Podcasts about Cancer immunotherapy

For decades, traditional cancer treatments like chemotherapy and radiation have targeted tumors directly—often with severe side effects and mixed results. But what if the key to treating cancer was already inside our bodies? Prof. Thomas Gajewski, a renowned oncologist at the University of Chicago, is leading a revolution by using the body's gut microbiome to fight cancer. His pioneering work in cancer immunotherapy focuses on why some patients with melanoma responded dramatically to immune-based therapies while others do not. In this episode, Gajewski discusses how training T-cells to recognize and attack tumors is transforming oncology, why the microbiome might hold the key to supercharging cancer treatments, and what it will take to make life-saving immunotherapies effective for every patient. Hosted by Simplecast, an AdsWizz company. See pcm.adswizz.com for information about our collection and use of personal data for advertising.

Cancer finally led Theresa Magistro to Yale Cancer Center where she took part in a study--now she celebrates 10 years of being cancer-free. Yale Cancer Center visit: http://www.yalecancercenter.org email: canceranswers@yale.edu call: 203-785-4095

"A good way of thinking about this is this is the survival of the fittest clone. There could be a portion of a cancer that naturally has some resistance or ability to survive a particular drug. And over time, as the other cells around it are dying off, that particular clone is able to replicate and continue to survive in the face of that drug therapy and eventually take over as being the fittest clone. At that point, we're often seeing disease progression," Danielle Roman, PharmD, BCOP, manager of clinical pharmacy services at the Allegheny Health Network Cancer Institute in Pittsburgh, PA, told Jaime Weimer, MSN, RN, AGCNS-BS, AOCNS®, manager of oncology nursing practice at ONS, during a conversation about resistance pathways.  Music Credit: "Fireflies and Stardust" by Kevin MacLeod Licensed under Creative Commons by Attribution 3.0  Earn 0.5 contact hours of nursing continuing professional development (NCPD), including 30 minutes of pharmacotherapeutic content, by listening to the full recording and completing an evaluation at courses.ons.org by August 7, 2027. Roman has served on advisory boards for Genetech, Pfizer, Regeneron, and Daiichi Sankyo and received honoraria payments from Pharmacy Times and Decera for faculty lectures. These financial relationships have been mitigated. ONS is accredited as a provider of nursing continuing professional development by the American Nurses Credentialing Center's Commission on Accreditation. Learning outcome: Learners will report increased knowledge related to resistance pathways in oncology care. Episode Notes  Complete this evaluation for free NCPD.  ONS Podcast™ episodes: Pharmacology 101 series Episode 423: Pharmacology 101: Interaction Pathways Episode 406: Drug Resistance Biomarkers and Their Impact on Cancer Treatment Choices ONS Voice articles: Predictive and Diagnostic Biomarkers Scientists Identify Protein Implicated in Tumor Growth, Treatment Resistance ONS book: Guide to Cancer Immunotherapy (second edition) Genomics and Precision Oncology Learning Library ONS Biomarker Database Pharmacogenomics Huddle Card CancerQuest: Cancer Drug Resistance National Comprehensive Cancer Network OncoKB.org Research To Practice To discuss the information in this episode with other oncology nurses, visit the ONS Communities.  To find resources for creating an ONS Podcast club in your chapter or nursing community, visit the ONS Podcast Library. To provide feedback or otherwise reach ONS about the podcast, email pubONSVoice@ons.org. Highlights From This Episode "As we look at drug resistance, this is the concept that cancer cells are no longer able to respond to a cancer treatment. The downstream of this is that we could end up with progression of the disease and need to look at alternative therapies that may be beneficial for the patient. This is unfortunately a very common phenomenon. Drug resistance is a major cause of treatment failure and poor patient outcomes with treatments. Unfortunately, this is an issue we see that increases over time on treatment." TS 2:29 "Genetics play a really big role in drug resistance. We know that drug resistance can be due to different things. It could be epigenetics. It could be the tumor microenvironment factors. But genetics often play a very big role in resistance pathways. It's generally considered to be a critical contributor to resistance, particularly in the way of acquired variants to drug targets or amplifications of certain oncogenes that can lead cancers to have progression. A well-known genetic alteration is the BRCA1/BRCA2 variant that helps to make the cancer more efficient at fixing DNA damage. So we're trying to get DNA damage with chemotherapy, and this particular variant helps at fixing that damage to allow the cancer to progress. So that is one genetic variant we see that plays a big role in a number of different cancers." TS 4:51 "These pathways are not mutually exclusive. Oftentimes we have multiple resistance pathways involved. I think it's important to understand some of those individually, but kind of thinking about this as we might be facing multiple resistance pathways. ... We can see resistance mechanisms that vary based on the type of treatment we use, for example, traditional cytotoxic chemotherapy. We may be more likely to see some resistance mechanisms that are working at DNA: repairing broken DNA or working on those efflux pumps that are being used to push chemotherapy out of cells. If we're talking more about the targeted therapies such as tyrosine kinase inhibitors or monoclonal antibodies, we may be more likely to see resistance mechanisms that are what we discussed with that drug target alteration: changing the way that the target agents are able to bind to the tumor cells to activate or inactivate pathways so we may see some changes there." TS 12:39 "One way to overcome this and to help to decrease the resistance from developing is using combination therapy: drugs that are targeting different pathways at once or potentially using combinations with things like chemotherapy in addition to immunotherapy. In this way, as we're getting these different targets, we can hopefully decrease the mechanism of resistance that may be developing." TS 14:48 "Biomarker testing is an incredibly important part of our practice. In many situations now, we are getting upfront, comprehensive biomarker testing to identify whether the patient may have any of those intrinsic or primary resistance mechanisms that might make it so a patient is never going to respond to a particular type of treatment. And in that case, we can spare the patient from the potential toxicities of that treatment if we don't think that there's going to be benefit there. So I think that that has become a really important way that we can tailor patients for understanding what treatments are going to be more effective. And then after that, there's usually additional biomarker testing that may be warranted at the time of progression in certain types of cancer. And that really helps us to understand that acquired resistance that might be developing." TS 17:32 "Nurses are really helpful with filling in the gaps and bringing back patient concerns that might be shared with them. And these might be early signs of progression. Better understanding how our patients are feeling and what's going on with them may help us to identify a patient that we need to do some additional testing for to understand whether there is drug resistance ongoing and potential progression of disease." TS 21:52

Good morning from Pharma Daily: the podcast that brings you the most important developments in the pharmaceutical and biotech world. Today, we're diving into some of the latest scientific advancements, regulatory milestones, and strategic business maneuvers shaping the industry. One of the standout developments comes from Otsuka with their drug Voyxact, which has shown promising results in stabilizing kidney function decline in patients with immunoglobulin A nephropathy (IgAN). In a Phase 3 trial, patients exhibited kidney function comparable to that of healthy adults. IgAN is a challenging autoimmune condition often leading to end-stage renal disease. This advancement, leveraging a monoclonal antibody to target specific pathways, could mark a new era in managing this chronic kidney disease. In oncology, Jiangsu Alphamab Biopharmaceuticals has been making waves through strategic collaborations, securing deals worth $125 million upfront and potential milestone payments reaching over $2 billion. Their focus on developing antibody-drug conjugates (ADCs) using AI and machine learning underscores the promise of precision oncology. ADCs marry the targeting precision of antibodies with potent anti-cancer drugs, highlighting robust investment and confidence in these cutting-edge therapies. Merck & Co. continues to expand its financial outlook, driven by the success of its flagship drugs like Keytruda. This monoclonal antibody remains pivotal in cancer immunotherapy, while drugs like Winrevair and Lipfendra are broadening Merck's reach into cardiovascular health. This growth trajectory reflects a strategic push toward diversifying product lines and leveraging breakthrough therapies to maintain strong financial performance. Additionally, Merck's $10.8 billion acquisition of Prometheus Biosciences aims to expand their therapeutic portfolio with targeted biologics. Although mid-stage trials showed mixed results for their anti-TL1A antibody therapy, such acquisitions are pivotal in addressing unmet medical needs. On the regulatory side, Sanofi's MenQuadfi vaccine has achieved EU approval for use in infants as young as six weeks. This approval enhances preventive measures against invasive meningococcal disease in vulnerable populations, representing a significant public health advancement. In research methodologies, Sethera Therapeutics' collaboration with Receptor.AI is notable. By integrating AI-driven platforms for polymacrocyclic peptide discovery aimed at hard-to-drug targets, they're paving the way for overcoming traditional drug discovery challenges through computational tools. However, not all news is about progress. Jazz Pharmaceuticals faced a setback by withdrawing its label indication for Zepzelca after failing Phase 3 trials for small-cell lung cancer. This underscores the inherent risks in clinical development pathways. From a financial standpoint, BioNTech has adjusted its 2025 sales forecast downward due to waning global demand for COVID-19 vaccines—a reflection of the volatile vaccine markets post-pandemic peaks. Meanwhile, Pfizer's discontinuation of its Phase 2 GIPR antagonist for obesity illustrates strategic pivots within R&D pipelines as companies reassess priorities based on trial outcomes and market potential. Recent corporate strategies include Pfizer's ambitious cost-saving plan totaling $9.7 billion through 2029. Amid economic pressures and patent expirations looming on key products like Eliquis, Pfizer is optimizing operations to stay competitive. Speculation around a possible merger between Bristol Myers Squibb (BMS) and AstraZeneca has stirred interest. With both facing patent cliffs, this merger could rejuvenate portfolios—though the strategic benefits for AstraZeneca are still debated. On the technological front, advancements in cellular therapies promise to revolutionize medicine production at the cellular level, potentially enhancing patient outcomes through more personalized treatments. The regulatory landscape is also evolving. There's a growing call for streamlining Investigational New Drug applications under the FDA's Trialblazer initiative—crucial for accelerating clinical trials and bringing innovative therapies to market swiftly. Finally, initiatives such as Boston Scientific's restructuring efforts highlight challenges within the medical device sector as companies adapt to shifting market dynamics. Overall, these developments underscore an industry in motion where innovation and adaptation are key to navigating complex landscapes and advancing patient care globally. As we look ahead, these trends will likely continue shaping the future of pharmaceuticals and biotech in profound ways.Support the show

Immune checkpoint inhibitors have rapidly reshaped care for triple-negative breast cancer (TNBC)—but surgical teams increasingly encounter their downstream perioperative consequences. In this episode, we define immunotherapy through the lens of checkpoint biology, review the landmark evidence supporting pembrolizumab in metastatic PD‑L1–positive TNBC (KEYNOTE‑355) and curative-intent stage II–III TNBC (KEYNOTE‑522), and translate immune-related adverse events (irAEs) into practical periop recognition, triage, and timing decisions—especially for endocrine, pulmonary, hepatic, dermatologic, and GI toxicities. Hosts:- Rashmi Kumar, MD, PhDResident, University of Michigan General Surgery Residency Program Twitter/X: @RashmiJKumar- Melissa Pilewskie, MDAttending Breast Surgical Oncologist, Co-Director of the Weiser Family Center for Breast Cancer, Michigan MedicineTwitter/X: @MPilewskie- Stephanie Downs-Canner, MDAttending Breast Surgical Oncologist & Physician-Scientist, Memorial Sloan Kettering Cancer Center, Program Director of the Breast Surgical Oncology Fellowship Training ProgramTwitter/X: @SDownsCannerLearning Objectives: Define immunotherapy and immune checkpoint inhibition in breast cancer  Summarize current clinical indications and pivotal evidence for pembrolizumab in TNBC  Equip perioperative clinicians to identify and manage immune-related adverse events (irAEs) or side effects of immunotherapy.  Rationale for Immunotherapy in Breast Cancer ReviewSelecting Triple Negative Breast Cancer Patients for Immunotherapy: https://pubmed.ncbi.nlm.nih.gov/37714640/Landmark Clinical Trials Discussed in this Episode KEYNOTE-355: https://pubmed.ncbi.nlm.nih.gov/33232653/ KEYNOTE-522: https://pubmed.ncbi.nlm.nih.gov/33232642/ IMpassion130: https://pubmed.ncbi.nlm.nih.gov/30345906/ IMpassion131: https://pubmed.ncbi.nlm.nih.gov/33930478/ Assessment of Surgical Outcomes in patients receiving chemoimmunotherapySurgical outcomes after neoadjuvant chemoimmunotherapy in triple-negative breast cancer: https://pubmed.ncbi.nlm.nih.gov/38332314/Immune Related Adverse Events and Management Schneider BJ, et al. Management of immune-related adverse events: https://pubmed.ncbi.nlm.nih.gov/34724392/ Brahmer JR, et al. SITC clinical practice guideline: https://pubmed.ncbi.nlm.nih.gov/34177534/ Please visit https://behindtheknife.org to access other high-yield surgical education podcasts, videos and more.  If you liked this episode, check out our recent episodes here: https://behindtheknife.org/listenBehind the Knife Premium: https://behindtheknife.org/premiumOral Board Review: https://behindtheknife.org/oral-boardOral Board Simulator: https://behindtheknife.org/oral-board/simulatorGeneral Surgery Oral Board Review Course: https://behindtheknife.org/premium/general-surgery-oral-board-reviewTrauma Surgery Video Atlas: https://behindtheknife.org/premium/trauma-surgery-video-atlasDominate Surgery: A High-Yield Guide to Your Surgery Clerkship: https://behindtheknife.org/premium/dominate-surgery-a-high-yield-guide-to-your-surgery-clerkshipDominate Surgery for APPs: A High-Yield Guide to Your Surgery Rotation: https://behindtheknife.org/premium/dominate-surgery-for-apps-a-high-yield-guide-to-your-surgery-rotationVascular Surgery Oral Board Review Course: https://behindtheknife.org/premium/vascular-surgery-oral-board-reviewColorectal Surgery Oral Board Review Course: https://behindtheknife.org/premium/colorectal-surgery-oral-board-reviewSurgical Oncology Oral Board Review Course: https://behindtheknife.org/premium/surgical-oncology-oral-board-reviewCardiothoracic Oral Board Review Course: https://behindtheknife.org/premium/cardiothoracic-surgery-oral-board-reviewOBGYN Oral Board Review Coures: https://behindtheknife.org/course/obgyn-oral-board-reviewEPA Playbook: https://behindtheknife.org/course/epa-playbookSurgical Instrument Flashcards: https://behindtheknife.org/course/surgical-instrument-flashcardsABSITE Review: https://behindtheknife.org/course/absite-2026-exam-reviewDownload our App:Apple App Store: https://apps.apple.com/us/app/behind-the-knife/id1672420049Android/Google Play: https://play.google.com/store/apps/details?id=com.btk.app&hl=en_US

