Abnormal mass of tissue as a result of abnormal growth or division of cells
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Just Shoot It: A Podcast about Filmmaking, Screenwriting and Directing
Will Bridges https://www.imdb.com/name/nm2782297/ shares his method for making every meeting an opportunity. And he explains what he did that let him come from 10 years of working random jobs and trying to make shorts here and there, to becoming the newly discovered talent, suddenly writing for hit series like “Black Mirror” and “Stranger Things” as well as being a co-creator with Charlie Brooker.Matt and Oren get Will to open up about what he learned from "Shaun of the Dead" and how those filmmakers pitched. And they break down the process of showing decision-makers a concept and the steps needed to get them to truly understand what it will look like, feel like, and clearly see the audiences it will resonate with.If you're looking for ideas to improve how you direct actors, you too will get a lot from this episode. And Will goes into the secret of freeing up established actors to do their best work. And he's got some warnings about key mistakes many directors often make---Help our Patreon! https://www.patreon.com/JustShootItPodMatt's Endorsement: "Paprika" https://www.imdb.com/title/tt0851578Oren's Endorsement: Mike Birbiglia's "Working It Out" podcast https://www.podpage.com/mike-birbiglias-working-it-out/ and Za'atar spice https://en.wikipedia.org/wiki/Za'atarWill's Endorsement: "Tumor", the graphic novel https://en.wikipedia.org/wiki/Tumor_%28comics%29 Hosted on Acast. See acast.com/privacy for more information.
To have Dr. Morse answer a question, visit: https://drmorses.tv/ask/ 00:00:00 - Intro - Foods - Dr. Morse History 00:18:05 - Tumors 00:29:58 - Reincarnation 00:18:05 - Tumors I'm a 50 year old female, and have a lump in my breast and head. 00:29:58 - Reincarnation When our bodies pass and we come into a new body in our next life — does any of the work we did on the body in this lifetime, pass to the next?
Hi friends! So thankful to be back with you guys today :) In this episode , I answer some more of your questions! We talk about my pituitary tumor symptoms, how to start recovery, coping when it's dark and cold outside, and my thoughts on "full" ed recovery. I hope this episode brings you peace! I'm so thankful for you!GabbiXx
To Health With That! Podcast Season 5, Episode 5. Thank you so much to Tony for generously sharing his story - the full interview was fabulous and included much more than we could put in one podcast episode, so we broke it into two. In this episode, Tony continues to share with the idea of MTHFR being a rebirth, new information he has about a tumor and his concerns about folate and tumor growth, and questions about MTHFR and anesthesia.00:00 - Introduction00:43 - Manageable steps01:07 - Symptom tracking01:23 - Staying in control (or not).02:03 - MTHFR as a rebirth02:45 - tumor03:10 - folate and tumor growth04:40 - Do we get enough B12 from food06:15 - B12 and lithium rotate07:15 - MTHFR and detox09:42 - mental health struggles and folic acid10:31 - MTHFR and anesthesia11:11 - MTHFR and nitrous oxide and preparing for surgery12:32 - MTHFR and antibiotics13:33 - Building back good gut floraThanks so much for watching! I have so many other resources for you. Here is the full version of this interview: https://youtu.be/SZmHnyCKd8UIf you would like to tell your own MTHFR story, you can schedule with Dr. Amy here: https://calendly.com/amy-tohealthwiththat/new-meetingCheck out the website first for lots of FREE stuff:WEBSITE: https://tohealthwiththat.com/ You can now Pre-order the book MTHFR Easy: Get Healthy For Life. https://www.amazon.com/MTHFR-Get-Started-Guide-Healthy-ebook/dp/B0FLFCY1YQ/ref=sr_1_2?crid=3E616JJOYSA12&dib=eyJ2IjoiMSJ9.7WXbrOZ6vkAu5Ncg9lJLavpPvim_O1kOvqp3LTim_snTq6Gahvu-NhWvC1mZurA6.XnOpY_FYGI_DbfEx9NmEwRrSM2USTXkw_HTykBFrMtw&dib_tag=se&keywords=amy+neuzil&qid=1755710249&sprefix=amy+neuzil%2Caps%2C98&sr=8-2 Look for Kindle, audiobook, and paperback versions also to be released on October 24, 2025.GENETIC ROCKSTARS (an MTHFR, methylation, and genetics community): https://community.tohealthwiththat.comThis story was shared graciously and generously with permission to post on the podcast, Youtube, and in print if that happens in the future.
Ian shares a bit of absolutely unofficial medical advice that you should only follow if you want a laugh
VetFolio - Veterinary Practice Management and Continuing Education Podcasts
It could be a bug bite. Or a harmless fatty lump. But it might be a mast cell tumor. In this episode of the VetFolio Voice podcast, we delve into mast cell tumors in dogs, including the unpredictable nature of these tumors, nuances around interpretation of cytology and histopathology reports, cytologic grading accuracy, and options for therapy including surgery, chemo, radiation and Stelfonta, an injectable mast cell tumor treatment for dogs. You'll learn about staging considerations and the role of newer prognostic panels as well as strategies for client communication about mast cell disease.
❣ Gratis 7 Tage Ernährungsplan nach Glykoplan: Hier klicken❣ Galactose: Hier klicken (✔ 10 % CODE: TAN34909)Die Datenlage ist klar: Zuckerarme oder zuckerfreie Ernährung mit wenig Kohlenhydraten und guten Fetten hilft immer, egal ob bei Alzheimer, Parkinson oder sogar Krebst. Dr. med. Kurt Mosetter zeigt auf, dass es mittlerweile 56 verschiedene Bezeichnungen für Zucker gibt und wie du dich ernähren kannst, sodass die Zellen und dein Körper sich selbst reparieren. Danke an @swissbiohealthkreuzlingen3586 für das herausragende Therapeutentreffen. ✨ Mehr Infos zu Dr. Kurt Mosetter: Kurts Homepage: https://www.myoreflex.de/Der Glycoplan: Hier klickenInhaltsverzeichnis: 00:00 Intro 02:36 DAS hemmt Tumorzellen? 07:12 Bioelektrische Felder steuern 09:48 Epigenetische Reparaturmechanismen 12:24 Natursubstanzen fördern Gesundheit✨ Mehr mr.broccoli: Blog YouTube Instagram Telegram-Community (für besonders brisante Themen) Newsletter▶▶▶ Meine 10 Favoriten für mehr Gesundheit
In this episode of SurgOnc Today, Mark Knab, Charles Vining, and Kelvin Allenson discuss how the anatomic location of duodenal adenocarcinoma—from the first to the fourth portion—fundamentally shapes surgical decision-making. Discussion highlights include criteria for pancreaticoduodenectomy versus segmental or limited resections, the role of margin status and lymphadenectomy, and evolving data guiding resection strategy for non-ampullary duodenal cancers. Designed for practicing surgical oncologists, this episode emphasizes operative judgment, outcomes data, and the balance between oncologic adequacy and surgical morbidity.
