which were not captured obviously in the single-gene testing, which would have just tried to look at BRAF? Dr. Dean Regier:So I did look at the data this morning because I thought that might come up in terms of my own questions that I had. I couldn't find it, but what we did see is that some patients went on to clinical trials. So, meaning that this multigene panel testing allowed, as you would hope in a learning healthcare system, patients to move on to clinical trials to have a better chance at more appropriate care if a target therapy was available. Dr. Rafeh Naqash:And the other question in that context, which is not necessarily related to the gene platform, but more on the variant allele frequency, so if you had a multigene panel that captured something that was present at a high VAF, with suspicion that this could be germline, did you have any of those patients? I'm guessing if you did, probably very low number, but I'm just thinking from a cost-effective standpoint, if you identify somebody with germline, their, you know, first-degree relative gets tested, that ends up, you know, prevention, etc. rather than somebody actually developing cancer subsequently. That's a lot of financial gains to the system if you capture something early. So did you look at that or maybe you're planning to look at that? Dr. Dean Regier:We did not look at that, but that is a really important question that typically goes unanswered in economic evaluations. And so, the short answer is yes, that result, if there was a germline finding, would be returned to the patient, and then the family would be able to be eligible for screening in the appropriate context. What we have found in economic evaluations, and we've recently published this research, is that that scope of analysis is rarely incorporated into the economic evaluation. So those downstream costs and those downstream benefits are ignored. And when you- especially also when you think about things like secondary or incidental findings, right? So it could be a germline finding for cancer, but what about all those other findings that we might have if you go with an exome or if you go with a genome, which by the way, we do have in British Columbia—we do whole-genome and transcriptome sequencing through something called the Personalized OncoGenomics program. That scope of evaluation, because it's very hard to get the right types of data, because it requires a decision model over the lifetime of both the patients and potentially their family, it becomes very complicated or complex to model over patients' and families' lifetime. That doesn't mean that we should not do it, however. Dr. Rafeh Naqash:So, in summary Dean, could you summarize some of the known and unknowns of what you learned and what you're planning in subsequent steps to this project? Dr. Dean Regier:Our North Star, if you will, is to really understand the entire system effect of next-generation sequencing panels, exome sequencing, whole genomes, or whole genomes and transcriptome analysis, which we think should be the future of precision oncology. The next steps in our research is to provide a nice base around multigene panels in terms of multigene versus single-gene testing, whether that be colorectal cancer, lung cancer, melanoma, etc., and to map out the entire system implications of implementing next-generation sequencing panels. And then we want to answer the questions around, “Well, what if we do exomes for all patients? What if we do whole genomes and transcriptomes for all patients? What are the comparative outcomes for a true tumor-agnostic precision oncology approach, accounting for, as you say, things like return of results with respect to hereditary cancers?” I think the challenge that's going to be encountered is really around the persistent high costs of something like a whole-genome and transcriptome sequencing approach. Although we do see the technology prices going down—the "$1,000 genome" or “$6,000 genome" on whatever Illumina machine you might have—that bioinformatics is continuing to be expensive. And so, there are pipelines that are automated, of course, and you can create a targeted gene report really rapidly within a reasonable turnaround time. But of course, for secondary or what I call level two analysis, that bioinformatics is going to continue to be expensive. And so, we're just continually asking that question is: In our healthcare system and in other healthcare systems, if you want to take a precision oncology approach, how do you create the pipelines? And what types of technologies really lend themselves to benefits over and above next-generation sequencing or multigene panels, allowing for access to off-label therapies? What does that look like? Does that actually improve patients? I think some of the challenges, of course, is because of heterogeneity, small benefiting populations, finding a signal if a signal is indeed there is really challenging. And so, what we are thinking through is, with respect to real-world evidence methods and emulating randomized controlled trials, what types of evidence methods actually allow us to find those signals if indeed those signals are there in the context of small benefiting populations? Dr. Rafeh Naqash:Thank you so much, Dean. Sounds like a very exciting field, especially in the current day and age where cost-effectiveness, financial toxicity is an important aspect of how we improve upon what is existing in oncology. And then lots more to be explored, as you mentioned. The last minute and a half I want to ask about you as an individual, as a researcher. There's very few people who have expertise in oncology, biomarkers, and health economics. So could you tell us for the sake of our trainees and early career physicians who might be listening, what was your trajectory briefly? How did you end up doing what you're doing? And maybe some advice for people who are interested in the cost of care, the cost of oncology drugs - what would your advice be for them very briefly? Dr. Dean Regier:Sure. So I'm an economist by training, and indeed I knew very little about the healthcare system and how it works. But I was recruited at one point to BC Cancer, to British Columbia, to really try to understand some of those questions around costs, and then I learned also around cost-effectiveness. And so, I did training in Scotland to understand patient preferences and patient values around quality of care, not just quantity of life, but also their quality of life and how that care was provided to them. And then after that, I was at Oxford University at the Nuffield Department of Population Health to understand how that can be incorporated into randomized control trials in children. And so, I did a little bit of learning about RCTs. Of course, during the way I picked up some epidemiology with deep understanding of what I call econometrics, what others might call biostatistics or just statistics. And from there, it was about working with clinicians, working with epidemiologists, working with clinical trialists, working with economists to understand the different approaches or ways of thinking of how to estimate efficacy, effectiveness, safety, and cost-effectiveness. I think this is really important to think through is that we have clinical trialists, we have people with deep understanding of biostatistics, we have genome scientists, we have clinicians, and then you add economists into the mix. What I've really benefited from is that interdisciplinary experience, meaning that when I talk to some of the world's leading genome scientists, I understand where they're coming from, what their hope and vision is. And they start to understand where I'm coming from and some of the tools that I use to understand comparative effectiveness and cost-effectiveness. And then we work together to actually change our methods in order to answer those questions that we're passionate about and curious about better for the benefit of patients. So, the short answer is it's been actually quite a trajectory between Canada, the UK. I spent some time at the University of Washington looking at the Fred Hutch Cancer Research Center, looking at precision oncology. And along the way, it's been an experience about interdisciplinary research approaches to evaluating comparative outcomes. And also really thinking through not just at one point in time on-off decisions—is this effective? Is it safe? Is it cost-effective?—not those on-off decisions, but those decisions across the lifecycle of a health product. What do those look like at each point in time? Because we gain new evidence, new information at each point in time as patients have more and more experience around it. And so what really is kind of driving our research is really thinking about interdisciplinary approaches to lifecycle evaluation of promising new drugs with the goal of having these promising technologies to patients sooner in a way that is sustainable for the healthcare system. Dr. Rafeh Naqash:Awesome. Thank you so much for those insights and also giving us a sneak peek of your very successful career. Thank you for listening to JCO Precision Oncology Conversations. Don't forget to give us a rating or review, and be sure to subscribe so you never miss an episode. You can find all ASCO shows at asco.org/podcast. Thank you. The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement.      