Send us Fan MailFor decades, the war on cancer has focused on destroying cancer cells directly - with chemotherapy, radiation, and targeted drugs. But what if the future of cancer treatment is not about attacking cancer ourselves...but teaching our own immune system to do it for us?Today we're exploring a new generation of immunotherapies designed to turn the body's own defenses into a precision weapon against cancer.Over the past decade, immunotherapies such as checkpoint inhibitors and CAR-T cell therapies have transformed the treatment landscape for many cancers. But major challenges remain - including limited response rates, treatment resistance, toxicity, and the enormous complexity and cost of manufacturing many next-generation therapies.Our guest today believes the next breakthrough may come from a new generation of personalized immunotherapies designed to activate a patient's own immune system against their cancer - while also being manufactured as an accessible, off-the-shelf treatment.Joining us is Dr. William Williams, MD - President and CEO of BriaCell Therapeutics ( https://briacell.com/ ).Dr. Williams brings more than 35 years of experience spanning academia and the biopharmaceutical industry. He has helped advance numerous medicines from discovery through clinical development, including work contributing to therapies such as Jakafi and Olumiant during his time at Incyte, and multiple oncology programs during his career at GlaxoSmithKline.Before entering industry leadership, Dr. Williams was a researcher at the University of Pennsylvania focused on molecular immunology, receptor biology, and early DNA vaccine approaches.Today we'll discuss the evolution of cancer immunotherapy, BriaCell's Bria-IMT platform, the challenges of treating advanced breast cancer, and whether the future of oncology lies in creating therapies that can truly mobilize each patient's own immune system.#CancerResearch #CancerImmunotherapy #Immunotherapy #CancerTreatment #Oncology #PrecisionMedicine #PersonalizedMedicine #Biotechnology #Biotech #LifeSciences #DrugDiscovery #ClinicalTrials #BreastCancer #MetastaticBreastCancer #CancerVaccine #CellTherapy #TumorImmunology #TCells #ImmuneSystem #MedicalInnovation #FutureOfMedicine #HealthcareInnovation #BiomedicalResearch #Pharma #PharmaceuticalInnovation #SciencePodcast #ProgressPotentialAndPossibilities #PPPShowSupport the show

Carnitine, with acknowledged muscle and brain benefits, may find a new role in supporting cancer immunity; Calcium and vitamin D's bone-building impact may be limited; Internal visceral fat may accelerate brain aging, MRI study finds; The remarkable benefits of a newly-discovered mitochondrial booster—urolithin A (Mitopure®️).

As part of the 2026 UCSF Patient Conference on Prostate Cancer, Dr. David Oh discusses immunotherapy. Series: "Prostate Cancer Patient Conference" [Health and Medicine] [Show ID: 41562]

As part of the 2026 UCSF Patient Conference on Prostate Cancer, Dr. David Oh discusses immunotherapy. Series: "Prostate Cancer Patient Conference" [Health and Medicine] [Show ID: 41562]

As part of the 2026 UCSF Patient Conference on Prostate Cancer, Dr. David Oh discusses immunotherapy. Series: "Prostate Cancer Patient Conference" [Health and Medicine] [Show ID: 41562]

"There are a lot of specifics that nurses need to keep in mind as they are administering this herpes simplex modified virus to patients because accidental exposure is of concern both to the patient, to their family members, as well as to healthcare workers. I always recommend nurses wear personal protective equipment, such as a gown, safety glasses, gloves, and/or a face shield," Heidi Finnes, PharmD, RPh, BCOP, director of clinical ambulatory practice at Mayo Clinic and assistant professor of pharmacy at Mayo Clinic Alix School of Medicine in Rochester, MN, told Jaime Weimer, MSN, RN, AGCNS-BS, AOCNS®, manager of oncology nursing practice at ONS, during a conversation about oncolytic viral therapy.  Music Credit: "Fireflies and Stardust" by Kevin MacLeod Licensed under Creative Commons by Attribution 3.0  Earn 0.5 contact hours of nursing continuing professional development (NCPD) by listening to the full recording and completing an evaluation at courses.ons.org by May 29, 2027. The planners and faculty for this episode have no relevant financial relationships with ineligible companies to disclose. ONS is accredited as a provider of nursing continuing professional development by the American Nurses Credentialing Center's Commission on Accreditation. Learning outcome: Learners will report an increase in knowledge about the use of oncolytic viruses to treat cancer. Episode Notes  Complete this evaluation for free NCPD.  ONS Podcast™ episodes: Pharmacology 101 series Episode 338: High-Volume Subcutaneous Injections: The Oncology Nurse's Role Episode 330: Stay Up to Date on Safe Handling of Hazardous Drugs Episode 273: Updates in Chemotherapy and Immunotherapy ONS Voice articles: Cutaneous Malignancies Have High Response to Oncolytic Virus Plus Immunotherapy Oncolytic Virus Kills Tumor Cells While Supporting T Cells What Nurses Need to Know About Talimogene Laherparepvec for Advanced Melanoma Clinical Journal of Oncology Nursing articles: Intralesional Therapy: Consensus Statements for Best Practices in Administration From the Melanoma Nursing Initiative Safe and Effective Standards of Care: Supporting the Administration of T-VEC for Patients With Advanced Melanoma in the Outpatient Oncology Setting Oncology Nursing Forum article: Administration and Handling of Talimogene Laherparepvec: An Intralesional Oncolytic Immunotherapy for Melanoma ONS book: Guide to Cancer Immunotherapy (second edition) ONS clinical practice resource: Safe Handling of Oncolytic Viruses ONS Huddle Card: Immunotherapy Association of Community Cancer Centers (ACCC) Drugs@FDA Hematology/Oncology Pharmacy Association (HOPA) Network for Collaborative Oncology Development and Advancement (NCODA) Patient Education Sheets To discuss the information in this episode with other oncology nurses, visit the ONS Communities.  To find resources for creating an ONS Podcast club in your chapter or nursing community, visit the ONS Podcast Library. To provide feedback or otherwise reach ONS about the podcast, email pubONSVoice@ons.org. Highlights From This Episode "[Oncolytic viruses] can have direct lysis to the tumor cells themselves, or they can cause immunogenic activation. They release tumor-associated antigens and then proinflammatory signals, so think of T cells, natural killer cells, those sorts of things, that can convert to immunologically cold tumors. Those are tumors that are immune silenced into hot tumors which are now immune activated. By doing that, they recruit those T cells and other cells to the area to attack both the primary tumors. But that's also thought to be how they work on distant or noninjected sites as well. This immunomodulatory capacity has led to the reclassification of oncolytic viruses as a form of cancer immunotherapy. So, think of it kind of similarly to how we think of immune checkpoint inhibitors in recruiting immune cells and leaving our immune system in the on position. This is also kind of a form of immunotherapy." TS 4:35 "One of the toxicities I know that is of significant concern to patients, family members, and healthcare workers is the incidence of herpes infections. Systemic herpetic infections are extremely rare and usually more common in patients who may be immunocompromised. In patients who also have other immune-related diseases—such as vitiligo, vasculitis, pneumonitis, sometimes worsening psoriasis—because you're mounting an immune response with these types of things, sometimes you can see a worsening of those types of immune symptoms. But for the most part, these types of side effects are very well tolerated in most patients." TS 9:07 "Talimogene is generally transmitted via bodily fluids or touch. It's not airborne. Herpes simplex virus isn't an airborne type of virus. Another thing to consider is where are you going to inject this? Are you going to do this in your infusion therapy unit? Are you going to do it in a dedicated room? Who's going to escort the patient to the room? How is the virus going to arrive at the room? How will you clean the room and all of the laboratory equipment or any of the exam tables that may be in there? I think having all of that discussed and assigned mitigates the consternation that can sometimes occur—the fear that occurs with administering a virus that is thought to be fairly communicable." TS 15:44 "Helping patients understand how this works [is important] because hearing that you're receiving a virus, particularly a herpes simplex virus, can be scary to a patient. I think understanding that it's modified or essentially we're taking the parts out of it so that we can directly inject a portion that recruits immune cells to that area, because the goal is for the oncolytic virus to attack cancer cells and then destroy them by triggering an immune response in the body." TS 20:51 "Sometimes patients are very concerned about urine in the toilet, bodily fluids, kissing loved ones, holding hands, hugging, you know, am I going to infect my loved one because I'm getting this type of an oncolytic virus therapy? I like to reassure patients that they can continue to hold hands and hug their loved ones as normal. Viral DNA is usually only present on the injection site. And as I mentioned previously, we want to cover that injection site with an occlusive dressing, at least with talimogene, for up to seven days. And particularly, if those injection sites are at all oozing or weeping, active virus is usually only on that injection site itself." TS 24:14

Send us Fan MailWhat if medicines could actually “decide” when and where to activate inside the body? MIT-trained synthetic biologist Dr. Jacob Becraft, Ph.D. is building programmable therapies that behave less like traditional drugs…and more like biological software.Dr. Becraft is Co-Founder and CEO of Strand Therapeutics ( https://www.strandtx.com/ ), a company pioneering what may become one of the next great frontiers in medicine: programmable mRNA therapeutics.Long before mRNA became a household term through COVID vaccines, Dr. Becraft and his colleagues at MIT were developing what has been described as the world's first synthetic biology programming language for mRNA - technology designed not simply to deliver genetic instructions, but to create logic-driven therapies capable of making decisions inside living cells.Now Strand is translating that vision into cancer therapeutics, with early clinical data from its lead candidate STX-001 showing responses in patients with advanced solid tumors who had exhausted conventional options - including evidence of systemic immune activity and even complete responses.Beyond the science, Jake is also a leading voice in synthetic biology, biotech entrepreneurship, and the future relationship between software, biology, and medicine.#StrandTherapeutics #JacobBecraft #SyntheticBiology #mRNA #ProgrammableMedicine #CancerImmunotherapy #Immunotherapy #Biotech #PrecisionMedicine #GeneTherapy #SyntheticBiologyEngineering #FutureOfMedicine #Oncology #CAR_T #mRNATherapeutics #Bioengineering #IL12 #RNA #MIT #CellTherapy #Longevity #Biotechnology #MedicalInnovation #NextGenMedicine #CancerResearch #AIinBiology #HealthcareInnovation #GeneticMedicine #ScientificBreakthrough #ProgressPotentialPossibilitiesSupport the show

Welcome to IDEA Collider. In this episode, host Alex Gray is joined by IDEA Pharma colleagues David Radwaner and Tom Brockbank to dissect the history, strategy, and future of immuno-oncology (IO). The trio explores how PD-1 and PD-L1 therapies revolutionized cancer treatment, acting as a brake on the immune system to offer unprecedented durability and long-term survival for patients.  They take a deep dive into the fascinating commercial and clinical race between Merck's Keytruda and BMS's Opdivo. Learn how Merck's strategic decisions—including smart statistical trial designs, targeted biomarker approaches in first-line non-small cell lung cancer, and tumor-agnostic labels like MSI-high—allowed Keytruda to secure market dominance. Finally, Alex, David, and Tom look ahead to the next ten years, discussing whether emerging players like AstraZeneca and China's Akeso / Summit will displace Keytruda, or if the future lies in combination therapies.    Episode Timestamps:  00:00:00 - Introduction: Meet David Radwaner, Tom Brockbank, and host Alex Gray.  00:01:45 - The Origins of IO: The Nobel Prize-winning discovery of PD-1 and CTLA-4 checkpoints.  00:03:55 - Why PD-1 / PD-L1 Won: The unique breadth of utility and unparalleled durability of long-term survival.  00:06:21 - Keytruda vs. Opdivo: How Merck's strategic trial design and smart statistical work outpaced BMS's early lead.  00:11:48 - The NSCLC Inflection Point: Why narrowing the patient population (PD-L1 - 50%) cemented Keytruda's foundation in first-line lung cancer.  00:14:20 - Tumor-Agnostic Success: Merck's bold move into MSI-high and broad biomarker-led strategies.  00:16:09 - Science or Luck? Analyzing Merck's aggressive and risky clinical development strategy.  00:18:00 - The Next 10 Years: Will anyone displace Keytruda? Assessing the future strategies of Merck, BMS, AstraZeneca, and Akeso/Summit    Don't forget to Like, Share, Subscribe, Rate, and Review!   Keep up with Alex Gray;  LinkedIn: https://www.linkedin.com/in/alexander-gray-934a653/    Keep up with David Radwaner;  LinkedIn: https://www.linkedin.com/in/david-radwaner-1b496343/    Keep up with Tom Brockbank;  LinkedIn: https://www.linkedin.com/in/tom-brockbank-159bb4116/      Follow IDEA Pharma On; Website: https://www.ideapharma.com/    Listen to more fantastic podcast episodes: https://ideacollider.simplecast.com/

Dr. Marty Makary out as FDA Commissioner—was he the victim of a BigPharma purge? Are “liquid biopsies” useful for predicting recurrences, as well as guiding therapy, for cancer? Nighttime smartphone by adolescents surges, eroding kids' sleep needs; Persistent itch may require an “all of the above” approach to break its vicious cycle—could topical vitamin B12 provide an answer? Study critiques research methods that fast-tracked new Alzheimer's drugs.