Shirts, long sleeves, and hoodies are back for a limited time! This batch has the podcast logo on the back and on the front is a simple name tag saying "Dental Technician". Be proud of what you do and show the WORLD that we exist. Shirts on sale until November 8, 2025. As always 100% of the profits go towards the Foundation For Dental Laboratory Technology (https://dentallabfoundation.org/)! https://www.bonfire.com/its-all-in-the-name160/ This week, Elvis and Barb cross the globe to chat with the legendary Marc Rondeau—a Sydney-based dental technician, educator, and yes, nightclub DJ. From being one of 30 accepted out of 300 applicants into Australia's only dental tech program, to running one of the country's top labs, Marc's journey is packed with hard work, humor, and heart. He shares how a near-fatal car accident—and the brain tumor it uncovered—completely reshaped his perspective on work-life balance, pushing him to give back through teaching and advocacy. Now the Vice President of the Australian Dental Technicians Association (https://www.australiandentaltechnicians.com.au/), Marc talks about the fight to keep technicians recognized, the shift from analog to CAD/CAM, and why he believes every tech should know how to “wax before they CAD.” * Dental Labs—The Ivoclar (https://www.ivoclar.com/en_us) Flash Sale Is On! * From November 3rd to 14th, Ivoclar is bringing you unbeatable deals on the equipment that will set your lab up for success in 2026. * Upgrade your mill, your furnace, or expand your workflow—and save big while doing it! * Plus, when you purchase a milling machine (https://www.ivoclar.com/en_us/products/product-list?page=1&limit=12&filters=%5B%7B%22id%22%3A%22professions%22%2C%22advancedFilter%22%3Afalse%2C%22values%22%3A%5B%22Lab%22%5D%7D%2C%7B%22id%22%3A%22categories%22%2C%22advancedFilter%22%3Afalse%2C%22value%22%3A%22Digital%20Equipment%22%7D%5D), you'll get delivery, installation, and training—all included. That means your lab will be production-ready from day one. * But hurry—these savings vanish after November 14th! * Contact your Ivoclar sales rep today and power up your lab for the year ahead. The right CAM software can completely transform your lab's workflow — and no one understands that better than FOLLOW-ME! Technology (https://www.follow-me-tech.com/), creators of hyperDENT (https://www.follow-me-tech.com/hyperdent/#product_overview). That's why Roland DGA (https://www.rolanddga.com/applications/dental-cad-cam) has partnered with FOLLOW-ME! North America to offer the Roland DGA x hyperDENT Bundle for their DWX-53D series mills. This collaboration gives labs optimized performance, smoother milling, and incredible efficiency gains — with some users reporting up to two hours saved per case cycle without sacrificing quality. And here's the best part: Roland is making this available to everyone through a hyperDENT trade-in promo for existing users. It's the perfect opportunity to upgrade your CAM and take full advantage of the technology you already have. Plus, Nowak Dental Supplies (https://www.nowakdental.com/) is participating in the promotion and adding an exclusive bonus for NOLA Lab Fest attendees: the Multiple Instances feature at no additional cost. Don't miss your chance to see the difference in person! Join Jordan Greenberg — the “hyperDENT dude” himself — at NOLA Lab Fest, November 7–8 (https://www.nolalabfest.com/), and discover how CAM can redefine what your Roland mill can do. Special Guest: Marc Rondeau.
Linktree: https://linktr.ee/AnalyticJoin The Normandy For Additional Bonus Audio And Visual Content For All Things Nme+! Join Here: https://ow.ly/msoH50WCu0KIn this Notorious Mass Effect segment, Analytic Dreamz delivers a comprehensive analysis of Rosalía's groundbreaking 2025 single “Berghain” featuring Björk and Yves Tumor, the lead track from her upcoming album Lux, releasing November 7 via Sony Music. Clocking in at 3:26, the Nicolás Méndez-directed video amassed 3M+ YouTube views in 24 hours and 6M+ by October 29, hitting #2 globally on Trending while debuting Top 5 on Spotify Spain and trending in Germany, Iceland, and Latin America. Filmed across Berlin and Barcelona, the multilingual masterpiece in German, English, and Spanish blends organ, choir, synth bass, and London Symphony Orchestra strings conducted by Daníel Bjarnason. Analytic Dreamz dissects symbolic scenes—from Catholic iconography and a wounded heart jewel to Snow White animal motifs, a dissolving sugar cube nod to Kieslowski's Three Colors: Blue, and a white dove ascension signifying rebirth post-heartbreak with subtle Rauw Alejandro references like the fox and garnet medallion. Fashion highlights include archival Alexander McQueen Fall 2002 shredded dress, Spring 2003 rosary sandals, Givenchy Spring 1997 fringed top, and Balenciaga Spring 2004 cutout piece, curated by José Carayol to evoke holiness and reincarnation. Lux's 18-song, four-movement structure features collaborators Carminho, Estrella Morente, Silvia Pérez Cruz, and shifts from Motomami's urban edge to orchestral spirituality, with 300K+ pre-saves and 1.2M+ Instagram likes signaling massive impact. Analytic Dreamz explores lyrics like “Ich halte viele Dinge in meinem Herzen” and Björk's “divine intervention” bridge, positioning “Berghain” as Rosalía's boldest evolution yet.Support this podcast at — https://redcircle.com/analytic-dreamz-notorious-mass-effect/donationsAdvertising Inquiries: https://redcircle.com/brandsPrivacy & Opt-Out: https://redcircle.com/privacy
Featuring an interview from Dr John Strickler, including the following topics: Prognostic value of molecular residual disease (MRD) as detected by circulating tumor DNA (ctDNA) and optimal incorporation of MRD assays into the care of patients with colorectal cancer (0:00) Potential use of MRD assays for patients with microsatellite instability (MSI)-high localized colorectal cancer or those with delayed progression or metastatic disease (16:09) Tumor-informed MRD assays under clinical development (20:36) Predictive role of ctDNA in Stage III colon cancer treated with celecoxib; effect of low-dose aspirin on response to celecoxib in patients with PI3K pathway alterations (24:19) Case: A man in his late 50s with resected Stage IIA colon cancer (30:06) Case: A woman in her late 40s with Lynch syndrome and MSI-H colon cancer with a solitary, small hepatic metastasis (34:57) MRD as a future clinical trial endpoint for solid tumors; increasing incidence of colorectal cancer in younger people (40:24) Antibody-drug conjugates in the treatment of colorectal cancer (45:13) Perspectives on promising areas of clinical research in colorectal cancer (48:23) CME information and select publications
Siggi Gunnars og Margrét Maack sáu um Poppland í dag. Bríet kom í heimsókn með nýtt lag. Andrea Jóns og Arnar Eggert dæmdu plötu vikunnar og Vilberg Andri sendi póstkort með laginu Spún. Máni Orrason – Pushing Brandi Carlile – Returning to Myself Hjaltalín – Stay by You St. Paul & The Broken Bones – Sushi and Coca-Cola Jónas Sigurðsson – Þessi endalausi vegur endar vel Hayley Williams & David Byrne – What Is the Reason for It Björk – Big Time Sensuality Björk Guðmundsdóttir, Rosalía, Tumor & Yves – Berghain Sigur Rós – Inní mér syngur vitleysingur The Rolling Stones – Angie Amy MacDonald – This Is the Life Taylor Swift – The Fate of Ophelia Daft Punk – Lose Yourself to Dance Shaboozey – A Bar Song (Tipsy) Sálin hans Jóns míns – Á nýjum stað Bríet – Cowboy Killer (Má spila 31.10.2025) Jón Jónsson ft. GDRN – Ef ástin er hrein Of Monsters and Men – Tuna in a Can Olivia Dean – Man I Need Veronica Maggio – Måndagsbarn The Temper Trap – Sweet Disposition Kraak & Smaak ft. Ivar – Travel Light Hjálmar & Mugison – Ljósvíkingur Rakel Sigurðardóttir – 11:11 Rakel Sigurðardóttir – Staður Rakel Sigurðardóttir – Pillows Skúli Sverrisson, Rakel Sigurðardóttir, Nanna Bryndís Hilmarsdóttir & Salóme Katrín – Pickled Peaches Lily Allen – West End Girl Lily Allen – Not Fair ABBA – The Winner Takes It All Hipsumhaps – Hjarta Grýlurnar – Valur og jarðaberjamaukið hans Royel Otis – Who's Your Boyfriend Vilberg Andri Pálsson – Spún Janelle Monáe – Make Me Feel Króli & CeaseTone – Stinga mér í samband Teddy Swims – The Door Digital Ísland – Eh plan? Violent Femmes – Gone Daddy Gone Joy Crookes – Somebody to You Hannes ft. Waterbaby – Stockholmsvy Cat Burns – There's Just Something About Her Daði Freyr – Me and You