Join us for the inaugural episode of "TWAD: Cancer, Cures and Coffee" with Dr. Ashwani Rajput and special guest Dr. Kelly Paulson. In this episode, we dive deep into the topic of Melanoma, one of the most serious types of skin cancer. Dr. Paulson, a medical oncologist at Swedish Cancer Institute First Hill in Seattle, shares her expertise on the importance of early detection, risk factors, and the latest advancements in treatment. Learn how to protect yourself and your loved ones from Melanoma and discover the role of the immune system in fighting cancer. Don't miss this informative and engaging discussion.Dr. Ashwani Rajput BioSee below Do you want to know more?Check out the Providence blog for more information on melanoma and other cancer related topics. ·       Cancer survivor speaks with doctor he credits for saving his life·       Saint Patrick HealthBreak - Skin Cancers·       A year to remember: Advancements, recognition and transitions To learn more about our mission programs and services, go to Providence.org.Follow us on social media to get continued information on other important health care topics. You can  connect with us on LinkedIn, Facebook, TikTok, Instagram and X.For all your healthcare information on the go, download the Providence app. Whether you're tracking symptoms, scheduling appointments, or connecting with your healthcare providers, the Providence app has your back.To learn more about the app, check out the Wellness Brief podcast episode. Wellness Brief: Simplifying Care-There's an App for That. We'd love to hear from you. You can contact us at FutureOfHealthPodcasts@providence.org Dr. Ashwani Rajput BioAshwani Rajput, MD, FACS, joined Providence Swedish in September 2024 as the regional executive medical director (EMD) of the Swedish Cancer Institute. Dr. Rajput comes to us from Johns Hopkins University, where he is a professor of Surgery and Oncology, as well as the director of the Hopkins Kimmel Cancer Center in the Washington, D.C. region. Dr. Rajput completed his medical school, general surgery training, and a post-doctoral fellowship in molecular genetics at Case Western Reserve University in Cleveland, Ohio. He went on to the Roswell Park Comprehensive Cancer Center in Buffalo, N.Y., for a fellowship in Complex General Surgical Oncology (CGSO). There, he was recruited to join the faculty at Roswell Park with appointments in GI Surgical Oncology as well as Pharmacology and Therapeutics. His laboratory investigated the key signal transduction pathways in colorectal metastases using novel orthotopic murine models. In 2009, Dr. Rajput was recruited to the University of New Mexico as the inaugural division chief of Surgical Oncology. During his tenure in New Mexico, he also served as the director of surgical services for the NCI-designated Comprehensive Cancer Center and vice-chair of surgery for academic affairs and faculty development. Under his leadership, an ACGME-approved fellowship in CGSO was created and launched. Throughout his roles in New Mexico and D.C., he has actively addressed cancer health care outcomes and health equity. Under Dr. Rajput's leadership, he will develop and implement a cancer strategic vision and enhance collaboration across our geography. He will oversee the SCI medical directors and partner with the Senior Director of Operations to deliver excellence in cancer care. Dr. Rajput and his wife, Sunita, have four children. Outside of work, he enjoys playing tennis, piano, the arts, and traveling.