In this episode of the IDEA Collider, host Mike Rea sits down with Reagan Jarvis, scientific founder and CEO of Anocca, to explore how TCR-T cell therapy could unlock the next frontier in cancer treatment—particularly for solid tumors.  While CAR-T therapy has transformed outcomes in hematologic cancers, its success has been limited in solid tumors due to a lack of suitable targets. Reagan explains how T-cell receptor (TCR) therapies overcome this challenge by targeting HLA-presented peptide antigens, enabling access to tumor-specific biology that CAR-T cannot reach.  Anocca is building a fully integrated platform that combines: Target mapping of HLA-peptide complexes Rapid generation of optimized T-cell receptors from healthy donors Non-viral gene editing for faster, lower-cost manufacturing End-to-end control from discovery through clinical development. The conversation also highlights Anocca's first clinical program targeting mutant KRAS in pancreatic ductal adenocarcinoma, using an umbrella trial design, early intervention strategies, and biomarkers such as circulating tumor DNA (ctDNA). Reagan shares insights on regulatory pathways for individualized therapies, the commercial challenges of patient segmentation, and how software, data, and machine learning are becoming essential to scaling cell therapy platforms.  This episode is a must-listen for anyone interested in cell therapy innovation, cancer immunotherapy, and the future of precision medicine.  Episode Timestamps  00:00 – Introduction to TCR-T and solid tumor challenges  00:48 – Meet Reagan Jarvis and Anocca  02:05 – From New Zealand to Sweden: founder journey  03:08 – Frustration that sparked the platform  04:33 – Why CAR-T struggles in solid tumors  07:24 – The advantage of vertical integration in biotech  09:23 – First non-viral clinical trial challenges  10:56 – Umbrella trials in pancreatic cancer (KRAS focus)  14:13 – Biomarkers and building a target library  17:08 – Software, data, and machine learning in TCR discovery  18:08 – Regulatory pathways for individualized therapies  19:19 – Commercial landscape and target bottlenecks  22:29 – Expanding beyond oncology and partnerships  23:51 – Building a biotech company in Sweden  27:12 – Misconceptions about T-cell biology  30:04 – Milestones and 5-year vision  32:32 – Advice for scientific founders  34:17 – Closing thoughts  Don't forget to Like, Share, Subscribe, Rate, and Review!      Keep up with Reagan Jarvis;  LinkedIn: https://www.linkedin.com/in/reagan-jarvis-063984142/  Website: https://www.anocca.com/     Follow IDEA Pharma  Website: https://www.ideapharma.com/  LinkedIn: https://www.linkedin.com/company/idea-pharma/   Listen to more fantastic podcast episodes: https://ideacollider.simplecast.com/

Gugs Mhlungu is joined by Dr. Omondi Ogude, a medical oncologito explain what mRNA vaccines for cancer are, how they work, and why they show promising potential in treating pancreatic cancer, known as one of the most aggressive and difficult cancers to manage. Gugs Mhlungu is your weekend companion for thoughtful conversations on lifestyle, health, culture, books, food, and everything happening around 702Land. Thanks for listening. Catch the 702 Weekend Breakfast with Gugs Mhlungu live on 702 every weekend morning from 6 am to 10 am (SA time). Find more from the show and catch-up podcasts on the Primedia+ app https://buff.ly/gk3y0Kj Subscribe to the 702 newsletters for more https://buff.ly/v5mfetc Let’s keep the conversation going online: 702 on Facebook: https://www.facebook.com/TalkRadio702 702 on TikTok: https://www.tiktok.com/@talkradio702 702 on Instagram: https://www.instagram.com/talkradio702/ 702 on X: https://x.com/Radio702 702 on YouTube: https://www.youtube.com/@radio702 See omnystudio.com/listener for privacy information.

"They are small, powerful little nuggets. They are actually small signaling proteins that our immune cells use to communicate. They really help regulate immune activation or inflammation and even the growth and survival of immune cells. When cytokines are used therapeutically in oncology, they help to stimulate immune cells such as T cells or natural killer cells to better recognize and attack cancer cells," Maribel Pereiras, PharmD, BCPS, BCOP, clinical pharmacy specialist at the John Theurer Cancer Center of Hackensack University Medical Center in New Jersey, told Jaime Weimer, MSN, RN, AGCNS-BS, AOCNS®, manager of oncology nursing practice at ONS, during a conversation about the cytokine drug class. Music Credit: "Fireflies and Stardust" by Kevin MacLeod Licensed under Creative Commons by Attribution 3.0  Earn 0.5 contact hours (including 30 minutes of pharmacotherapeutic content) of nursing continuing professional development (NCPD) by listening to the full recording and completing an evaluation at courses.ons.org by April 24, 2027. The planners and faculty for this episode have no relevant financial relationships with ineligible companies to disclose. ONS is accredited as a provider of nursing continuing professional development by the American Nurses Credentialing Center's Commission on Accreditation. Learning outcome: Nurses caring for people with cancer require knowledge of cytokines to provide appropriate education and to safely administer related therapies. Episode Notes  Complete this evaluation for free NCPD.  ONS Podcast™ episodes: Pharmacology 101 series Episode 256: Cancer Symptom Management Basics: Hematologic Complications Episode 196: Oncologic Emergencies 101: Bleeding and Thrombosis ONS Voice articles: FDA Approves Nogapendekin Alfa Inbakicept-Pmln for BCG-Unresponsive Non–Muscle Invasive Bladder Cancer Manage Cancer-Associated Anemia With Erythropoietin-Stimulating Agents Oncology Drug Reference Sheet: Motixafortide ONS books: Chemotherapy and Immunotherapy Guidelines and Recommendations for Practice (second edition) and 2024 Drug Supplement Clinical Guide to Antineoplastic Therapy: A Chemotherapy Handbook (fourth edition) Guide to Cancer Immunotherapy (second edition) Clinical Journal of Oncology Nursing article: Tumor-Infiltrating Lymphocyte Therapy for Melanoma: Nursing Considerations What's Old Is New Again, Unfortunately ONS Symptom Interventions Colony-Stimulating Factors Including Biosimilars for At-Risk Patients for Prevention of Infection: General Platelet Growth Factors for Prevention of Bleeding National Comprehensive Cancer Network To discuss the information in this episode with other oncology nurses, visit the ONS Communities. To find resources for creating an ONS Podcast club in your chapter or nursing community, visit the ONS Podcast Library. To provide feedback or otherwise reach ONS about the podcast, email pubONSVoice@ons.org. Highlights From This Episode "Cytokines are actually among some of the earliest forms of immunotherapy used in the treatment of cancer, and it really goes back to the 1980s and the 1990s. We're talking therapies like interferon [alpha] or interleukin-2 that were used to stimulate the immune system, with the idea that they would recognize and attack cancer cells, particularly in diseases like metastatic melanoma and renal cell carcinoma. What made these therapies unique was that although the overall response rates were relatively modest, when patients did respond, those responses could be very durable and sometimes long lasting. And that observation was really important for the field of oncology, because it was part of the process that demonstrated that the immune system could potentially control cancer in really meaningful ways." TS 1:49 "One nice new example of an engineered cytokine is nogapendekin alfa inbakicept, which is quite the tongue twister to say. … This agent is really interesting because it's an engineered interleukin-15 receptor agonist that works on stimulating natural killer cells and CD8-positive T cells. And what makes this so interesting is that it's used in combination with a medication that probably some of us are familiar with—good old BCG—for patients specifically with invasive bladder cancer. The other really interesting thing about this new therapy is the fact that it is one of our first ones to be engineered in a combination fashion. So the nogapendekin alfa is combined with a receptor component that is called inbakicept. And what happens is it forms a complex to enhance signaling and prolong the activity of the cytokine." TS 7:50 "When you're looking at our therapeutic cytokines, those tend to produce larger-scale systemic inflammatory effects leading to much more global side effect reactions, while your supportive care cytokines are more commonly associated with either bone marrow stimulation effects or hematologic changes." TS 14:01 "Regardless of what type of cytokine therapy may you be using, across the board, early recognition of the symptoms and proactive supportive care are really important. And this is where many of our oncology nurses play such a critical role in identifying changes that are happening in real time to the patient's condition and helping to coordinate, relay information to the rest of the providing team so that timely interventions can occur for the best care of the patient." TS 18:01 "The other fascinating thing about these cytokines is that they're not being used as monotherapy anymore. They're now being looked at in combination with other therapies or even other immunotherapies like our checkpoint inhibitors. They're being looked at in the sense that they may be able to help expand and further activate immune cells that our current therapies rely on. And so it's really interesting that while cytokines were some of the earliest forms of cancer immunotherapy, they're now being reimagined as part of modern combination strategies designed to really further help enhance the immune responses against cancer." TS 29:08

Recorded at the 2026 SCbio Annual Conference in Charleston, Heather and Matthew are joined by Dr. Besim Ogretmen, an internationally recognized cancer researcher at MUSC and Co-Founder and CEO of Lipo‑Immuno Tech. Dr. Ogretmen shares how his team is developing novel chemoimmunotherapy approaches designed to enhance immune cell function and improve outcomes for patients with advanced cancers. We also discussed building a biotech company from academic research, securing non‑dilutive funding, scaling manufacturing, and leveraging AI to support research and regulatory efforts. Tune in for an inside look at how their unique treatments are changing and extending patients' lives!

"You want to try to act quickly and be able to know what the pathways are for appropriate escalating when a patient is having symptoms that are reflective of cytokine release syndrome (CRS) or neurotoxicity. These toxicities are very manageable and treatable when recognized early. To summarize, choosing the right patient, knowing the toxicity profile for each product, and acting early is really what helps to prevent severe outcomes with chimeric antigen receptor (CAR) T-cell therapy," Maribel Pereiras, PharmD, BCPS, BCOP, clinical pharmacy specialist at the John Theurer Cancer Center at Hackensack University Medical Center in New Jersey, told Jaime Weimer, MSN, RN, AGCNS-BS, AOCNS®, manager of oncology nursing practice at ONS, during a conversation about CAR T-cell immunotherapy. Music Credit: "Fireflies and Stardust" by Kevin MacLeod Licensed under Creative Commons by Attribution 3.0  Earn 0.75 contact hours of nursing continuing professional development (NCPD) by listening to the full recording and completing an evaluation at courses.ons.org by March 20, 2027. The planners and faculty for this episode have no relevant financial relationships with ineligible companies to disclose. ONS is accredited as a provider of nursing continuing professional development by the American Nurses Credentialing Center's Commission on Accreditation. Learning outcome: Learners will report an increase in knowledge related to CAR T-Cell immunotherapy in the treatment of cancer. Episode Notes  Complete this evaluation for free NCPD.  ONS Podcast™ episodes: Pharmacology 101 series Episode 267: Side-Effect Management for CAR T-Cell Therapy for Hematologic Malignancies Episode 261: CAR T-Cell Therapy for Hematologic Malignancies Requires Education and Navigation Episode 176: Oncologic Emergencies 101: Cytokine Release Syndrome ONS Voice articles: A Body of Evidence Helps Nurses Manage CAR T-Cell Therapy Toxicities CAR T-Cell Therapy Programs Oncology Clinical Social Workers Add Layers of Support for Patients and Families During CAR T-Cell Therapy Studies Show Best Practices to Manage CAR T-Cell Therapies' irAEs and Improve Outcomes ONS Voice oncology drug reference sheet: Lisocabtagene Maraleucel Clinical Journal of Oncology Nursing articles: CAR T-Cell Therapy for Relapsed/Refractory Aggressive Large B-Cell Lymphoma CAR T-Cell Therapy: Updates in Nursing Management Nursing Considerations in Navigating Patients Receiving CAR T-Cell Therapy ONS book: Guide to Cancer Immunotherapy (second edition) ONS Huddle Cards: Chimeric Antigen Receptor T-Cell Therapy Cytokine Release Syndrome Immune Effector Cell–Associated Neurotoxicity Syndrome Immunotherapy Immuno-Oncology Learning Library American Society of Gene and Cell Therapy: Learning Center American Society for Transplantation and Cellular Therapy: Learning Center National Comprehensive Cancer Network home page To discuss the information in this episode with other oncology nurses, visit the ONS Communities.  To find resources for creating an ONS Podcast club in your chapter or nursing community, visit the ONS Podcast Library. To provide feedback or otherwise reach ONS about the podcast, email pubONSVoice@ons.org. Highlights From This Episode "CAR T-cell therapy combines an adoptive cell transfer with genetic engineering. And what that really means is that we are harvesting a patient's own T cells and then we engineer them with a synthetic receptor that helps them recognize that cancer. And all of this work has evolved through many decades of stepwise advances in how we design and activate the T cells. That led us to several landmark trials and ultimately the first CAR T-cell therapy approved by the U.S. Food and Drug Administration in 2017, which was tisagenlecleucel for pediatric and young adult patients that had acute lymphoblastic leukemia." TS 3:34 "If a patient has higher disease burden or an inflammatory biology, that does tend to correlate with higher toxicity risk. And then that might influence the way we monitor the patients who are getting the CAR T therapy. And then finally, baseline neurologic examinations, because neurotoxicity can occur with these agents. It's very important that we as a whole healthcare team really understand what the patient looks like at baseline to be able to determine if they're having any altered changes or confusion. If I had to summarize it, we want to confirm the target and make sure that we have the right CAR T product for the patient. We want to confirm that the patient, physiologically and mentally, is ready for the CAR T therapy." TS 10:53 "I think the two [toxicities] that every nurse will hear about almost immediately when talking about CAR T therapy are CRS or ICANS, which stands for immune effector cell–associated neurotoxicity syndrome. ... ICANS can either follow or even occur alongside CRS. And this can present as something as simple as just being slightly confused or altered, leading into progressively more severe elements such as word-finding difficulties, tremors, or changes in handwriting. Or even more severe cases that lead to seizures or decreased levels of consciousness. So, in this setting, neurologic assessments and knowing and understanding what your patient's baseline neurologic status is is so important. Those are really the two largest side effects that cross the board when it comes to CAR T therapies." TS 16:02 "In terms of the more practical aspects of administration, this is not a typical medication infusion. CAR T cells are living cells. So the way they are handled and administered is very specific. The majority of CAR T products are given as a single IV infusion. The cells come to us frozen either from a cellular lab or they will come from the pharmacy department. So those cells are typically thawed, and timing is of the essence. You really need to coordinate the timing of [thawing] to when they get infused to your patient. They tend to have a short shelf life once they're not frozen anymore." TS 26:34 "Now that therapy has, in many places, transitioned to be administered in the outpatient setting, education becomes absolutely critical. The patient is coming for their daily visit to clinic and then they're going home. And it's really up to the caregiver, who is usually not a nurse, who has to recognize early signs of toxicity. They need to be educated about what a fever is, what number constitutes a fever, what does confusion look like, what does hypotension look like? ... Do they have access to a thermometer? If you are asking them to look at blood pressure, do they have access to a blood pressure monitor? And sometimes those can be subtle things that might be overlooked. So, the emphasis in outpatient quality education is teaching those caregivers what to watch for, how to act quickly, and who to call immediately. You need to make sure that they have that information readily available if something happens." TS 30:55