In this episode of JCO PO Article Insights, host Dr. Jiasen He summarizes the article, "Somatic Mutation Profiles of Colorectal Cancer by Birth Cohort" by Gilad, et al published October 11, 2025. TRANSCRIPT Jiasen He: Hello, and welcome to the JCO Precision Oncology Article Insights. I am your host, Jiasen He, and today, we will be discussing the JCO Precision Oncology article, "Somatic Mutation Profiles of Colorectal Cancer by Birth Cohort," by Dr. Gilad and colleagues. Early-onset colorectal cancer is defined as colorectal cancer diagnosed before the age of 50. Several reports have suggested that early-onset colorectal cancer has unique characteristics. Compared with late-onset colorectal cancer, early-onset colorectal cancer cases are more commonly found in the distal colon or rectum, tend to be diagnosed at more advanced stages, and may display unfavorable histologic features. Although the overall incidence of colorectal cancer has declined in recent decades, the incidence of early-onset colorectal cancer continues to rise. This increase appears to be driven by birth cohort effects. The reasons behind this rise remain unclear but are likely multifactorial, involving changes in demographics, diet, lifestyle, environmental exposures, and genetic predisposition. At the same time, studies have shown conflicting results regarding whether there are differences in the mutation profiles between early-onset and late-onset colorectal cancer. Therefore, it is crucial to explore whether colorectal cancer somatic mutational landscape differs across birth cohorts, as this could provide important insight into generational shifts in colorectal cancer incidence. To address this question, the authors conducted a retrospective study to characterize the mutation spectrum of colorectal cancer across different birth cohorts. Consecutive colorectal cancer patients who underwent somatic next-generation sequencing at the University of Chicago pathology laboratory between 2015 and 2022 were retrospectively identified. Tumors were tested for 154 to 168 genes and categorized as either microsatellite stable or high according to established thresholds. Patients with hereditary cancer syndromes or inflammatory bowel disease were excluded. Participants were then grouped into birth cohorts by decades, as well as into two major groups: those born before 1960 and after 1960. Genes that were identified in at least 5% of the sample were selected and grouped into 10 canonical cancer signaling pathways. These genes and pathways were then included in the analysis to explore their association with colorectal cancer across different birth cohorts and age groups. A total of 369 patients were included in the study, with a median birth year of 1955 and a median age at colorectal cancer diagnosis of 62.9 years. 5.4% were identified as having microsatellite-high tumors. The median tumor mutational burden was 5 mutations per megabase for microsatellite-stable tumors and 57.7 mutations per megabase for microsatellite-high tumors. Patients with microsatellite-high tumors tended to have earlier birth years and were diagnosed at an older age. However, after adjusting for potential confounders, neither birth year nor age remained statistically significant. Similarly, after controlling for confounders, no significant associations were observed between birth year or age and mutation burden. In this cohort, APC, TP53, and KRAS were the most frequently mutated genes. No statistically significant differences in the prevalence of gene mutations were observed across birth cohorts. Correspondingly, the most affected signaling pathways were the Wnt, TP53, and (RTK)/RAS pathways. Similar to the gene-level finding, no significant differences in the prevalence of these pathways were identified among birth cohorts. When examining patients born before and after 1960, the authors found that the older birth cohorts were diagnosed at an older age and had higher tumor mutational burden. However, no significant differences were observed in any of the genes or pathways analyzed. Among microsatellite-stable tumors, 18.3% were classified as early-onset colorectal cancer, while 81.1% were late-onset colorectal cancer. Consistent with previous reports, early-onset colorectal cancers in this cohort were more likely to be left-sided and more common among more recent birth cohorts. However, no significant differences were identified in any of the examined genes or pathways when comparing early-onset to late-onset colorectal cancer. In this cohort, a higher prevalence of early-onset colorectal cancer was observed among more recent birth cohorts, consistent with previous reports. Still, no distinct mutational signature was identified between the early and late birth cohorts. The authors proposed that the lack of distinct mutational profile by age or birth cohort may be due to the limited number of key molecular pathways driving colorectal cancer. Although environmental exposures likely differ across generations, the downstream effects may have converged on similar biological mechanisms, leading to comparable somatic mutations across cohorts. Alternately, they proposed that the observed birth cohort differences in colorectal incidence may be driven by distinct mutation signatures, epigenetic alterations, or changes in the immune microenvironment rather than variations in canonical gene mutations. As the authors noted, given the retrospective nature of this study, its modest sample size, and the predominance of advanced-stage tumors, larger prospective studies are needed to validate these findings. In summary, this study found no significant differences in the mutational landscape of colorectal cancer across birth cohorts or age groups. The authors proposed that the generational shift in colorectal cancer incidence is unlikely to be driven by changes in the underlying tumor genomics. However, larger prospective studies are needed to validate these findings. Thank you for tuning in to JCO Precision Oncology Article Insights. Do not forget to subscribe and join us next time as we explore more groundbreaking research shaping the future of oncology. 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.
#ROSALÍA #Björk #YvesTumor #Latin #PopSeason 11 BEGINS! For Let's Talk About It: MUSIX REVIEWS. The Music Critic is gearing up ready to deliver a action packed season. Daily episodes are fully back! This SEASON is the first yearly long season! Get ready for the wild RIDE OF S11! Fun Pop Reviews, Rap Reviews AND MORE! ROSALÍA, Björk, Yves Tumor, Berghain, music collaboration, electronic music, avant-garde pop, experimental artists, music video, live performance, underground music, Spanish singer, Icelandic artist, alternative music, modern music, club culture, music reviews, genre fusion, indie music
Are cats the forgotten patients in oncology? Dr. Sue Ettinger is back on the Purr Podcast to elaborate on cancer tests, treatments, and why cats deserve more. Why are clinical trials and funding so limited for cats? What is the next big leap in feline oncology? What is the best practice for early cancer detection in cats? Dr. Sue Cancer Vet joins our hosts, Dr. Susan Little and Dr. Jolle Kirpensteijn, live from WVC 2025 to tackle one of veterinary medicine's biggest questions: Why are cancer diagnostics and treatments for cats lagging behind dogs?Thanks for tuning in to the Purr Podcast with Dr. Susan and Dr. Jolle!If you enjoyed today's episode, don't forget to subscribe, rate, and leave us a review—it really helps other cat lovers and vet nerds find the show. Follow us on social media for behind-the-scenes stories, cat trivia, and the occasional bad pun. And remember: every day is better with cats, curiosity, and maybe just a little purring in the background. Until next time—stay curious, stay kind, and give your cats an extra chin scratch from us. The Purr Podcast – where feline medicine meets feline fun.