Are you or a loved one facing a diagnosis of bladder cancer, melanoma, or skin cancer? Tune in to this essential episode of Navigating Cancer TOGETHER for expert guidance and compassionate insights. Join host Talaya Dendy as she welcomes back Dr. Thomas Eanelli, a highly respected radiation oncologist based in New York. We also feature Angel Santana, co-host of The CROC Podcast, sharing powerful motivational perspectives. In observance of May Cancer Awareness, this special episode dives into critical aspects of three specific cancers: bladder, melanoma, and skin cancer. Dr. Eanelli provides invaluable medical expertise on the latest cancer treatments, diagnosis, and management of these diseases. Angel Santana offers heartfelt inspiration and emphasizes the power of support and positivity throughout the cancer journey. This episode is packed with vital information and moving stories to offer hope and guidance for anyone navigating cancer.

Jason talks with dermatologist Dr. Mohiba Tareen about skin cancer awareness month and the simple steps you can take to prevent a deadly form of cancer.

3pm Hour: Jason talks about some of the latest controversy surrounding President Trump. Is the President just trolling people? Then he's joined by dermatologist Dr. Mohiba Tareen to talk about skin cancer awareness month.

In today's episode, supported by Replimune, we had the pleasure of speaking with Anna C. Pavlick, BSN, MSc, DO, MBA, about the use of RP1 plus nivolumab (Opdivo) for the treatment of patients with advanced melanoma. Dr Pavlick is a professor of medicine in the Division of Hematology & Medical Oncology at Weill Cornell Medicine in New York, New York; as well as the founding director of the Cutaneous Oncology Program at Weill Cornell Medicine and NewYork-Presbyterian. In our exclusive interview, Dr Pavlick discussed the rationale for investigating this combination in patients with advanced melanoma who have received prior immune checkpoint inhibition, key efficacy and safety findings from the phase 1/2 IGNYTE trial (NCT03767348), and where the future may be headed regarding the use of oncolytic viruses in melanoma.