What began as a harmless looking spot on Kevin Donaghy's forearm turned into a pair of diagnoses of skin cancer.  The first was Stage II in 2018, but 18 months later, it returned and was diagnosed Stage IV metastatic melanoma BRAF+.  The urologist said Kevin, an IT specialist from Melrose, Scotland, may have six months to live unless he underwent a newly-approved immunotherapy known as pembroluzimab.  That was in 2020, and Kevin is still with us.  The immunotherapy triggered a bout of ulcerative colitis, which left him bedridden for six months, but Kevin says his health is no different than it was before his diagnosis.   In late 2017, Kevin didn't give much thought to a spot he saw on his forearm.  He thought he might have cut himself and didn't know it.  When the spot didn't go away, he sought medical attention.  His doctor said the spot did not look cancerous, prescribed some cream for Kevin to rub on it, and said if the spot changes in size, shape or color, to come back.  The spot made none of those changes, but it also didn't go away.   Kevin was referred to a dermatologist, who called for a biopsy.  He was away on a business trip when he received an urgent phone call stating that Kevin needed to come in that afternoon.  He came in two days later and the dermatologist said the biopsy indicated Kevin had a cancerous tumor in his forearm.  Another biopsy was conducted to see if the cancer had spread to any lymph nodes and thankfully it hadn't.   Not long after the tumor was removed, Kevin received a phone call from the oncologist while walking in downtown Edinburgh.  The doctor told Kevin he was cancer free.  On the sidewalk, he dropped to his knee and wept, overcome with relief.  He thought the worst was over.   However, his health took a turn for the worse some 18 months later when he experienced severe back pain and sought medical attention.  Another biopsy revealed that the melanoma had spread, bypassing his lymph nodes, but resulting in tumors on his right lung and one next to his spine, which was the source of back pain.   Kevin was told he had six months to live unless a procedure involving an immunotherapy called pembroluzimab was successful.  The operation seemed to go well, but at its conclusion, Kevin had to periodically come in for CT scans.  A couple years later, Kevin was contacted by his urologist who said the immunotherapy had shrunk the tumors and again, he was told he was cancer free.   There was one more problem for Kevin.  The immunotherapy triggered ulcerative colitis, a chronic inflammatory disease.  He was bedridden for six months, but eventually survived that as well.   These days Kevin Donaghy says his health is just as sharp as it was prior to his diagnosis, and that going forward he "wants to do more."   He has gone on to write a book, "Stories of Hope and Cancer."  Thousands of copies have been donated to cancer charities around the United Kingdom.  It chronicles the stories of 39 cancer survivors.   Additional Resources:   Kevin's book: "Stories of Hope and Cancer," available on Amazon, with proceeds going to cancer charities throughout the United Kingdom.  

Today, Ivelisse talks with Dr. Dan Rubin, a naturopathic oncologist and co-founder of Naturopathic Specialists in Scottsdale, Arizona, about an emerging cancer treatment called dendritic cell therapy.Dr. Rubin explains in simple terms how dendritic cells act like “generals” of the immune system—gathering information about a tumor and teaching the body's T cells how to recognize and attack cancer. He discusses Immunocine's “double-loaded” dendritic cell therapy, which uses information from a patient's own tumor to help train the immune system in a more personalized way. This treatment is currently offered in Cancun and is also being studied in U.S. clinical trials for certain cancers, including glioblastoma and pancreatic cancer.They walk through what the process looks like for patients—from application and medical record review, to traveling for tumor sampling, collecting immune cells, and receiving a series of injections. Dr. Rubin also shares how tumor tissue can be stored for possible future use and talks honestly about outcomes, cost, and the importance of ongoing testing to determine who may benefit most.This episode provides hope-filled, easy-to-understand insight into a personalized, immune-based approach to cancer care for patients and caregivers alike.Learn more about Dr. Dan Rubin. Suggested Resources:Naturopathic Specialists in Scottsdale, AZAiresTech Products for EMF protectionHAVN by Lambs - EMF defracting productsImmunocine (Cancun)Immunocine Preserve (Biobank in Scottsdale)Send us Fan Mail! Click here >Your donations power our podcast's mission to support cancer patients with hope, insights, and resources. Every contribution fuels our ability to uplift and empower. Join us in making a lasting impact. Donate now!

Sarah Poland, MD, lead author of a recently published article in the journal ONCOLOGY titled Advances in Immunotherapy for Breast Cancer, highlighted key findings from her review in a conversation with CancerNetwork®.1 Throughout the discussion, she spoke about: Shifting Perspectives on Immunogenicity: Historically, breast cancer was considered a “cold,” poorly immunogenic tumor due to low tumor mutational burden (TMB) and few tumor-infiltrating lymphocytes (TILs). Poland highlighted how clinical research has shifted this perspective, particularly through the study of triple-negative breast cancer (TNBC), which often exhibits higher PD-L1 expression and immune infiltration.Key Clinical Milestones: The review highlighted foundational data that established immunotherapy as a standard of care: Early-Stage TNBC: The phase 3 KEYNOTE-522 trial (NCT03036488) established pembrolizumab (Keytruda) plus chemotherapy as a standard neoadjuvant treatment for stage II to III TNBC.2 Metastatic TNBC: The phase 3 KEYNOTE-355 trial (NCT02819518) demonstrated the benefit of pembrolizumab in PD-L1–positive metastatic disease.3 Managing Toxicity and Rechallenge: Poland addressed the feasibility of pembrolizumab rechallenge after an immune-related adverse effect (irAE), emphasizing that while possible, it requires a highly individualized approach based on the severity and timing of the initial toxicity.The Future Landscape: Beyond PD-1/PD-L1 inhibitors, the discussion covered emerging technologies that are poised to redefine treatment: Antibody-Drug Conjugates (ADCs): Exploration of novel combinations of ADCs with immunotherapy. Emerging Modalities: The potential role of bispecific antibodies and vaccine trials utilizing tumor antigens. Subtype Expansion: Emerging evidence supporting the efficacy of immunotherapy in hormone receptor–positive and HER2-positive subtypes, moving beyond the traditional focus on TNBC. Unmet Educational Needs: Poland emphasized the importance of resources that connect providers and patients, particularly in translating complex trial data into clinical practice and addressing patient concerns regarding the newest therapies and trials.Poland is from the Department of Medicine in the Section of Hematology/Oncology at The University of Chicago.References1.        Poland S, de Oliveira Andrade M, Nanda R. Advances in immunotherapy for breast cancer. Oncology (Williston Park). 2026;40(1):8-15. doi:10.46883/2026.259210612.        Schmid P, Cortes J, Pusztai L, et al. Pembrolizumab for early triple-negative breast cancer. N Engl J Med. 2020;382(9):810-821. doi:10.1056/NEJMoa19105493.        Cortes J, Rugo HS, Cescon DW, et al. Pembrolizumab plus chemotherapy in advanced triple-negative breast cancer. N Engl J Med. 2022;387(3):217-226. doi:10.1056/NEJMoa2202809

"Because the premise of immune checkpoint blockade centers around elevating the immune function, we should always take a great deal of caution around those patients who have high immune risks. Those include patients with autoimmune disorders. That's one of our biggest questions that we ask, usually every consult that we're seeing with solid tumor. 'Do you have any history of autoimmune disorders? Tell me a little bit more about it. Is it being treated? What are your symptoms like?' And then also patients who have undergone organ transplants. Now, interestingly, this does include stem cell transplants," Kelsey Finch, PharmD, BCOP, oncology pharmacist practitioner at Columbus Regional Health in Indiana, told Jaime Weimer, MSN, RN, AGCNS-BS, AOCNS®, manager of oncology nursing practice at ONS, during a conversation about checkpoint inhibitors. Music Credit: "Fireflies and Stardust" by Kevin MacLeod Licensed under Creative Commons by Attribution 3.0  Earn 0.5 contact hours of nursing continuing professional development (NCPD) by listening to the full recording and completing an evaluation at courses.ons.org by February 20, 2027. Kelsey Finch has disclosed a speakers bureau relationship with AstraZeneca. This financial relationship has been mitigated. ONS is accredited as a provider of nursing continuing professional development by the American Nurses Credentialing Center's Commission on Accreditation. Learning outcome: Learners will report an increase in knowledge related to checkpoint inhibitors in the treatment of cancer. Episode Notes  Complete this evaluation for free NCPD.  ONS Podcast™ episodes: Pharmacology 101 series Episode 273: Updates in Chemotherapy and Immunotherapy Episode 174: Administer Pembrolizumab Immunotherapy With Confidence Episode 139: How CAR and Other T Cells Are Revolutionizing Cancer Treatment ONS Voice articles: Here's Why Oncology Nurses Are Pivotal in Managing Immune-Related Adverse Events Make Subcutaneous Administration More Comfortable for Your Patients Nursing Considerations for ICI-Related Myocarditis Oncology Nurses Navigate the Changing Landscape of Immuno-Oncology Postdischarge ICI Patient Education Eliminates Hospital Readmissions Shorter Administration Times Still Require High-Acuity Care ONS Voice oncology drug reference sheets: Dostarlimab-Gxly Nivolumab and Hyaluronidase-Nvhy Nivolumab and Relatlimab-Rmbw Pembrolizumab and Berahyaluronidase Alfa-Pmph Retifanlimab-Dlwr Toripalimab-Tpzi ONS books: Chemotherapy and Immunotherapy Guidelines and Recommendations for Practice (second edition) Guide to Cancer Immunotherapy (second edition) ONS course: ONS/ONCC® Chemotherapy Immunotherapy Certificate™ Clinical Journal of Oncology Nursing articles: Immune Checkpoint Inhibitor–Related Myocarditis: Recognition, Surveillance, and Management Immune Checkpoint Inhibitor Therapy: Key Principles When Educating Patients Triple M Syndrome: Implications for Hematology-Oncology Advanced Practice Providers ONS Huddle Cards: Checkpoint Inhibitors Immunotherapy ONS Learning Libraries: Genomics and Precision Oncology Learning Library Immuno-Oncology Learning Library Drugs@FDA package inserts National Comprehensive Cancer Network homepage OncoLink: All About Immunotherapy To discuss the information in this episode with other oncology nurses, visit the ONS Communities.  To find resources for creating an ONS Podcast club in your chapter or nursing community, visit the ONS Podcast Library. To provide feedback or otherwise reach ONS about the podcast, email pubONSVoice@ons.org. Highlights From This Episode "Before immune checkpoint blockade, the two-year overall survival rate in metastatic melanoma was hovering around 10%. After these agents came to market, depending on the trial and the agents used, that number actually increased to about 50%–65%. So, five times the amount of patients were actually living at the two-year mark. Not surprisingly, studies then exploded across several tumor types, leading to approvals in all sorts of cancers, mostly in the solid tumor. But there are a couple hematologic as well. Lung cancer, kidney cancer, head and neck, Hodgkin lymphoma, hepatocellular, the list goes on. So, it's really just transforming the stage IV setting across all tumors, specifically from uniformly fatal prognosis to one where durable responses and long-term survival is also possible." TS 3:03 "There are four different mechanisms officially being used in therapies that are approved by the U.S. Food and Drug Administration (FDA). Those are cytotoxic T-lymphocyte–associated protein 4, programmed cell death protein 1, and programmed cell death ligand 1, which I'm counting as two different mechanisms, even though they somewhat work together. And lymphocyte-activation gene 3 is the fourth one that's in there. So, all these mechanisms impact the T cell in our immune system. The T cell is traditionally responsible for protecting our body from harmful things like bacteria, viruses, and cancer. When the tumor binds to cytotoxic T-lymphocyte–associated protein 4 receptors, that happens on the T cell itself. And that inhibits the activation of the T cells, essentially allowing that tumor to then live. So when developing medications that block this receptor, they noted an added benefit that it actually increased the T-cell proliferation as well as keeping that T cell active. So not only are we not blocking the T cells, we're making them more productive." TS 5:38  "If you have a chance of any sort of tissue rejection, specifically with allogeneic stem cell transplants or where we see that focusing on it, there's a little bit of controversy, mixed bag on opinions as far as autologous stem cell transplants. But it's best to at least exercise a little bit of caution. If they have a chance of organ rejection, is that worth the risk of the therapy that we're looking to give? And then, patients with HIV, any sort of immunologic concerns at baseline that we could potentially worsen." TS 14:37 "As a rule of thumb, with immune checkpoint blockade, regardless of what mechanism you're looking at, if something in your body can get inflamed, that can wind up as an adverse event. So, whenever I talk to my patients, the key word is anything ending in '-itis.' ... The most common adverse events that we end up seeing are dermatitis and hypothyroidism. Immune checkpoint blockade can cause both hyper- and hypothyroidism. Very often, we actually start in the hyper- and then end up, for lack of better words, burning out the thyroid, ultimately leading to a sustained hypothyroidism." TS 18:34 "The half-life of immune checkpoint inhibitors is usually around 30 days, meaning that once these agents are given, the drug will be in the patient's system for up to five months. Specifically, it will probably build month to month, so often we don't even see a lot of our adverse events until month three or four. Usually, when we're that far into treatment, we're not looking for new adverse events in things like chemotherapy. But these drugs do build over time." TS 24:28 "As far as safe handling is concerned, these agents are not chemotherapy. That makes drug compounding and administration pretty straightforward. When looking at the follow-up care, the most important thing, in my opinion, is to engage in meaningful dialogue with your patients. A lot of the side effects can be nonspecific. So, really listening to the patient and evaluating changes in their lifestyle, I think it'll get you far. We usually hark in on the new, worsening, or persistent whenever we're talking to patients because they'll be looking for things as well. So, just having a dialogue of how their life has changed can certainly help." TS 26:17