Dr. Brooke Britton discusses degranulation events—a scary potential when a dog has mast cell tumors. Learn what degranulation is, why it happens, and how it can affect your dog. Also: practical tips for managing symptoms, potential connections between allergies and cancer, and how to care for dogs with mast cell tumors. Topics Discussed: • What is a degranulation event? • How mast cell tumors cause degranulation • Symptoms dogs may experience during a degranulation event • The role of allergies and chronic inflammation in mast cell tumor risk • Medications and treatments to manage symptoms • Low-histamine diets and their role in comfort care • Tips for preventing future mast cell tumor growth • The importance of early detection and regular vet check-ups Your Voice Matters! If you have a question for our team, or if you want to share your own hopeful dog cancer story, we want to hear from you! Go to https://www.dogcancer.com/ask to submit your question or story, or call our Listener Line at +1 808-868-3200 to leave a question. Related Videos: https://www.youtube.com/watch?v=Al7jjCXVhuE https://www.youtube.com/watch?v=6eb4GrcH_f8 Related Links: Our article on mast cell tumors: https://www.dogcancer.com/articles/types-of-dog-cancer/mast-cell-tumors-in-dogs/ Chapters: 00:00 Introduction 01:15 What Are Mast Cell Tumors? 02:30 The Role of Mast Cells in Normal Immune Response04:00 What Happens During a Degranulation Event?06:45 Symptoms Dogs May Experience During Degranulation09:00 How Dogs Might Feel During Degranulation Events11:00 Stomach Upset and Ulcers in Dogs with Mast Cell Tumors13:00 The Link Between Allergies and Mast Cell Tumors16:00 Managing Allergies in Dogs to Reduce Risk18:30 Diet Considerations: Low-Histamine and Commercial Diets22:00 Medications for Degranulation Symptoms: Benadryl and Tagamet25:00 The Truth About Diet and Cancer Prevention27:30 Why Balanced Diets Are Key for Dogs with Cancer29:45 Closing Thoughts on Degranulation and Mast Cell Tumors34:00 Outro: Support and Resources for Dog Owners Get to know Dr. Brooke Britton: https://www.dogcancer.com/people/brooke-britton-dvm-dacvim-oncology/ For more details, articles, podcast episodes, and quality education, go to the episode page: https://www.dogcancer.com/podcast/ Learn more about your ad choices. Visit megaphone.fm/adchoices
Tumor components and immune response indicators can be found in cerebrospinal fluid, or CSF, when someone has a brain tumor, in a new test developed by Chetan Bettagowda, director of neurosurgery at Johns Hopkins and one of the test's developers. … Cerebrospinal fluid may hold the keys to brain cancer identification and treatment, Elizabeth Tracey reports Read More »
In this podcast, experts Tina Cascone, MD, PhD; Christina Baik, MD, MPH; and David Planchard, MD, PhD discuss data-driven treatment for EGFR-mutant non-small cell lung cancer.
This is a text-to-speech (TTS) AI reading of our most recent blog post: 6 Facts Every Clinician Needs to Know About Tumor Lysis Syndrome.https://www.pointofcaremedicine.com/blog-post/6-facts-every-clinician-needs-to-know-about-tumor-lysis-syndrome-2025Tumor Lysis Syndrome (NEJM, 2025)Bociek RG, Lunning M. Tumor Lysis Syndrome. N Engl J Med. 2025;393(11):1104-1116. doi:10.1056/NEJMra2300923Related ContentTumor Lysis Syndrome Admission Template
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BUFFALO, NY – October 20, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on October 16, 2025, titled “Widespread folate receptor expression in pediatric and adolescent solid tumors – opportunity for intraoperative visualization with the novel fluorescent agent pafolacianine.” In this study, led by first author Ashley C. Dodd from Ann & Robert H. Lurie Children's Hospital and corresponding author Timothy B. Lautz from the same institution and Northwestern University Feinberg School of Medicine, researchers discovered that folate receptor beta (FRβ) is widely expressed in various pediatric and adolescent solid tumors. This finding highlights FRβ as a promising target for improving the accuracy of tumor surgery using a fluorescent imaging agent known as pafolacianine. Pediatric cancers are often challenging to remove completely during surgery, particularly when tumors spread or form small metastases. Fluorescence-guided surgery is a method that helps surgeons better identify tumors during operations using special imaging dyes. However, commonly used dyes such as indocyanine green are not tumor-specific and rely on general features of blood vessel permeability, limiting their precision. In this study, researchers investigated the potential of pafolacianine, a next-generation dye that targets folate receptors, for pediatric use. Folate receptors are proteins commonly found on the surface of cancer cells. Pafolacianine is already FDA-approved for adults with ovarian and lung cancers due to its ability to bind these receptors and highlight tumors during surgery. The research team analyzed tissue samples from 13 young patients diagnosed with various cancers, including Wilms tumor, osteosarcoma, synovial sarcoma, rhabdomyosarcoma, Ewing sarcoma, and neuroblastoma. The results showed that FRα was predominantly absent, whereas FRβ was present in 100% of the tumor samples. Notably, FRβ appeared both on the tumor cells and in the surrounding tumor microenvironment but showed little to no expression in normal tissue, making it an excellent candidate for targeted imaging. “In this study, we performed immunohistochemistry staining on slides obtained from a range of pediatric patients with solid tumors.” This consistent expression of FRβ in pediatric tumors is a significant and novel finding. Earlier studies primarily linked FRβ to immune cells called tumor-associated macrophages. This study reveals that FRβ is also expressed directly on tumor tissue, which could help surgeons better distinguish cancer from healthy tissue during procedures. Based on these results, the team has launched a clinical trial to evaluate pafolacianine in children undergoing surgery for metastatic lung tumors. If successful, this method could make pediatric cancer surgery safer and more effective. Overall, this study suggests that targeting FRβ with pafolacianine could serve as a tumor-agnostic imaging strategy, applicable across a wide range of pediatric solid tumors. This represents a potential advancement in real-time surgical imaging and a step forward in pediatric cancer care. DOI - https://doi.org/10.18632/oncotarget.28772 Correspondence to - Timothy B. Lautz - TLautz@luriechildrens.org Abstract video - https://www.youtube.com/watch?v=0its0QkOcwM Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM
Nuestro guía por la sanidad pública, el nefrólogo Borja Quiroga, nos conduce hasta Dani, el paciente con tumor de páncreas que ayudó a desvelar chatGPT. ¿Cómo puede la IA dar superpoderes a los médicos? Conversamos con un experto en la aplicación de la IA en la sanidad, el neurólogo y director de Savana Ignacio Hernández Medrano.
In this episode of Healthy Mind, Healthy Life, host Avik welcomes Riza August, who shares her inspiring journey of resilience and self-discovery following a brain tumor diagnosis. Riza discusses her decision to reclaim her life through an 1845-mile bike journey, the emotional and spiritual growth she experienced, and the importance of sharing her story to help others heal. The conversation emphasizes the power of perspective, the significance of taking small steps towards recovery, and the ongoing journey of personal transformation. Takeaways Riza made a conscious decision to live after her diagnosis. The bike journey was a spiritual testament to perseverance. Healing can be facilitated through sharing one's story. Vulnerability is a powerful form of medicine for the soul. Asking 'What can I do?' can shift one's perspective. Even small steps can lead to extraordinary outcomes. Riza's journey opened her up to new experiences and opportunities. Embracing change is essential for personal growth. Healing and growth are lifelong practices. We are all worthy of healing and transformation. Chapters 00:00 Introduction to Riza's Journey 02:02 The Decision to Live 03:44 Reflecting on Life's Choices 05:23 The Spiritual Journey of Biking 06:49 Healing Through Sharing 09:51 Overcoming Limitations 12:19 Embracing Change and Growth 13:46 Continuing the Journey of Transformation Watch Video: https://youtu.be/XHyzG1sC-ns Reach Risa: Facebook: https://www.facebook.com/risa.august.unleashed/ Instagram: https://www.instagram.com/risaunleashed/ LinkedIn: www.linkedin.com/in/risa-august-9b130524a Disclaimer: This video is for educational and informational purposes only. The views expressed are the personal opinions of the guest and do not reflect the views of the host or Healthy Mind By Avik™️. We do not intend to harm, defame, or discredit any person, organization, brand, product, country, or profession mentioned. All third-party media used remain the property of their respective owners and are used under fair use for informational purposes. By watching, you acknowledge and accept this disclaimer. ----- Healthy Mind By Avik™️ is a global platform redefining mental health as a necessity, not a luxury. Born during the pandemic, it's become a sanctuary for healing, growth, and mindful living. Hosted by Avik Chakraborty storyteller, survivor, wellness advocate this channel shares powerful podcasts and soul-nurturing conversations on: • Mental Health & Emotional Well-being • Mindfulness & Spiritual Growth • Holistic Healing & Conscious Living • Trauma Recovery & Self-Empowerment With over 4,500+ episodes and 197.4K+ global listeners, join us as we unite voices, break stigma, and build a world where every story matters.