As tennis players, we know the sun can be just as much of an opponent in our sport from finding the right SPF and avoiding sun damage. Enter BLOQUV.  Founder and sun sport enthusiast, Corina Biton, joins us in this episode to help educate us on all things UPF apparel. As someone who loves to run, walk, paddleboard and play tennis.  After noticing white spots on my arms, she founded BloqUV when finding skin damage even though she always wore long-sleeve T-shirts. Turns out plain T-shirts only block 5% of the sun's rays! Corina created BloqUV with BloqTek, their proprietary fabric with minimum Ultraviolet Protection Factor 50 that blocks 98% UVA/UVB rays; the protection is chemical-free, inherent to the fabric and unaffected by laundering. After 15 years, BloqUV has emerged as a market leader in sun protection: unique in design, fit and sun protection technology; they're moisture-wicking and quick-dry, allowing for a wide range of uses on land and water!  Learn even more & stay tuned for a chance to win some BloqUV gear!  If you have any further questions or want to continue the conversation?! Email us at podcast@tennis-warehouse.com   Shop with us for all your TENNIS needs all over the WORLD:

Hey Heal Squad! The Roundtable is BACK and this week Maria and the squad are tackling sun myths that'll totally change your morning routine. Think sunglasses protect your eyes? Wait till you hear how ditching them could actually turn back the clock on aging! Plus, could morning sun exposure be your skin's new BFF and not the enemy we've been warned about? The squad spills it all. We're also diving deep into the lymphatic system—aka your body's secret to glowing skin and lasting energy. Dr. Alison and Christina Gomes break down easy lymphatic hacks you'll obsess over (rebounding, anyone?). Dry brushing, bed elevation, and more wellness tips you never knew you needed! Hit play and get ready to rethink everything you thought you knew about the sun, skin, and your energy levels. Trust us, your body will thank you! — HEAL SQUAD SOCIALS IG: https://www.instagram.com/healsquad/ TikTok: https://www.tiktok.com/@healsquadxmaria HEAL SQUAD RESOURCES: Heal Squad Website: https://www.healsquad.com/ Maria Menounos Website: https://www.mariamenounos.com Heal Squad x Patreon: https://www.patreon.com/HealSquad/membership  My Curated Macy's Page: Shop My Macy's Storefront Delete Me: https://bit.ly/43rkHwi   code: SQUAD Prenuvo: Prenuvo.com/MARIA for $300 off HEADLINES & RESOURCES Chart Source: https://academic.oup.com/jnci/article-abstract/97/3/195/2544082 Rubberband hack on TikTok EPISODE RESOURCES: ABOUT MARIA MENOUNOS: Emmy Award-winning journalist, TV personality, actress, 2x NYT best-selling author, former pro-wrestler and brain tumor survivor, Maria Menounos' passion is to see others heal and to get better in all areas of life. ABOUT HEAL SQUAD x MARIA MENOUNOS: A daily digital talk-show that brings you the world's leading healers, experts, and celebrities to share groundbreaking secrets and tips to getting better in all areas of life. DISCLAIMER: This Podcast and all related content ( published or distributed by or on behalf of Maria Menounos or http://Mariamenounos.com and http://healsquad.com ) is for informational purposes only and may include information that is general in nature and that is not specific to you. Any information or opinions provided by guest experts or hosts featured within website or on Company's Podcast are their own; not those of Maria Menounos or the Company. Accordingly, Maria Menounos and the Company cannot be responsible for any results or consequences or actions you may take based on such information or opinions. This podcast is presented for exploratory purposes only. Published content is not intended to be used for preventing, diagnosing, or treating a specific illness. If you have, or suspect you may have, a health-care emergency, please contact a qualified health care professional for treatment.