In this episode of Curing with Sound, we speak with Natasha Sheybani, PhD, assistant professor of biomedical engineering at the University of Virginia (UVA) and research director of the UVA Focused Ultrasound Cancer Immunotherapy Center. Dr. Sheybani shares insights into her groundbreaking work using focused ultrasound–based immunotherapy approaches in patients with metastatic breast cancer and other solid tumors. She explains how precisely delivered sound waves can do more than destroy tumors—helping to reshape the tumor microenvironment, overcome immune evasion, and activate the immune system to recognize and attack cancer cells. The conversation also explores Dr. Sheybani's strong commitment to mentorship and interdisciplinary training, as well as her efforts to integrate patient advocates directly into the research process. Discussion Highlights: Sheybani Lab Research: The lab explores how focused ultrasound can help activate the immune system and improve the delivery of immunotherapy drugs to solid tumors, including brain cancers such as glioblastoma and metastatic breast cancer. Era of Hope Scholar Award: Learn about the prestigious $5.5 million Department of Defense grant awarded to Dr. Sheybani—the first ever at UVA—to accelerate the development of focused ultrasound technologies that improve the safety, effectiveness, and precision of immunotherapy for patients with breast cancer. Patient-Centered Science: Hear how Dr. Sheybani is redefining the research process by integrating breast cancer survivors directly into her grant writing and experimental design, fostering scientific innovation that is deeply informed by real-world patient experience.  EPISODE TRANSCRIPT ---------------------------- QUESTIONS? Email podcast@fusfoundation.org if you have a question or comment about the show, or if you would you like to connect about future guest appearances.  Email info@fusfoundation.org if you have questions about focused ultrasound or the Foundation.  FUSF SOCIAL MEDIA LinkedIn X Facebook Instagram TikTok YouTube FUSF WEBSITE https://www.fusfoundation.org SIGN UP FOR OUR FREE NEWSLETTER https://www.fusfoundation.org/newsletter-signup/ READ THE LATEST NEWSLETTER https://www.fusfoundation.org/the-foundation/news-media/newsletter/ DOWNLOAD "THE TUMOR" BY JOHN GRISHAM (FREE E-BOOK) https://www.fusfoundation.org/read-the-tumor-by-john-grisham/

How has immunotherapy evolved in the last decade? In this episode of The Chain, Laszlo Radvanyi, professor of immunology at the University of Toronto, discusses his years-long research on cancer immunotherapy, including his time at MD Anderson, with host Rakesh Dixit. He shares his thoughts on agonist antibodies, the true breakthroughs that are moving the needle for patients, reducing the CD-28 pathway so that it doesn't produce cytokine toxins, and what is the next frontier in immunotherapy. Links from this episode:  EpiVax University of Toronto, Department of Immunology University of Toronto  

Broadcast from KSQD, Santa Cruz on 1-01-2025: An emailer asks about omega-3 supplementation for memory at age 72. Dr. Dawn advises checking that fish oil capsules contain adequate DHA—at least 1,000 mg—since many omega-3 products have low DHA levels. She notes Medicare covers the same testing at standard labs as proprietary labs like OmegaQuant that charge patients directly. Beyond omega-3s, she emphasizes glucose control (hemoglobin A1c below 5.6) since the enzyme that breaks down insulin also clears beta-amyloid, and weight training to raise brain-derived neurotrophic factor (BDNF), which promotes new synapse formation essential for memory. Dr. Dawn reviews Popular Science's top 2025 health innovation: eye drops from Lens Therapeutics containing aceclidine that correct age-related farsightedness for 10 hours. The drops shrink the pupil to increase depth of field, improving near vision by three or more lines on eye charts within 30 minutes without affecting distance vision. Side effects include eye irritation, dimmed night vision, and headache. She describes Duke University's breakthrough allowing heart transplants from circulatory death donors using an on-table reanimation technique. This could expand the pediatric donor pool by 20%—critical since up to 20% of children die waiting for transplants. Dr. Dawn celebrates CAR-T immunotherapy for multiple myeloma, which saved her husband's life. Of 97 heavily pretreated patients, 38% achieved complete remission still present at five years, with over 50% total survival. The therapy removes T-cells, uses CRISPR to add receptors targeting cancer cell antigens, then reinfuses the modified cells. She highlights a UC Davis study showing remote blood pressure monitoring with home technology, education, and coaching dropped patients' average blood pressure from 150/80 to 125/74 in months—low-tech with high impact. Dr. Dawn explains the Nano Knife for prostate cancer, which uses localized electrical pulses delivered through thin wires to destroy tumors while sparing surrounding nerves. This minimally invasive approach could reduce erectile dysfunction and incontinence common with traditional surgery. She describes Gilead's Sunlenca, a twice-yearly injection for HIV prevention that's 99% effective. At $14,000 per injection in the US, proceeds help fund access in resource-limited countries where it can be distributed like a vaccination. Dr. Dawn discusses Journavx (suzetrigine), a new non-opioid pain medication working on sodium channels to block pain signals before reaching the brain. At $30 for 50 pills on GoodRx, it offers an alternative for surgical pain in patients with addiction history or genetic vulnerability to opioid dependence. She details the landmark case of Baby KJ, the first person to receive personalized CRISPR gene therapy. Born with a CPS1 enzyme deficiency causing toxic ammonia buildup, KJ was too small for liver transplant. Scientists identified his specific mutation and used CRISPR base editing delivered via lipid nanoparticles to correct a single DNA letter—changing an A to G—in his liver cells which restored enough function to be discharged home. Dr. Dawn reports surprising findings that COVID mRNA vaccines amplify cancer immunotherapy. Lung cancer patients who received COVID vaccination within 100 days of checkpoint inhibitor treatment had 56% three-year survival versus 31% for unvaccinated patients. The mechanism is unknown but may involve mRNA generally alerting the immune system. She revisits research showing Zostavax shingles vaccination reduced dementia risk by 20% over seven years. A natural experiment in Wales—where an age cutoff created comparable vaccinated and unvaccinated groups—provided strong evidence that preventing herpes zoster inflammation protects brain health. Dr. Dawn concludes with Huntington's disease breakthrough: microRNA therapy delivered by virus directly into the brain slowed disease progression by 75% over three years. The microRNA binds to Huntington protein mRNA, preventing ribosome translation and toxic protein production. Some patients returned to work; others expected to need wheelchairs are still walking.

In this episode of Spark Time!, we speak with Øystein Rekdal, co-founder and CEO of Lytix Biopharma, about how the company reimagined host-defense peptides as a new class of oncolytic molecules for cancer immunotherapy.Øystein shares the full arc of Lytix's development, from an academic discovery in Norway to a clinical-stage platform built around locally administered oncolytic molecules designed to activate the immune system where standard treatments fall short. We explore how Lytix isolated and engineered naturally occurring peptides into drug candidates with clinical momentum, and why this approach differs fundamentally from both traditional cytotoxic agents and oncolytic viruses.The conversation dives into how Lytix's lead program induces immunogenic cell death, exposes tumor antigens, and initiates a broad immune response that extends beyond the treated lesion. We also discuss the company's strategic focus on combination and neo-adjuvant settings, its rationale for intratumoral delivery, and how this platform is positioned to address non-responsive solid tumors.A thoughtful discussion for biotech leaders, investors, and partners interested in differentiated immunotherapy platforms and the strategic decisions required to translate novel biology into real clinical relevance.

Good morning from Pharma Daily: the podcast that brings you the most important developments in the pharmaceutical and biotech world. Today, we are diving into a series of significant breakthroughs and updates that are shaping the industry landscape.Starting with a remarkable scientific advancement, researchers have made headway in the development of a new class of antibiotics that shows promise against drug-resistant bacteria. This comes as a beacon of hope in the ongoing battle against superbugs, a problem that has been escalating over the past few decades. The new antibiotics work by targeting bacterial cell walls in a novel way, which may bypass the resistance mechanisms that have rendered many traditional antibiotics ineffective. This innovation could potentially extend the lifespan of existing drugs and provide new treatment options for infections that are currently difficult to manage. It's crucial to monitor how these developments will proceed through clinical trials and regulatory scrutiny, as successful outcomes could revolutionize our approach to bacterial infections.Shifting focus to regulatory news, the FDA has recently approved a groundbreaking gene therapy for a rare genetic disorder affecting children. The therapy is designed to target and correct specific genetic mutations, offering hope for families affected by this debilitating condition. This approval not only marks a milestone for personalized medicine but also sets a precedent for future gene therapies targeting other rare diseases. The implications of such advancements are vast, as they open doors to tailored treatments that address the root causes of genetic disorders rather than just managing symptoms. As we continue to explore the potential of gene editing technologies like CRISPR, it's important to consider both the ethical and logistical challenges that accompany these scientific leaps.In clinical trial news, a late-stage study has shown promising results for a new cancer immunotherapy targeting non-small cell lung cancer. This therapy leverages the body's immune system to identify and destroy cancer cells more effectively than traditional treatments. The trial demonstrated significant improvements in patient survival rates and quality of life, underscoring the potential of immunotherapies to transform oncology care. These findings add to a growing body of evidence supporting immunotherapy as a cornerstone of future cancer treatment regimens. However, it is essential to continue researching how these therapies can be optimally combined with existing treatments to enhance outcomes and minimize side effects.Turning our attention to industry trends, there is an increasing emphasis on digital health solutions in drug development processes. Pharmaceutical companies are integrating artificial intelligence and machine learning technologies to streamline clinical trials and accelerate drug discovery. These digital tools enable more efficient data analysis, patient monitoring, and predictive modeling, which can significantly reduce development timelines and costs. As this trend gains momentum, it will be important to assess how these technologies can be best utilized without compromising data integrity or patient safety.Lastly, let's discuss an interesting development in sustainable biomanufacturing practices. Companies are investing in greener production methods that reduce environmental impact while maintaining high-quality standards for pharmaceuticals. This includes optimizing energy use, minimizing waste, and incorporating renewable resources into manufacturing processes. As regulatory bodies increasingly prioritize sustainability, we can expect these practices to become more widespread across the industry.These stories highlight how innovation continues to drive progress within pharmaceuticals and biotechnology, offering new possibilities for treatment and care. As always, it's eSupport the show

Drs Joseph Mikhael and Shaji Kumar discuss the future of multiple myeloma, including enhanced diagnostics for detecting myeloma, frontline therapy, and durable responses. Relevant disclosures can be found with the episode show notes on Medscape https://www.medscape.com/viewarticle/1002718. The topics and discussions are planned, produced, and reviewed independently of advertisers. This podcast is intended only for US healthcare professionals. Resources Multiple Myeloma https://emedicine.medscape.com/article/204369-overview Updated Diagnostic Criteria and Staging System for Multiple Myeloma https://pubmed.ncbi.nlm.nih.gov/27249749/ Mass Spectrometry for the Evaluation of Monoclonal Proteins in Multiple Myeloma and Related Disorders: An International Myeloma Working Group Mass Spectrometry Committee Report https://pubmed.ncbi.nlm.nih.gov/33563895/ Multiple Myeloma Imaging https://emedicine.medscape.com/article/391742-overview Next-Generation Biomarkers in Multiple Myeloma: Understanding the Molecular Basis for Potential Use in Diagnosis and Prognosis https://pubmed.ncbi.nlm.nih.gov/34299097/ Monoclonal Gammopathy of Undetermined Significance https://www.ncbi.nlm.nih.gov/books/NBK507880/ Primary Plasma Cell Leukemia: Consensus Definition by the International Myeloma Working Group According to Peripheral Blood Plasma Cell Percentage https://pubmed.ncbi.nlm.nih.gov/34857730/ Advancing MRD Detection in Multiple Myeloma: Technologies, Applications, and Future Perspectives https://pubmed.ncbi.nlm.nih.gov/40214184/ Genomic Landscape of Multiple Myeloma and Its Precursor Conditions https://pubmed.ncbi.nlm.nih.gov/40399554/  Quadruplet Regimens for Patients With Newly Diagnosed Multiple Myeloma: A Systematic Review and Meta-Analysis https://pubmed.ncbi.nlm.nih.gov/39348665/ Subcutaneous Daratumumab (Dara) + Bortezomib/Lenalidomide/Dexamethasone (VRd) With Dara + Lenalidomide (DR) Maintenance in Transplant-Eligible (TE) Patients With Newly Diagnosed Multiple Myeloma (NDMM): Analysis of Sustained Minimal Residual Disease Negativity in the Phase 3 PERSEUS Trial https://ascopubs.org/doi/10.1200/JCO.2025.43.16_suppl.7501 Isatuximab, Carfilzomib, Lenalidomide, and Dexamethasone Induction in Newly Diagnosed Myeloma: Analysis of the MIDAS Trial https://pubmed.ncbi.nlm.nih.gov/39841461/ Comparing Combinations of Drugs to Treat Newly Diagnosed Multiple Myeloma (NDMM) When a Stem Cell Transplant Is Not a Medically Suitable Treatment https://www.clinicaltrials.gov/study/NCT05561387 Cytokine Release Syndrome and Associated Neurotoxicity in Cancer Immunotherapy https://pubmed.ncbi.nlm.nih.gov/34002066/ The Role of CELMoD Agents in Multiple Myeloma https://pmc.ncbi.nlm.nih.gov/articles/PMC12399888/ Phase 2 Study of Talquetamab + Teclistamab in Patients With Relapsed/Refractory Multiple Myeloma and Extramedullary Disease: REDIRECTT-1 https://library.ehaweb.org/eha/2025/eha2025-congress/4173809/shaji.kumar.phase.2.study.of.talquetamab.2B.teclistamab.in.patients.with.html Discovery of a Novel Class NSD2 Inhibitor for Multiple Myeloma With t(4;14) https://pubmed.ncbi.nlm.nih.gov/40949769/ Long-Term (≥5 Year) Remission and Survival After Treatment With Ciltacabtagene Autoleucel (Cilta-Cel) in CARTITUDE-1 Patients (Pts) With Relapsed/Refractory Multiple Myeloma (RRMM) https://ascopubs.org/doi/10.1200/JCO.2025.43.16_suppl.7507