Cats deserve cancer breakthroughs too! Dr. Sue Ettinger, DVM, DACVIM (Oncology), shares what's on the horizon for feline cancer testing in the next episode of the Purr Podcast. Known on social media as Dr. Sue Cancer Vet, she is an international speaker, author, & vlogger. She is a board-certified specialist in medical oncology. She received her veterinary training at Cornell University College of Veterinary Medicine. She completed her residency in medical oncology at the Animal Medical Center in NYC in 2003.Thanks for tuning in to the Purr Podcast with Dr. Susan and Dr. Jolle!If you enjoyed today's episode, don't forget to subscribe, rate, and leave us a review—it really helps other cat lovers and vet nerds find the show. Follow us on social media for behind-the-scenes stories, cat trivia, and the occasional bad pun. And remember: every day is better with cats, curiosity, and maybe just a little purring in the background. Until next time—stay curious, stay kind, and give your cats an extra chin scratch from us. The Purr Podcast – where feline medicine meets feline fun.
BUFFALO, NY – October 14, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on October 13, 2025, titled “Treatment of glioblastoma with tumor-specific amplitude-modulated radiofrequency electromagnetic fields.” The study, led by Hugo Jimenez from Wayne State University School of Medicine, Karmanos Cancer Institute, introduces a novel treatment approach for glioblastoma, an aggressive and often treatment-resistant brain cancer. The findings open a new potential path for patients who currently have limited therapeutic options. The approach uses a device developed by TheraBionic that delivers extremely low levels of radiofrequency electromagnetic fields, tuned to frequencies associated with glioblastoma. In laboratory experiments, this therapy significantly slowed the growth of multiple glioblastoma cell lines. It was especially effective against tumor stem cells, which are known to resist standard treatments and drive cancer reappearance. Researchers also found that the treatment's effects depend on a calcium channel in tumor cells known as Cav3.2 (CACNA1H). When this channel was blocked, the therapy lost its effectiveness, highlighting the channel's essential role in how tumor cells respond to the signal. The therapy also disrupted the process of cell division by interfering with the mitotic spindle, a structure critical for cell replication. This disruption was associated with changes in the expression of genes that regulate cell division, particularly those involved in the “Mitotic Roles of Polo-Like Kinase” pathway. These effects were specific to tumor-targeted frequencies, as non-matching signals had no measurable impact. The study also includes data from two patients with difficult-to-treat brain tumors who received the therapy through compassionate use. One patient with recurrent glioblastoma showed signs of clinical and radiographic improvement after one month of treatment. Another patient with oligodendroglioma tolerated the therapy well and had stable disease during follow-up imaging. Neither patient experienced serious side effects, further supporting the safety of the therapy. “There was evidence of clinical and radiological benefit in a 38-year-old patient with recurrent GB and evidence of safety and feasibility in a 47-year-old patient with oligodendroglioma.” This is the first study to demonstrate that tumor-specific radiofrequency therapy can suppress both tumor growth and cancer stem cells in glioblastoma. Similar results had previously been observed in liver and breast cancers. These findings contribute to the growing body of evidence supporting a new class of systemic, non-toxic cancer therapies. Further clinical trials will be crucial to confirm these results and fully assess the potential of this approach for treating brain cancer. DOI - https://doi.org/10.18632/oncotarget.28770 Correspondence to - Hugo Jimenez - hugo.jimenez@wayne.edu Abstract video - https://www.youtube.com/watch?v=uxYnWcNKYfg Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28770 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, oncology, amplitude-modulated radiofrequency electromagnetic fields, glioblastoma, TheraBionic, CACNA1H, Cav3.2 To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM
Check your ego at the door! In this BackTable MSK Brief, Dr. Mark Amsbaugh and Dr. Ran Lador share their multidisciplinary approach to the treatment of spinal tumors at the University of Texas and Memorial Hermann in Houston. They highlight the distinctive aspects of their practice, including their extensive collaboration and support system for patients, the intricate process of managing spinal tumors, and the unique challenges and solutions they encounter. The doctors emphasize the importance of teamwork, minimally invasive techniques, and comprehensive patient-centered care to improve treatment outcomes for patients with spinal tumors. Episode Outline 00:00 - Introduction 03:18 - Addressing Potential Barriers in Receiving Spinal Tumor Treatment 04:32 - The Multidisciplinary Approach in Action 07:46 - Minimally Invasive Techniques and Their Impact 09:49 - Navigating Patient Care and Referrals 14:29 - Final Thoughts Resources Dr. Mark Amsbaugh, MD https://med.uth.edu/neurosciences/dr-mark-j-amsbaugh-md/ Dr. Ran Lador, MD https://med.uth.edu/ortho/2022/11/02/ran-lador-md/ Dr. Alexa Levey, MD https://medicine.yale.edu/profile/alexa-levey/
Dr. Hope Rugo and Dr. Giuseppe Curigliano discuss recent developments in the field of bispecific antibodies for hematologic and solid tumors, including strategies to optimize the design and delivery of the immunotherapy. TRANSCRIPT Dr. Hope Rugo: Hello and welcome to By the Book, a podcast series from ASCO that features engaging conversations between editors and authors of the ASCO Educational Book. I am your host, Dr. Hope Rugo. I am the director of the Women's Cancers Program and division chief of breast medical oncology at the City of Hope Cancer Center. I am also the editor-in-chief of the Educational Book. Bispecific antibodies represent an innovative and advanced therapeutic platform in hematologic and solid tumors. And today, I am delighted to be joined by Dr. Giuseppe Curigliano to discuss the current landscape of bispecific antibodies and their potential to reshape the future of precision oncology. Dr. Curigliano was the last author of an ASCO Educational Book piece for 2025 titled, "Bispecific Antibodies in Hematologic and Solid Tumors: Current Landscape and Therapeutic Advances." Dr. Curigliano is a breast medical oncologist and the director of the Early Drug Development Division and chair of the Experimental Therapeutics Program at the European Institute of Oncology in Milan. He is also a full professor of medical oncology at the University of Milan. You can find our disclosures in the transcript of this episode. Dr. Curigliano, Giuseppe, welcome and thanks for being here. Dr. Giuseppe Curigliano: Thanks a lot for the invitation. Dr. Hope Rugo: Giuseppe, I would like to first ask you to provide some context for our listeners on how these novel therapeutics work. And then perhaps you could tell us about recent developments in the field of bispecific antibodies for oncology. We are at a time when antibody-drug conjugates (ADCs) are all the rage and, trying to improve on the targeting of specific antigens, proteins, receptors in the field of oncology is certainly a hot and emerging topic. Dr. Giuseppe Curigliano: So, thanks a lot. I believe really it was very challenging to try to summarize all the bispecific antibodies that are under development in multiple solid tumors. So, the first thing that I would like to highlight is the context and the mechanism of action of bispecific antibodies. Bispecific antibodies represent a groundbreaking advancement in cancer immunotherapy, because these engineered molecules have the unique ability to target and simultaneously bind to two distinct antigens. That is why we call them bispecific. So typically, one antigen is expressed on the tumor cell and the other one is expressed on the immune effectors, like T-cell or natural killer cells. So this dual targeting mechanism offers several key advantages over conventional monoclonal antibodies because you can target at the same time the tumor antigen, downregulating the pathway of proliferation, and you can activate the immune system. So the primary mechanism through which bispecific antibodies exert their therapeutic effects are: First, T-cell redirecting. I mean, many bispecific antibodies are designed to engage tumor-associated antigens like epidermal growth factor receptor, HER2, on the cancer cell and a costimulatory molecule on the surface of T-cell. A typical target antigen on T-cell is CD3. So what does it mean? That you activate the immune system, immune cells will reach the tumor bed, and you have a dual effect. One is downregulating cell proliferation, the other one is activation of the immune system. This is really important