"I'll go back to the backpack analogy. When your kids come home with a backpack, all of a sudden their homework is not on the desk where it's supposed to be. It's in the kitchen; it kind of spreads all over the place, but it's still in the house. When we give antibody–drug conjugates (ADCs), the chemotherapy does go in, but then it can kind of permeate out of the cell membrane and something right next to it—another cancer cell that might not look exactly like the cancer cell that the chemotherapy was delivered into—is affected and the chemotherapy goes over to that cancer cell and kills it," ONS member Marisha Pasteris, OCN®, office practice nurse in the breast medicine service at Memorial Sloan Kettering Cancer Center in New York, NY, told Jaime Weimer, MSN, RN, AGCNS-BS, AOCNS®, manager of oncology nursing practice at ONS, during a conversation about ADCs in metastatic breast cancer. Music Credit: "Fireflies and Stardust" by Kevin MacLeod Licensed under Creative Commons by Attribution 3.0  This podcast is sponsored by Gilead and is not eligible for NCPD contact hours. ONS is solely responsible for the criteria, objectives, content, quality, and scientific integrity of its programs and publications.  Episode Notes  This episode is not eligible for NCPD. ONS Podcast™ episodes: Episode 391: Pharmacology 101: Antibody–Drug Conjugates Episode 378: Considerations for Adolescent and Young Adult Patients With Metastatic Breast Cancer Episode 368: Best Practices for Challenging Patient Conversations in Metastatic Breast Cancer Episode 350: Breast Cancer Treatment Considerations for Nurses Episode 303: Cancer Symptom Management Basics: Ocular Toxicities ONS Voice articles: An Oncology Nurse's Guide to Cancer-Related Ocular Toxicities Black Patients With Metastatic Breast Cancer Are Less Informed About Their Clinical Trial Options Communication Case Study: Talking to Patients About Progressive Metastatic Breast Cancer What Is HER2-Low Breast Cancer? ONS Voice drug reference sheets: Belantamab mafodotin-blmf Datopotamab deruxtecan-dlnk Enfortumab vedotin-ejfv Fam-trastuzumab deruxtecan-nxki ONS books: Chemotherapy and Immunotherapy Guidelines and Recommendations for Practice (second edition) Guide to Breast Care for Oncology Nurses Guide to Cancer Immunotherapy (second edition) ONS courses: ONS Fundamentals of Chemotherapy and Immunotherapy Administration™ ONS/ONCC® Chemotherapy Immunotherapy Certificate™ Clinical Journal of Oncology Nursing article: Antibody–Drug Conjugates and Ocular Toxicity: Nursing, Patient, and Organizational Implications for Care The Association Between Hormone Receptor Status and End-of-Life Care Among Patients With Metastatic Breast Cancer Oncology Nursing Forum article: Impact of Race and Area Deprivation on Triple-Negative Metastatic Breast Cancer Outcomes ONS huddle cards: Altered Body Image Huddle Card Chemotherapy Huddle Card Targeted Therapy Huddle Card Foundations of Antibody–Drug Conjugate Use in Metastatic Breast Cancer: A Case Study ONS Biomarker Database (refine by breast cancer) ONS Breast Cancer Learning Library American Society of Clinical Oncology (ASCO) homepage Drugs@FDA package inserts National Comprehensive Cancer Network homepage Susan G. Komen metastatic breast cancer page To discuss the information in this episode with other oncology nurses, visit the ONS Communities.  To find resources for creating an ONS Podcast club in your chapter or nursing community, visit the ONS Podcast Library. To provide feedback or otherwise reach ONS about the podcast, email pubONSVoice@ons.org. Highlights From This Episode "What an ADC is doing is taking the antibody and linking it to a cytotoxic chemotherapy with the idea of delivering it directly into the cell. How I explain this to new nurses or patients is a backpack analogy. If we think of it as a HER2 molecule wearing a chemo backpack, it's going to find the HER2 receptor attached to it and then drop the chemotherapy into the cell via the backpack. Similar to how we come home from work, we open the key to our door, we're carrying all of our items, and then we drop our own personal items in our house." TS 2:30 "The reason that so many patients with metastatic breast cancer are able to receive ADC therapy is because they are targeting two very common antibodies that we see in breast cancer. One is HER2 and the other is trophoblast cell surface antigen 2 (TROP2). These are seen across the board. We see these on triple-negative breast cancers, hormone receptor–positive cancers, and HER2-positive breast cancers. And now we have a new way to talk about HER2, which is a HER2-low. ... Recently, we have found that patients who express low levels of HER2 are able to receive ADC therapy, specifically fam-trastuzumab deruxtecan." TS 4:21 "Another [ADC] that has just been approved is datopotamab deruxtecan. This is another ADC that targets the TROP2 receptor on a cancer cell. This one carries a lot of side effects. I mentioned earlier that you need an ophthalmology clearance because there is a lot of ocular toxicity around this one. We see a lot of blepharitis, conjunctivitis, there can be blurred vision. Another thing we monitor on this one is mucositis. In the package insert, there's a recommendation for using ice chips while receiving the treatment. ... Then in the HER2-positive and HER2-low space is the big one, which is fam-trastuzumab deruxtecan. This was approved in 2019 for the HER2-positive patients, then more recently in the HER2-low [patients]. The big [side effect] with this one is interstitial lung disease." TS 10:11 "Interstitial lung disease is an inflammation or a little bit of fibrosis within the lung that causes an impaired exchange between the oxygen and carbon dioxide. This was seen in the clinical trials, specifically around fam-trastuzumab deruxtecan. During the trials, they had a very small percentage, I think it was 1%, that died due to interstitial lung disease. So, this is a very important side effect for us as nurses to be aware of. It typically presents in patients like a dyspnea. A lot of times, it's like, 'Well, I used to be able to walk my kid to the bus stop, but now when I walk there, I feel really short of breath.' Or 'I've had this dry cough for the past couple weeks and I've tried medications, but haven't had that relieved.' So, we really need to be aware of that because early intervention in interstitial lung disease is key." TS 12:57 "ADCs are toxic drugs. They have the benefit of being targeted, but we know that they carry a lot of side effects. ... Their specificity makes them so wonderful and we've seen amazing responses to these drugs. But also, we want patients to be safe. We want to give these drugs safely. So, we have to assess our patients and make sure that this is an appropriate patient to give this therapy to. I think that's an open conversation that clinicians need to have with patients regarding these drugs." TS 18:08

"It's critical to identify those mutations found that are driving the cancer's growth and guide the personalized treatment based on those results. And important to remember, too, early testing is crucial for patients with non-small cell lung cancer (NSCLC). In studies, it has been found to be associated with improved survival outcomes and reduced mortality," ONS member Vicki Doctor, MS, BSN, BSW, RN, OCN®, precision medicine director at the City of Hope Atlanta, GA, Chicago, IL, and Phoenix, AZ, locations, told Jaime Weimer, MSN, RN, AGCNS-BS, AOCNS®, manager of oncology nursing practice at ONS, during a conversation about the oncology nurse's role in NSCLC biomarker testing. Music Credit: "Fireflies and Stardust" by Kevin MacLeod Licensed under Creative Commons by Attribution 3.0  This podcast is sponsored by Lilly Oncology and is not eligible for NCPD contact hours. ONS is solely responsible for the criteria, objectives, content, quality, and scientific integrity of its programs and publications. Episode Notes  This episode is not eligible for NCPD. ONS Podcast™ episodes: Episode 363: Lung Cancer Treatment Considerations for Nurses Episode 359: Lung Cancer Screening, Early Detection, and Disparities Episode 238: Cancer Genomics for Every Oncology Nurse Episode 157: Biomarker Testing Improves Outcomes for Patients With Non-Small Cell Lung Cancer ONS Voice articles: Non-Small Cell Lung Cancer Prevention, Screening, Diagnosis, Treatment, Side Effects, and Survivorship Only a Third of Patients With Advanced Cancer Get Biomarker Testing, Limiting Use of Potentially Effective Precision Therapies Precision Medicine in Lung Cancer: How Comprehensive Testing Optimizes Patient Outcomes Targeted Therapies Are Transforming the Treatment of Non-Small Cell Lung Cancer ONS book: Guide to Cancer Immunotherapy (second edition) ONS course: Genomic Foundations for Precision Oncology Clinical Journal of Oncology Nursing article: Using Nurse Navigators to Improve Timeliness of Biomarker Testing for Non-Small Cell Lung Cancer Oncology Nursing Forum article: Precision Medicine Testing and Disparities in Health Care for Individuals With Non-Small Cell Lung Cancer: A Narrative Review Other ONS resources: Best Practices for Biomarker Testing in Non-Small Cell Lung Cancer: A Case Study Genomics and Precision Oncology Learning Library Genomics Case Study: Precision Medicine in the Setting of Metastatic Non-Small Cell Lung Cancer Biomarker Database (refine by non-small cell lung cancer) Genomic Biomarkers Huddle Card Targeted Therapy Huddle Card National Comprehensive Cancer Network homepage To discuss the information in this episode with other oncology nurses, visit the ONS Communities.  To find resources for creating an ONS Podcast club in your chapter or nursing community, visit the ONS Podcast Library. To provide feedback or otherwise reach ONS about the podcast, email pubONSVoice@ons.org Highlights From This Episode "These biomarkers are used to provide information about cancer's characteristics or behavior. In oncology precision medicine specifically, molecular tests can help with diagnosing a cancer that is maybe an unknown primary. It can help with monitoring response to therapy, detect recurrence of disease before other tests can find that, predict prognosis or how aggressive the cancer may be, and guide treatment decisions for targeted therapies." TS 3:14 "Some of the key biomarkers recommended by the National Comprehensive Cancer Network (NCCN) to be tested in patients who have NSCLC are EGFR, ALK, KRAS, BRAF, MET exon 14 skipping mutation, HER2 which is a protein expression from an ErbB protein, PD-L1 which is a protein expression that's used to guide immunotherapy choices, and then finally there are three fusions: ROS1, RET, and NTRK. [These] are pretty rare but really important to be tested for in patients who have NSCLC." TS 3:46 "Another important challenge for nurses related to this topic is that these results may not reveal a targeted mutation for the patient and that could be very disappointing. So, being able to provide that emotional support to a patient if they have that result … you can actually reinforce with them that if [they] go onto another treatment that the physician decides to put [them] on, the tumor can change. New pathogenic variants can develop based on the treatment that they're getting, and another test can be done. And maybe at that time—a new biomarker that could be targeted—we'd be seeing on the new test." TS 7:32  "Another circumstance we didn't talk about yet is that maybe the result came back saying that the quality was not sufficient. And sometimes that happens, but that doesn't mean that we're at the end of the road, necessarily. So, you could explain to the patient that that may mean that possibly, a new biopsy would be ordered by the physician. Or if a new biopsy or another tissue sample is not available, then maybe the physician would pivot to sending a blood specimen for the molecular testing. So that would definitely be a way [nurses] could support their patients." TS 11:52 "In the case of patients with NSCLC, early testing is so important. So, advocating for that prompt biomarker testing to be done, making sure that it's comprehensive, that it's actually looking for all of those—I think it was 12 biomarkers—that I mentioned earlier. That this testing is done as soon as possible after diagnosis or progression. Something that I talk about all the time—personalized care, precision medicine—really matters. So, tailoring treatments for patients based on the biology of the tumor that's driving the cancer's growth is really crucial if you're going to be working as an oncology nurse. Another crucial thing, because it's changing so quickly, is to stay informed." TS 16:23

Professor Aideen Ryan, Professor in Tumour Immunology at University of Galway's College of Medicine, Nursing and Health Sciences. Photo: Andrew Downes Researchers at the University of Galway have revealed the results of a world-first study into how bowel cancer shuts down the immune system, and how this can be reversed to improve treatment. The findings have been published in the Journal for ImmunoTherapy of Cancer (JITC). Breakthrough for bowel cancer immunotherapy The research team showed how structural stromal cells switch off the immune system and how the body's own killer cells can be switched back on, opening up the opportunity for a completely new approach to optimising immunotherapy for patients. Colorectal cancer - commonly referred to as bowel cancer - is one of the world's most common cancers and the second leading cause of cancer death worldwide. Diagnoses in people under 50 have been climbing in recent decades, with recent global analysis showing these early-onset cases have almost doubled since 1990. In Ireland, the disease affects more than 2,500 people a year. Professor Aideen Ryan, Professor in Tumour Immunology at University of Galway's College of Medicine, Nursing and Health Sciences, said: "While immunotherapy has revolutionised care in cancers such as melanoma and lung cancer, it has shown very limited benefit in bowel cancer, leaving patients with advanced disease with few treatment options and poor survival outcomes." The breakthrough research discovery is the first to demonstrate that tumour stromal cells - the structural cells that support cancer growth - are directly reprogramming the immune system. They do this by switching off, or hijacking, two of our body's most important tumour-fighting cells - the natural killers (NK) and macrophages - rendering them unable to attack the cancer. Professor Ryan said: "The interaction between the cancer, our body's healthy cells and our defence mechanism is a complex one, but our research shows that the cancer is essentially creating an immune brake - it is blocking the body's natural response and fight mechanism." What has been discovered in relation to how the cancer interacts with the human body? Tumour stromal cells are the structural cells which allow the cancer to grow. They are coated in sugars called sialoglycans. These interact with receptors on the body's immune cells called Siglecs. This interaction causes the body's natural defence response to be switched off and unresponsive when immunotherapy is used, and therefore unable to attack the cancer. The research identified a specific enzyme that drives this process of 'switching off', as it produces the Siglec-binding sugars on stromal cells. When the researchers blocked this pathway using drugs called sialidases, they could show that the body's most important tumour-fighting cells - the natural killers (NK) and macrophages - reactivated. It showed that the tumours shrank and the spread of cancer, known as metastasis, was prevented. The multidisciplinary research was conducted in collaboration with colorectal surgeons and pathologists at Galway University Hospital, led by Professor Aisling Hogan and Professor Sean Hynes; as well as experts in colorectal cancer - Dr Philip Dunne, Queen's University Belfast and experts in targeting sialoglycans at Palleon Pharmaceuticals, MA, USA, who have developed sialidase drugs that disrupt the sialoglycan-Siglec interaction. Professor Ryan added: "Our research is a clear breakthrough in our understanding of bowel cancer and how immunotherapy could be more successful. This world-first finding shows that some of the bowel cancer cells are not just passive bystanders, they are actively reprogramming the body's immune cells, preventing them from doing their job. We have uncovered an entirely new checkpoint and by focusing on it we can reactivate the immune system and improve our body's innate ability to fight the disease, and even target metastasis." Michael O'Dwyer, Pro...

New research into bowel cancer has identified ways to reactivate the immune system, to help tackle the spread of the condition. For more Professor Aideen Ryan is a Professor in Tumour Immunology at University of Galway.

Bioengineer Michael Fischbach studies alternative vaccine delivery methods, like self-administered creams with no needles, health professionals, or side effects. He teases a day when vaccines that don't make you feel bad come in the mail in ketchup-style packets. Such innovations would greatly improve vaccine uptake, especially in developing countries, and speed global response to novel viruses. It would change how we think about vaccines, Fischbach tells host Russ Altman on this episode of Stanford Engineering's The Future of Everything podcast.Have a question for Russ? Send it our way in writing or via voice memo, and it might be featured on an upcoming episode. Please introduce yourself, let us know where you're listening from, and share your question. You can send questions to thefutureofeverything@stanford.edu.Episode Reference Links:Stanford Profile: Michael FischbachConnect With Us:Episode Transcripts >>> The Future of Everything WebsiteConnect with Russ >>> Threads / Bluesky / MastodonConnect with School of Engineering >>> Twitter/X / Instagram / LinkedIn / FacebookChapters:(00:00:00) IntroductionRuss Altman introduces guest Michael Fischbach, a professor of bioengineering at Stanford University.(00:04:24) Cream-Based VaccinesThe discovery that revealed the skin's ability to spark systemic immunity.(00:07:36) Engineering ImmunityModifying staph epidermidis to carry antigens and test immune response.(00:09:38) Tumor RegressionHow engineered bacteria triggered tumor-killing immunity in mice.(00:12:53) Antibody DiscoveryEvidence that skin exposure can generate long-lasting antibodies.(00:17:02) Antibody Response in HumansWhether humans show antibody responses to their own skin bacteria.(00:18:42) Turning Bacteria into VaccinesEmbedding harmless pathogen fragments into bacterial surface proteins.(00:20:55) Immunity Without ShotsHow mice achieved vaccine-level immunity through topical application.(00:24:00) Reimagining Vaccine DeliveryThe potential for self-applied, needle-free, and multiplexed vaccines.(00:26:50) Mechanism Behind Skin ImmunityHow skin immune cells may constantly sample microbes for defence.(00:28:14) Next Steps in DevelopmentThe path toward testing safety, dosage, and delivery in higher models.(00:29:57) Choosing Vaccine TargetsViruses and diseases that could be targets for early skin-based vaccines.(00:31:11) Safety and ReversibilityEnsuring safety with reversible bacteria and limited trial participants.(00:33:04) Transitioning to BiotechTransitioning research from Stanford to large-scale biotech development.(00:34:31) Future In a MinuteRapidfire Q&A: creative science, vaccine innovation, and biology's future.(00:36:56) Conclusion Connect With Us:Episode Transcripts >>> The Future of Everything WebsiteConnect with Russ >>> Threads / Bluesky / MastodonConnect with School of Engineering >>>Twitter/X / Instagram / LinkedIn / Facebook Hosted by Simplecast, an AdsWizz company. See pcm.adswizz.com for information about our collection and use of personal data for advertising.

“I think that this is an area that is exploding. Working with drug development, I see new agents all the time, with unique targets I've never heard about, with targets I have heard about used in a different way. So, I really think we're going to see more and more bispecifics. A lot of these drugs are used second line, third line, fourth line. I would not be surprised if they moved up in treatment, especially as we learn safer ways to give these drugs,” ONS member Moe Schwartz, PharmD, BCOP, FHOP, professor of pharmacy practice at the James L. Winkle College of Pharmacy at the University of Cincinnati, OH, told Jaime Weimer, MSN, RN, AGCNS-BS, AOCNS®, manager of oncology nursing practice at ONS, during a conversation about bispecific antibodies.  Music Credit: “Fireflies and Stardust” by Kevin MacLeod Licensed under Creative Commons by Attribution 3.0  Earn 0.5 contact hours of nursing continuing professional development (NCPD) by listening to the full recording and completing an evaluation at courses.ons.org by October 3, 2026. The planners and faculty for this episode have no relevant financial relationships with ineligible companies to disclose. ONS is accredited as a provider of nursing continuing professional development by the American Nurses Credentialing Center's Commission on Accreditation. Learning outcome: Learner will report an increase in knowledge related to the use of bispecific antibodies in the treatment of cancer. Episode Notes  Complete this evaluation for free NCPD. ONS Podcast™ episodes: Pharmacology 101 series Episode 275: Bispecific Monoclonal Antibodies in Hematologic Cancers and Solid Tumors Episode 261: CAR T-Cell Therapy for Hematologic Malignancies Requires Education and Navigation Episode 176: Oncologic Emergencies: Cytokine Release Syndrome ONS Voice articles: An Oncology Nurse's Guide to Bispecific Antibodies Bispecific Antibodies Cross-Discipline Cancer Care ONS Voice oncology drug reference sheets: Amivantamab-Vmjw Blinatumomab Epcoritamab-Bysp Glofitamab-Gxbm Mosunetuzumab-Axgb Tebentafusp-Tebn Teclistamab-Cqyv ONS book: Guide to Cancer Immunotherapy (second edition) ONS course: ONS/ONCC® Chemotherapy Immunotherapy Certificate™ Clinical Journal of Oncology Nursing article: Optimizing Transitions of Care in Multiple Myeloma Immunotherapy: Nurse Roles Other ONS resources: Bispecific Antibodies Video Bispecifics Huddle Card Cytokine Release Syndrome Huddle Card Immune Effector Cell–Associated Neurotoxicity Syndrome Huddle Card DailyMed homepage Hematology/Oncology Pharmacy Association late-breaking news article: The Emerging Use of Bispecific Antibodies with Chemotherapy in Diffuse Large B-Cell Lymphoma To discuss the information in this episode with other oncology nurses, visit the ONS communities.  To find resources for creating an ONS Podcast club in your chapter or nursing community, visit the ONS Podcast Library. To provide feedback or otherwise reach ONS about the podcast, email pubONSVoice@ons.org Highlights From This Episode “It was 2014 that most of us think of as the beginning of bispecifics in cancer, and that was with approval of blinatumomab. That was granted accelerated approval for the treatment of patients with Philadelphia chromosome–negative relapsed or refractory B-cell precursor acute lymphoblastic leukemia. It is a bispecific that targets CD19-expressing tumor cells and CD3 on T cells. It's the original bispecific T-cell engager and is often called a ‘BiTE.'” TS 2:11 “The term ‘bispecific' means that this is an artificial protein that's developed to hit two different antigens simultaneously. They can be two different epitopes on the same antigen. They can be an antigen on a cancer cell and CD3 on a T cell that kind of recruits the T cell to the cancer. So, there are different types [of bispecific antibodies]. The subtype that we often talk about are bispecific T-cell engagers, which are those bispecifics that do target the T cell. And currently, the target on the T cell that's utilized is the CD3 molecule. That's not the only one that will be used in the future because there's a lot of work being done on other types of T-cell engagers.” TS 4:21 “The targets for lymphoma are CD20. Those are bispecific T-cell engagers that hit CD20 on the lymphoma cell, as well as CD3 on a T cell. ... In myeloma, we have two different targets that have been utilized. One is BCMA or B-cell maturation antigen. That sits on the surface of myeloma cells and on some healthy B cells. ... There's also a target used in myeloma that's called GPRC5D, which stands for G protein–coupled receptor, class C, group 5, member D. ... In small cell lung cancer, there's delta-like ligand 3 (DLL3); it's part of the NOTCH pathway. ... And then this year, we've had a couple agents come out that target HER2.” TS 6:52 “[Toxicities] are very dependent on what your target is. ... The bispecific T-cell engager that's used in myeloma that targets the GPRC5D is also expressed on tissues that produce hard keratin like hair follicles and actually, within the tongue. So the toxicities that we see with that agent are something you wouldn't expect to see if you were using a myeloma agent. You see nail and skin issues. You see taste problems. So it's very specific about the target, which says to me, that every time a new one of these agents comes out, I have to learn about the target that helps me learn about the toxicity. I find that fascinating and really appreciate that.” TS 16:19 “Cytokine release syndrome has been one of the areas that drug development has really focused on to see how they can help mitigate the severity [of it]. ... [One of] the strategies that has been incorporated and studied in clinical trials is the step-up dosing scheme. [It's] where you give initial small doses and over time, increase the dose to the dose you're going to continue with. Usually, monitoring in the hospital is required by the FDA approval for anywhere from 28–48 hours for the first couple of doses. And that's a real common strategy that you'll see. Premedication with H2 blockers, H1 blockers, sometimes steroids. These are also things that are incorporated within the approvals of these drugs and are important to look at.” TS 20:53

“The proteasome itself, it really helps us unfold or get rid of misfolded proteins or degradations of different cells. We used to have garbage disposals in our sinks, and we used to put food product in there. If your garbage disposal is clogged, then everything backs up. So that's kind of what's really going on in the cell itself, is that I'm building up these unnecessary proteins that we should be getting rid of, and it actually causes apoptosis or cell death,” ONS member Daniel Verina, DNP, RN, ACNP-BC, nurse practitioner for the multiple myeloma program at Mount Sinai Medical Center in New York, NY, told Lenise Taylor, MN, RN, AOCNS®, BMTCN®, oncology clinical specialist at ONS, during a conversation about the proteasome inhibitor drug class. Music Credit: “Fireflies and Stardust” by Kevin MacLeod Licensed under Creative Commons by Attribution 3.0  Earn 0.75 contact hours (including 40 minutes of pharmacotherapeutic content) of nursing continuing professional development (NCPD) by listening to the full recording and completing an evaluation at courses.ons.org by July 18, 2026. The planners and faculty for this episode have no relevant financial relationships with ineligible companies to disclose. ONS is accredited as a provider of nursing continuing professional development by the American Nurses Credentialing Center's Commission on Accreditation. Learning outcome: Learner will report an increase in knowledge related to the use of proteasome inhibitors in the treatment of cancer. Episode Notes  Complete this evaluation for free NCPD.  ONS Podcast™ Pharmacology 101 series ONS Voice article: AI Multiple Myeloma Model Predicts Individual Risk, Outcomes, and Genomic Implications ONS books: Chemotherapy and Immunotherapy Guidelines and Recommendations for Practice (second edition) Clinical Guide to Antineoplastic Therapy: A Chemotherapy Handbook (fourth edition) Guide to Cancer Immunotherapy (second edition) Multiple Myeloma: A Textbook for Nurses (third edition) Clinical Journal of Oncology Nursing article: Optimizing Transitions of Care in Multiple Myeloma Immunotherapy: Nurse Roles Oncology Nursing Forum articles: Changes in Health-Related Quality of Life During Multiple Myeloma Treatment: A Qualitative Interview Study Facilitators of Multiple Myeloma Treatment: A Qualitative Study ONS Guidelines™ and Symptom Interventions Adherence to Oral Anticancer Medication Peripheral neuropathy ONS Hematology, Cellular Therapy, and Stem Cell Transplantation Learning Library American Society of Hematology International Myeloma Foundation Leukemia and Lymphoma Society Multiple Myeloma Research Foundation To discuss the information in this episode with other oncology nurses, visit the ONS Communities. To find resources for creating an ONS Podcast club in your chapter or nursing community, visit the ONS Podcast Library. To provide feedback or otherwise reach ONS about the podcast, email pubONSVoice@ons.org. Highlights From This Episode “When we look at the administration, we also want to make sure that we're looking at the blood counts, right? Because proteasome inhibitors are well known for causing thrombocytopenia and neutropenia. So making sure that the patients do meet eligibility for the treatment for that day, and do they have anemia or lower red blood cell counts. You want to make sure that, because of these therapies, that the patient has no symptoms or infections going into each therapy for that day.” TS 10:19 “[Bortezomib], interesting enough, it can cause hypotension, cardiac failure, and sometimes pulmonary edema. Switching that up a little bit, what makes it slightly different, carfilzomib … a lot of times we saw, even in the clinical trial, that there was a lot of hypertension or cardiomyopathies, or arrythmias that we saw with carfilzomib and different dosages that they have indicated from the FDA. So again, monitoring the hypertension … or heart failure.” TS 15:16 “We also want to keep in mind another adverse effect, and especially in myeloma—our patients come in the door already immunocompromised just by the disease state alone. But now I'm giving them therapies that can drop their neutrophil count, so neutropenia and thrombocytopenia, so they are at a higher risk of having serious infections, even including like pneumonia or having outbreaks of herpes zoster or shingles.” TS 16:50 “If the patient has shortness of breath or symptoms, hold the therapy. I think that's one of my biggest messages when it comes to cancer treatments and educating other healthcare providers, or even educating our patients and their caregivers or the care partners with them, is that we need to sometimes hold the therapy for safety.” TS 22:02 “I say keep a log, keep a book. Let me know when the symptoms happen. Are they happening the day of treatment? Are they happening two days later from the treatment? Are they happening a week later from the treatment? And being able to kind of guide which therapy is causing some of these adverse events or side effects alone. So, making them have calendars. When did you take the drug, when did you get your last infusion or your last [subcutaneous] injection? Always talk to your care team, whether it's in the academic center or next to your house in the community.” TS 26:17 “It's us learning how to listen to the patient going forward. We have tasks to do—we all have tasks to do in our lives—but we have to take a breath, be mindful who's in front of us, listen to them first, and then be able to talk to them and care for them upfront and see what the symptoms are. I think that's what we need to do. We have to take a breath in cancer.” TS 39:35