in hematological malignancies, where we have a lot of bispecifics already approved, like acute lymphoblastic leukemia or non-Hodgkin lymphoma. The second, in fact, is the engagement of the tumor microenvironment. So, if you engage immune effector cells like NK cells or macrophages, usually the bispecific antibodies can exploit the immune system's ability to recognize and kill the immune cells, even if there is a lack of optimal antigen presentation. And finally, the last mechanism of action, this may have a role in the future, maybe in the early cancer setting, is overcoming immune evasion. So bispecific antibodies can overcome some of the immune evasion mechanisms that we see in cancer. For example, bispecific antibodies can target immune checkpoint receptors, like PD-L1 and CTLA-4. Actually, there is a bispecific under development in breast cancer that has a dual targeting on vascular endothelial growth factor receptor and on PD-L1. So you have a dual effect at the same time. So, what is really important, as a comment, is we need to focus first on the optimal format of the bispecific, the optimal half-life, the stability, because of course even if they are very efficient in inducing a response, they may give also a lot of toxicities. So in clinical trials already, we have several bispecifics approved. In solid tumors, very few, specifically amivantamab for non-small cell lung cancer, but we have a pipeline of almost 40 to 50 bispecifics under development in multiple solid tumors, and some of them are in the context of prospective randomized trials. Dr. Hope Rugo: So this is really a fascinating area and it's really exciting to see the expansion of the different targets for bispecific antibodies. One area that has intrigued me also is that some of the bispecifics actually will target different parts of the same receptor or the same protein, but presumably those will be used as a different strategy. It's interesting because we have seen that, for example, in targeting HER2. Dr. Giuseppe Curigliano: Oh, yes, of course. You may consider some bispecifics like margetuximab, I suppose, in which you can target specifically two different epitopes of the same antigen. This is really an example of how a bispecific can potentially be more active and downregulating, let us say, a pathway, by targeting two different domains of a specific target antigen. This is an important point. Of course, not all the bispecifics work this way, because some of the target antigen may dimerize, and so you have a family of target antigen; an example is epidermal growth factor receptor, in which you have HER1, HER2, HER3, and HER4. So some of them can inhibit the dimerization between one target antigen and the other one, in order to exert a more antiproliferative effect. But to be honest, the new generation of them are more targeting two different antigens, one on the tumor and one on the microenvironment, because according to the clinical data, this is a more efficient way to reduce proliferation and to activate the immune system. Dr. Hope Rugo: Really interesting, and I think it brings us to the next topic, which is really where bispecific antibodies have already shown success, and that is in hematologic malignancies where we have seen very interesting efficacy and these are being used in the clinic already. But the expansion of bispecific antibodies into solid tumors faces some key challenges. It's interesting because the challenges come in different shapes and forms. Tell us about some of those challenges and strategies to optimize bispecific antibody design, delivery, patient selection, and how we are going to use these agents in the right kind of clinical trials. Dr. Giuseppe Curigliano: This is really an excellent question because despite bispecific antibodies having shown a remarkable efficacy in hematological malignancies, their application in solid tumors may have some challenges. The first one is tumor heterogeneity. In hematological malignancy, you have a clear oncogene addiction. Let us say that 90% of the cells may express the same antigen. In solid tumors, it is not the same. Tumor heterogeneity is a typical characteristic of solid tumors, and you have high heterogeneity at the genetic, molecular, and phenotypic levels. So tumor cells can differ significantly from one another, even if within the same tumor. And this heterogeneity sometimes makes it difficult to identify a single target antigen that is universally expressed in an hematological malignancy. So furthermore, sometimes the antigen expressed on a tumor cell can be also present on the normal tissue. And so you may have a cross-targeting. So let's say, if you have a bispecific against epidermal growth factor receptor, this will target the tumor but will target also the skin with a lot of toxicity. The second challenge is the tumor microenvironment. The solid tumor microenvironment is really complex and often immunosuppressive. It is characterized by the presence of immunosuppressor cells like the T regulators, myeloid derived suppressor cells, and of course the extracellular matrix. All these factors hinder immune cell infiltration and also may reduce dramatically the effectiveness of bispecific antibodies. And as you know, there is also an hypoxic condition in the tumor. The other challenge is related to the poor tumor penetration. As you know also with antibody-drug conjugate, only 1 to 3% of the drug will arrive in the tumor bed. Unlike hematological malignancies where tumor cells are dispersed in the blood and easily accessible, the solid tumors have a lot of barriers, and so it means that tumor penetration can be very low. Finally, the vascularity also of the tumor can be different across solid tumors. That is why some bispecifics have a vascular endothelial growth factor receptor or vascular endothelial growth factor as a target. Of course, what do we have to do to overcome these challenges? First, we have to select the optimal antigen. So knowing very well the biology of cancer and the tumor-associated antigens can really select a subgroup of epitopes that are specifically overexpressed in cancer cells. And so we need to design bispecifics according to the tumor type. Second, optimize the antibody format. So there are numerous bispecific antibody formats. We can consider the dual variable domain immunoglobulin, we specified this in our paper. The single chain variable fragments, so FC variable fragments, and the diabodies that can enhance both binding affinity and stability. And finally, the last point, combination therapies. Because bispecific antibodies targeting immune checkpoint, we have many targeting PD-1 or PD-L1 or CTLA-4, combined eventually with other immune checkpoint inhibitors. And so you may have more immunostimulating effect. Dr. Hope Rugo: This is a fascinating field and it is certainly going to go far in the treatment of solid tumors. You know, I think there is some competition with what we have now for antibody-drug conjugates. Do you see that bispecifics will eventually become bispecific ADCs? Are we going to combine these bispecific antibodies with ADCs, with chemotherapy? What is the best combination strategy do you think looking forward? Dr. Giuseppe Curigliano: So, yes, we have a bispecific ADC. We have actually some bispecifics that are conjugated with a payload of chemotherapy. Some others are conjugated with immunoactivation agents like IL-2. One of the most effective strategies for enhancing bispecific activity is the combination therapy. So which type of combination can we do? First, bispecific antibodies plus checkpoint inhibitors. If you combine a bispecific with an immune checkpoint, like anti-PD-1, anti-PD-L1, or anti-CTLA-4, you have more activity because you have activation of T-cells, reduction of immunosuppressive effect, and of course, the capability of this bispecific to potentiate the activity of the immune checkpoint inhibitor. So, in my opinion, in a non-small cell lung cancer with an expression of PD-L1 more than 50%, if you give pembrolizumab plus a bispecific targeting PD-L1, you can really improve both response rate and median progression-free survival. Another combination is chemotherapy plus bispecific antibodies. Combining chemotherapy with bispecific can enhance the cytotoxic effect because chemotherapy induces immunogenic cell death, and then you boost with a bispecific in order to activate the immune system. Bispecific and CAR T-cells, until now, we believe that these are in competition, but this is not correct. Because CAR T-cells are designed to deliver an activation of the immune system with the same lymphocytes engineered of the patients, with a long-term effect. So I really do not believe that bispecifics are in competition with CAR T-cells because when you have a complete remission induced by CAR T-cell, the effect of this complete remission can last for years. The activity of a bispecific is a little bit different. So there are some studies actually combining CAR T-cells with bispecifics. For example, bispecific antibodies can direct CAR T-cells in the tumor microenvironment, improving their specificity and enhancing their therapeutic effect. And finally, monoclonal antibody plus bispecific is another next generation activity. Because if you use bispecific antibodies in combination with existing monoclonal antibodies like anti-HER2, you can potentially increase the immune response and enhance tumor cell targeting. In hematological malignancies, this has been already demonstrated and this approach has been particularly effective. Dr. Hope Rugo: That's just so fascinating, the whole idea that we have these monoclonal antibodies and now we are going to add them to bispecifics that we could maybe attach on different toxins to try and improve this, or even give them with different approaches. I suppose giving an ADC with a bispecific would sort of be similar to that idea of giving a monoclonal antibody with the bispecific. So it is certainly intriguing. We also will need to understand the toxicity and cost overall and how we are going to use these, the duration of treatment, the assessment of biomarkers. There are just so many different aspects that still need to be explored. And then with that idea, can you look ahead five or ten years from now, and tell us how you think bispecific antibodies will shape our next generation cancer therapies, how they will be incorporated into precision oncology, and the new combinations and approaches as we move forward that will help us tailor treatment for patients both with solid tumors and hematologic malignancies? Are we going to be giving these in early-stage disease in solid tumors? So far, the studies are primarily focusing on the metastatic setting, but obviously one of the goals when we have successful treatments is to move them into the early stage setting as quickly as possible. Dr. Giuseppe Curigliano: Let us try to look ahead five years rather than ten years, to be more realistic. So, personally I believe some bispecifics can potentially replace current approaches in specifically T-cell selected population. As we gather more data from ongoing clinical trials and we adopt a deeper understanding of the tumor immuno microenvironment, of course we may have potentially new achievement. A few days ago, we heard that bispecifics in triple negative breast cancer targeting VEGF and PD-L1 demonstrated an improvement in median progression-free survival. So, how to improve and to impact on clinical practice both in the metastatic and in the early breast cancer setting or solid tumor setting? First, personalized antigen selection. So we need to have the ability to tailor bispecific antibody therapy to the unique tumor profile of individual patients. So the more we understand the biology of cancers, the more we will be able to better target. Second, bispecific antibodies should be combined. I can see in the future a potential trial in which you combine a bispecific anti-PD-L1 and VEGF with immune checkpoint inhibitor selected also to the level of expression of PD-L1, because integration of antibody bispecific with a range of immunotherapies, and this cannot be only immune checkpoint inhibitors, but can be CAR T-cells, oncolytic viruses, also targeted therapy, will likely be a dominant theme in the coming years. This combination will be based on the specific molecular and immuno feature of the cancer of the patient. Then we need an enhanced delivery system. This is really important because you know now we have a next generation antibody. An example are the bicyclic. So you use FC fragment that are very short, with a low molecular weight, and this short fragment can be bispecific, so can target at the same time a target antigen and improving the immune system. And so the development of this novel delivery system, including also nanoparticles or engineered viral vectors, can enhance the penetration in the tumor bed and the bioavailability of bispecific antibodies. Importantly, we need to reduce toxicity. Until now, bispecifics are very toxic. So the more we are efficient in delivering in the tumor bed, the more we will reduce the risk of toxicity. So it will be mandatory to reduce off-target effects and to minimize toxicity. And finally, the expansion in new indication. So I really believe you raised an excellent point. We need to design studies in the neoadjuvant setting in order to better understand with multiple biopsies which is the effect on the tumor microenvironment and the tumor itself, and to generate hypotheses for potential trials or in the neoadjuvant setting or in those patients with residual disease. So, in my opinion, as we refine design, optimize patient selection, and explore new combination, in the future we will have more opportunity to integrate bispecifics in the standard of care. Dr. Hope Rugo: I think it is particularly helpful to hear what we are going to be looking for as we move forward to try and improve efficacy and reduce toxicity. And the ability to engineer these new antibodies and to more specifically target the right proteins and immune effectors is going to be critical, of course, moving forward, as well as individualizing therapy based on a specific tumor biology. Hearing your insights has been great, and it really has opened up a whole area of insight into the field of bispecifics, together with your excellent contribution to the ASCO Educational Book. Thank you so much for sharing your thoughts and background, as well as what we might see in the future on this podcast today. Dr. Giuseppe Curigliano: Thank you very much for the invitation and for this excellent interview. Dr. Hope Rugo: And thanks to our listeners for joining us today. You will find a link to the Ed Book article we discussed today in the transcript of this episode. It is also, of course, on the ASCO website, as well as on PubMed. Please join us again next month on By the Book for more insightful views on the key issues and innovations that are shaping modern oncology. 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. Hope Rugo @hope.rugo Dr. Giuseppe Curigliano @curijoey Follow ASCO on social media: @ASCO on X (formerly Twitter) ASCO on Bluesky ASCO on Facebook ASCO on LinkedIn Disclosures: Dr. Hope Rugo: Honoraria: Mylan/Viatris, Chugai Pharma Consulting/Advisory Role: Napo Pharmaceuticals, Sanofi, Bristol Myer Research Funding (Inst.): OBI Pharma, Pfizer, Novartis, Lilly, Merck, Daiichi Sankyo, AstraZeneca, Gilead Sciences, Hoffman La-Roche AG/Genentech, In., Stemline Therapeutics, Ambryx Dr. Giuseppe Curigliano: Leadership: European Society for Medical Oncology, European Society of Breast Cancer Specialists, ESMO Open, European Society for Medical Oncology Honoraria: Ellipses Pharma Consulting or Advisory Role: Roche/Genentech, Pfizer, Novartis, Lilly, Foundation Medicine, Bristol-Myers Squibb, Samsung, AstraZeneca, Daiichi-Sankyo, Boerigher, GSK, Seattle Genetics, Guardant Health, Veracyte, Celcuity, Hengrui Therapeutics, Menarini, Merck, Exact Sciences, Blueprint Medicines, Gilead Sciences Speakers' Bureau: Roche/Genentech, Novartis, Pfizer, Lilly, Foundation Medicine, Samsung, Daiichi Sankyo, Seagen, Menarini, Gilead Sciences, Exact Sciences Research Funding: Merck Travel, Accommodations, Expenses: Roche/Genentech, Pfizer, Daiichi Sankyo, AstraZeneca
WFR Radio 447 How Big Is Your Tax Tumor by Tony Walker Financial
Kidney cancer management is evolving. How are experts adapting? In this installment of BackTable Tumor Board, Dr. Brandon Manley (Urologic Oncology, Moffitt Cancer Center), Dr. Raquibul Hannan (Radiation Oncology, UT Southwestern), and Dr. Rana McKay (Medical Oncology, UC San Diego) join guest host Mark Ball (Urologic Oncology, National Cancer Institute) to share their multidisciplinary perspectives on challenging, real-world kidney cancer cases.---This podcast is supported by:Ferring Pharmaceuticalshttps://ad.doubleclick.net/ddm/trackclk/N2165306.5658203BACKTABLE/B33008413.420220578;dc_trk_aid=612466359;dc_trk_cid=234162109;dc_lat=;dc_rdid=;tag_for_child_directed_treatment=;tfua=;gdpr=${GDPR};gdpr_consent=${GDPR_CONSENT_755};gpp=${GPP_STRING_755};gpp_sid=${GPP_SID};ltd=;dc_tdv=1---SYNPOSISThe conversation covers diagnostic dilemmas, navigating the treatment options of surgery, systemic therapy, and radiation, and the importance of a multidisciplinary approach. Through detailed case reviews, the panel highlights practical pearls, emerging clinical trials, and collaborative approaches that exemplify modern kidney cancer care.---TIMESTAMPS0:00 - Introduction02:20 - Case 1 (Incidental Renal Mass)16:52 - Case 2 (Bilateral Renal Masses)37:22 - Case 3 (Locally Advanced Renal Mass)56:34 - Case 4 (Symptomatic, Metastatic Disease)01:14:00 - Final Takeaways
Krebs bei jungen Menschen; Quarks Radio; KI kann Gefühle; Kommentar: Nobelpreis - ein veraltetes Ritual?; Nobelpreis Physik; Wie kann guter Umgang mit TikTok aussehen?; Wie sinnvoll sind Trigger-Warnungen?; Warum Frauen länger leben als Männer; Risiken und Nebenwirkungen von Psychotherapie; Moderation: Marlis Schaum. Von WDR 5.