Broadcast from KSQD, Santa Cruz on 6-26-2025: Dr. Dawn opens with groundbreaking results from Vertex Pharmaceuticals' stem cell treatment for severe type 1 diabetes. The experimental therapy, Zimislecel, converts stem cells into pancreatic islet cells and infuses them into patients. In a 12-person study, 10 patients no longer need insulin after one year. The cells migrated to the liver and began producing insulin in response to glucose levels. Patients with hypoglycemic unawareness saw complete elimination of dangerous episodes after three months. However, patients must take lifelong immunosuppressive drugs to prevent rejection. The research represents 25 years of work by Harvard's Doug Melton. A caller asks about Keytruda treatment for melanoma. Dr. Dawn explains it's an immunotherapy drug targeting programmed death receptors that cancer cells hijack to evade immune response. The drug can cause serious immune overreactions but is standard for metastatic melanoma. Treatment protocols depend on cancer staging. For young patients with decades to lose, aggressive treatment is often justified despite risks. An email about morning arthritis pain leads to chronotherapy research discussion. Macrophages have energy levels that peak in the morning when inflammasome activation is quicker and more robust, explaining why arthritis pain is worst after overnight rest. Treatment timing could optimize anti-inflammatory medications by taking them at bedtime. Another email about eye irritation prompts diagnostic discussion. Dr. Dawn recommends examining for bacterial blepharitis before assuming food allergies and testing antihistamine drops. For elimination diets, common allergens include wheat, dairy, corn, soy, and peanuts. However, without other symptoms, food allergies are unlikely causes of isolated eye problems. Dr. Dawn explores advancing CAR-T cell therapy using RNA technology. Traditional therapy costs up to $500,000 per patient requiring lab reprogramming. New RNA-containing nanoparticles temporarily create antigen receptors for about one week. Mouse studies eliminated detectable tumors at highest doses. While effects are temporary, this could dramatically reduce costs and complexity. She discusses DNA forensics evolution from O.J. trial era to current technologies. New paleogenomics technology can analyze fragmented DNA from hair, previously considered unusable. Mitochondrial DNA analysis can definitively exonerate suspects. This led to Charles Fane's release after 17 years on death row when hair evidence proved innocence and identified the actual perpetrator. Dr. Dawn introduces Barrett's esophagus screening replacing invasive endoscopy. Patients swallow a capsule containing a compressed sponge that expands in the stomach and is pulled out via string, collecting esophageal cells. The test identifies abnormalities with 100-fold increased cancer risk when positive and 98% accuracy when negative, allowing targeted endoscopy only for high-risk patients. She concludes discussing body composition analysis superiority over BMI. Studies found overweight BMI showed 3.6 times higher heart disease risk, while large waist circumference showed four times higher risk. However, BMI had no significant relationship with overall mortality. Dr. Dawn advocates for bioimpedance analysis devices to measure body fat percentage and track muscle loss.

Broadcast from KSQD, Santa Cruz on 6-26-2025: Dr. Dawn opens with groundbreaking results from Vertex Pharmaceuticals' stem cell treatment for severe type 1 diabetes. The experimental therapy, Zimislecel, converts stem cells into pancreatic islet cells and infuses them into patients. In a 12-person study, 10 patients no longer need insulin after one year. The cells migrated to the liver and began producing insulin in response to glucose levels. Patients with hypoglycemic unawareness saw complete elimination of dangerous episodes after three months. However, patients must take lifelong immunosuppressive drugs to prevent rejection. The research represents 25 years of work by Harvard's Doug Melton. A caller asks about Keytruda treatment for melanoma. Dr. Dawn explains it's an immunotherapy drug targeting programmed death receptors that cancer cells hijack to evade immune response. The drug can cause serious immune overreactions but is standard for metastatic melanoma. Treatment protocols depend on cancer staging. For young patients with decades to lose, aggressive treatment is often justified despite risks. An email about morning arthritis pain leads to chronotherapy research discussion. Macrophages have energy levels that peak in the morning when inflammasome activation is quicker and more robust, explaining why arthritis pain is worst after overnight rest. Treatment timing could optimize anti-inflammatory medications by taking them at bedtime. Another email about eye irritation prompts diagnostic discussion. Dr. Dawn recommends examining for bacterial blepharitis before assuming food allergies and testing antihistamine drops. For elimination diets, common allergens include wheat, dairy, corn, soy, and peanuts. However, without other symptoms, food allergies are unlikely causes of isolated eye problems. Dr. Dawn explores advancing CAR-T cell therapy using RNA technology. Traditional therapy costs up to $500,000 per patient requiring lab reprogramming. New RNA-containing nanoparticles temporarily create antigen receptors for about one week. Mouse studies eliminated detectable tumors at highest doses. While effects are temporary, this could dramatically reduce costs and complexity. She discusses DNA forensics evolution from O.J. trial era to current technologies. New paleogenomics technology can analyze fragmented DNA from hair, previously considered unusable. Mitochondrial DNA analysis can definitively exonerate suspects. This led to Charles Fane's release after 17 years on death row when hair evidence proved innocence and identified the actual perpetrator. Dr. Dawn introduces Barrett's esophagus screening replacing invasive endoscopy. Patients swallow a capsule containing a compressed sponge that expands in the stomach and is pulled out via string, collecting esophageal cells. The test identifies abnormalities with 100-fold increased cancer risk when positive and 98% accuracy when negative, allowing targeted endoscopy only for high-risk patients. She concludes discussing body composition analysis superiority over BMI. Studies found overweight BMI showed 3.6 times higher heart disease risk, while large waist circumference showed four times higher risk. However, BMI had no significant relationship with overall mortality. Dr. Dawn advocates for bioimpedance analysis devices to measure body fat percentage and track muscle loss.

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

In today's episode, we sat down for part 2 of our discussion with Elizabeth Mittendorf, MD, PhD, MHCM, the 2026-2027 president-elect of the American Society of Clinical Oncology (ASCO). Dr Mittendorf holds numerous leadership roles, including the Robert and Karen Hale Distinguished Chair in Surgical Oncology and vice chair for research in the Department of Surgery at Brigham and Women's Hospital; co-leader of the Breast Program and director of the Breast Immuno-Oncology Program at the Dana-Farber Brigham Cancer Center; co-leader of the Parker Institute for Cancer Immunotherapy at the Dana-Farber Cancer Institute; and a professor of surgery at Harvard Medical School, all in Boston, Massachusetts. In this discussion, Dr Mittendorf shared how ASCO is strategically preparing to address the long-term implications of proposed federal research funding cuts. She emphasized the significant return on investment generated by sustained NIH support, underscoring its role in fostering scientific innovation and stimulating the broader economy. She also advocated for structural reforms to be developed collaboratively with researchers, institutions, and policymakers to ensure continued progress in oncology is maintained, particularly in underfunded areas, such as prevention research. Dr Mittendorf also previewed her broader vision for ASCO, including expanding global collaboration and advancing equitable access to cancer care. She noted that these efforts will be complemented by continued emphasis on multidisciplinary care delivery and mentorship, which she discussed in more detail in part one of our conversation.

In today's episode, we had the pleasure of speaking with Elizabeth Mittendorf, MD, PhD, MHCM, the 2026 president-elect of ASCO. Dr Mittendorf is the Robert and Karen Hale Distinguished Chair in Surgical Oncology and the vice chair for research in the Department of Surgery at the Brigham and Women's Hospital; co-leader of the Breast Program and director of the Breast Immuno-Oncology Program at the Dana-Farber Brigham Cancer Center; co-leader of the Parker Institute for Cancer Immunotherapy at the Dana-Farber Cancer Institute; and a professor of surgery at Harvard Medical School, all in Boston, Massachusetts.  In our exclusive interview, Dr Mittendorf discussed her priorities for advancing oncology practice and improving patient outcomes during her presidency. These include multidisciplinary cancer care, workforce well-being, leveraging artificial intelligence to enhance efficiency, and addressing global cancer care. She also emphasized the importance of mentorship and sponsorship for early career professionals, highlighting her personal experience with multiple mentors and her commitment to supporting the next generation of oncology professionals. 

A patient beats grim cancer survival rates. Learn about the immunotherapy and other strategies that give people hope. Plus, we discuss survivor's guilt when you defy the odds.

“The most effective therapies for solid tumors are also the most toxic — and we need to fix that,” says Dr. John Connolly, chief scientific officer of the Parker Institute for Cancer Immunotherapy. In this episode of the Vanguards of Health Care podcast, Connolly tells Bloomberg Intelligence pharmaceutical analyst Sam Fazeli why managing toxicity is the key to unlocking CAR-T’s potential in solid tumors. They explore the rise of in vivo cell therapies, evolving views on the tumor microenvironment and why foundational cancer vaccines may shape the future of all immunotherapy. Connolly also shares the clinical trials he’s watching closely, the ones that could flip the script on cancer care.See omnystudio.com/listener for privacy information.

Vidcast:  https://www.instagram.com/reel/DHDygk-shuL/Immunotherapy has been a resounding success for melanoma skin cancer and small cell lung cancer.  Not so for ovarian cancer.  Cancer immunologists at the University of Virginia have now discovered what underlies this failure.Their research discovered that flagellin protein from gut bacteria blocks the effectiveness of the checkpoint inhibitors that power most current immunotherapy.  This bacterial flagellin inhibits immune cell communication helping tumors flourish rather than die. Using a mouse model and blocking flagellin action restored immunotherapeutic effectiveness with 80% of treated animals enjoying long-term tumor control. If this approach is effective for human ovarian cancer patients, coupling flagellin blocking with checkpoint immunotherapy may be a winning therapeutic strategy …..someday soon.https://newsroom.uvahealth.com/2025/02/11/ovarian-cancer-discovery-could-turn-ailed-treatment-into-lifesaver/https://aacrjournals.org/cancerimmunolres/article-abstract/doi/10.1158/2326-6066.CIR-24-0513/751676/TLR5-signaling-causes-dendritic-cell-dysfunction?redirectedFrom=fulltext#immunotherapy #checkpointinhibitor #ovarian #cancer #biome #flagellin

In this episode of the Veterinary Cancer Pioneers Podcast, host Dr. Rachel Venable welcomes Dr. Mark Mamula, an immunologist and professor at Yale University School of Medicine, to discuss his groundbreaking work in canine cancer immunotherapy. Dr. Mamula shares how his background in autoimmune diseases led him to develop an experimental vaccine targeting EGFR and HER2 proteins in dogs with cancer. He explains the science behind this therapy, its clinical trial progress, and its potential to improve survival outcomes for cancers such as osteosarcoma and hemangiosarcoma. They also explore the challenges of bringing new therapies to veterinary medicine, the role of combination treatments, and the importance of accessible, cost-effective options for pet owners. Tune in for an insightful conversation on the evolving landscape of canine cancer treatment and the promising future of immunotherapy.

Daniel Laheru , MD, is the Professor of Oncology and Co-Director of Skip Viragh Center for Pancreatic Cancer Research at the Sidney Kimmel Comprehensive Cancer Center at The Johns Hopkins Hospital. He holds the Ian MacMillian Professorship in Clinical Pancreatic Cancer Research. Dr. Laheru has developed a vaccine along with Dr. Elizabeth Jaffee, that supercharges the immune system and causes immune cells, which tend to be tolerant of cancer, to seek out and kill pancreatic cancer cells throughout the body. He is a Member of the Miller-Coulson Academy of Clinical Excellence, Member of Bloomberg-Kimmel Institute for Cancer Immunotherapy, and Associated Director of the Institute for Convergence Science.  “There's no job that's insignificant here. Whatever you're doing, you need to do it to the best of your abilities.” A monumental lesson from Dr. Daniel Laheru's parents taught him to notice the janitor who moves by silently in the corner, the nurse who works overtime without appreciation, and the security guard who passes a silent glance at every passerby. In this episode of The Medicine Mentors, Dr. Daniel Laheru explains recognizing the interconnected nature of every person's role in the infrastructure of medicine, instilling gratitude in our practice, and paying it back by paying it forward. Pearls of Wisdom:   1. Enjoy the time that you're a student because you'll wonder what you did with all your time after. The future is entirely open to you, the ceiling is what you make it. 2. I'm happy doing what I'm doing right now, and if I can do this five years from now, I'll be ecstatic.  3. The fellows, residents, and medical students are the lifeblood of the institution and the next generation so don't be shy about asking somebody if they have time to meet with you.  4. A good mentor is like a parent in the sense that they put your goals ahead of their own. My mentor really saw my future before I was able to understand it for myself. 5. The little things in the course of a day actually make a big difference. Thanking and appreciating someone goes a long way. 

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If you only listen to one show this year make it this one! With Producer Sean leaving early for INTERGEO, DD was joined this week by Peta Cox for this heartfelt and inspiring story. Our guest was Claire Masikewich. Claire is a seasoned marketing and communications professional at GeoVerra with a passion for advocacy that transcends her corporate career.  In May 2023, Claire's career paused when her five-year-old daughter was diagnosed with stage 4 neuroblastoma, a rare and aggressive pediatric cancer. This life-altering event ignited a new purpose: using her marketing expertise to raise awareness and advocate for more research in the severely underfunded area of pediatric cancer. Claire's story is not only one of professional success but also of personal resilience. She has faced and overcome challenges with anxiety and depression, which once felt overwhelming. Yet, with her daughter's diagnosis, Claire channeled her strength and transformed her pain into purpose, becoming a fierce advocate while navigating her daughter's treatment. By August 2024, just before Childhood Cancer Awareness Month, the Strong Like Sloane Foundation—named in honor of her daughter—became an official charitable organization in Alberta. Since launching fundraising efforts in October 2023, the foundation has raised over $155,000 for pediatric cancer research at Calgary's Riddell Centre for Cancer Immunotherapy.  Claire is a testament to the power of resilience, personal growth, and the unwavering love of a parent. Her life's journey is an inspiration to all who face personal challenges and a reminder that, with determination and support, we can find strength and light even in the most difficult of circumstances. "You don't know what you're capable of until you're asked to be capable." Music by Zach Bryan!