Functional synapses between brain cells and cancer cells are key to the metastatic growth, according to new findings from two independent teams.
In this episode with Meagan Lindquist, you’ll discover the world of AHCC, a cultured mushroom extract with a remarkable range of health benefits. We explore its origins, patented culturing process in Japan, and what makes AHCC uniquely bioavailable compared to other mushroom supplements. Meagan shares her health journey, her experiences supporting patients, and her passion for spreading awareness about AHCC’s research-backed potential—from cancer and HPV to Lyme disease and overall immune function. The conversation highlights AHCC’s role as an immunomodulator, antioxidant, and anti-inflammatory compound, reviewing studies that demonstrate its benefits for general immune support and as complementary therapy for serious conditions, such as cancer and chronic infections. Practical topics include supplement quality, dosing, and how to find credible sources. By the end, you’ll have insights and actionable information to evaluate AHCC as part of a thoughtful, science-driven approach to immune optimization and integrative health. Meagan (Mimi) Lindquist (@mimi_themedicin) is the co-founder of The Medicin, alongside her husband Chase. Together, they provide high-quality mushroom products to the world. With her background as a clinical dental hygienist, nutrition guide, and AHCC educator, she has been helping others prevent disease for over 12 years. Now, Mimi is dedicated to sharing the benefits of Immune Intel AHCC, a mushroom product unlike any other, to as many people as possible. She hosts monthly live calls with Dr. Nathan Riley for women trying to clear HPV naturally using AHCC. In her words, it is her "life's passion to spread the word about how powerful it is." Full show notes: bengreenfieldlife.com/ahccpodcast Episode Sponsors: Organifi Shilajit Gummies: Harness the ancient power of pure Himalayan shilajit anytime you want with these convenient and tasty gummies. Get them now for 20% off at organifi.com/Ben. BlockBlueLight: BlockBlueLight BioLights are the only lights extensively tested and recommended by building biologist Brian Hoyer as truly flicker-free, ultra-low EMF, and circadian-friendly, with three modes (day, evening, night) that support natural rhythms and optimize sleep quality. Get 10% off your first order at blockbluelight.com/Ben (discount autoapplied at checkout). Fatty15: Fatty15 is on a mission to optimize your C15:0 levels and help you live healthier, longer. You can get an additional 15% off their 90-day subscription Starter Kit by going to fatty15.com/BEN and using code BEN at checkout. LVLUP Health: I trust and recommend LVLUP Health for your peptide needs as they third-party test every single batch of their peptides to ensure you’re getting exactly what you pay for and the results you’re after! Head over to bengreenfieldlife.com/lvluphealth and use code BEN15 for a special discount on their game-changing range of products. BiOptimizers Magnesium Breakthrough: The 7 essential forms of magnesium included in this full spectrum serving help you relax, unwind, and turn off your active brain after a long and stressful day so you can rest peacefully and wake up feeling refreshed, vibrant, and alert. Go to bioptimizers.com/ben and use code ben15 for 15% off any order.See omnystudio.com/listener for privacy information.
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10-03-25 - New Update On Tumor Listener Gary His Wife Who Flew To See Him In Hospital - BOSee Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.
Is microwave ablation only for simple liver tumors, or can it be a versatile ‘Swiss Army knife' for a wide range of complex cases? In this episode, Dr. Driss Raissi of the University of Kentucky returns to BackTable to join host Dr. Chris Beck for a deep dive into advanced and unconventional microwave ablation techniques. They cover strategies for tackling a wide range of cases, from desmoid tumors to enterocutaneous fistulas.---This podcast is supported by:Medtronic Emprinthttps://www.medtronic.com/emprint---SYNPOSISDr. Raissi shares his ‘pre-burn' technique that desiccates tissue and reduces complications like capsular burst and bleeding. He elaborates on his method for tackling large liver tumors with a single probe through overlapping ablations, needle placement techniques and his ‘lung seal technique' to prevent pneumothorax. Dr. Raissi also shares how his previous experience in the ICU promotes close communication with anesthesiologists and how he ups his ablation game through collaboration, optimizing conditions for safe and effective ablation.The episode explores a series of unique, real-world applications beyond the usual scope of IRs. Dr. Raissi walks us through his novel approach to challenging cases, including cauterization of enterocutaneous fistulas, endometriomas and desmoid tumors. He also compares using microwave or cryoablation for renal cell carcinoma, explaining thought processes based on lesion location and the need for speed and simplicity. The discussion provides an overview of ablation physics and careful techniques that expand treatment possibilities for IR patients.---TIMESTAMPS00:00 - Introduction 04:08 - Advanced Techniques for Liver Tumor Ablation06:06 - Pre-Burning Ablation and Ablating a Range of Lesions16:38 - Lung Ablation22:00 - Partnering with Anesthesia28:53 - Managing Postoperative Pain and Nerve Injuries29:42 - Treating Enterocutaneous Fistulas, Endometriomas & Desmoid Tumors38:49 - Adrenal Gland Ablation: A Case Study44:50 - Microwave vs. Cryoablation for Renal Cell Carcinoma49:06 - Preventing Pneumothorax in Lung Ablation
Guest: Danielle O'Laughlin, PA-C, MS Hosts: Danielle O'Laughlin, PA-C, MS and Jenna Wygant, APRN, CNP, DNP In this episode, Danielle O'Laughlin discusses benign breast tumor conditions and other non-cancerous growths. Listeners will gain insight into the clinical presentation, diagnostic evaluation, and management strategies for these common breast findings. Learning Objectives: Review the types of benign breast tumors and their clinical features. Differentiate between symptoms, diagnostic approaches, and treatment options for various benign breast conditions. Learn more about this series: Mayo Clinic Talks: Obstetric and Gynecologic Health | Mayo Clinic School of Continuous Professional Development Connect and listen with Mayo Clinic Podcasts | Mayo Clinic School of Continuous Professional Development
MOJO Rising: How to Make Cancer Suck Less with Julie Stevens
In this groundbreaking episode, we dive deep into MOJO Health's "Data Iceberg" concept that's revolutionizing cancer care. Many people make life-changing medical decisions using only 2 types of data - biopsy results and imaging scans. If you go to the most advanced cancer centers, you likely use 6, but there are 7 additional categories of health data hiding beneath the surface that will transform your healing strategy.What You'll Discover:- Why most healthcare operates on "tip of the iceberg" data- The 13 hidden data categories that predict treatment success- How molecular DNA profiling creates personalized treatment roadmaps- The power of circulating tumor DNA (liquid biopsies) for real-time monitoringPerfect for: Cancer patients, survivors, caregivers, healthcare advocates, and anyone who wants to transform from reactive to proactive healthcare.Remember: Data G's don't just hope their treatment is working. They know.Resources Mentioned:For our downloadable Guide to Be a Data G, please go to mojohealth.org/datagguideTo set up an appointment with Oscar Sierra, please reach out to https://www.sierracollaborativemed.com/To see National Cancer Institute's page the blood biomarkers: https://www.cancer.gov/about-cancer/diagnosis-staging/diagnosis/tumor-markers-listAnd here for information on different types of data to request: https://www.mojohealth.org/be-a-data-g-1Other Podcasts to watch:#4 A Data G's Guide to Beating Cancer w/ Julie Stevens and Oscar Sierra, L.Ac.#6 BRCA2 Data Dilemma: Lessons in Gene Expression#8 How Genomic Testing Can Transform Your Cancer JourneyWhat tests do you need your doctor to order? Biopsy, Imaging, Circulating Tumor DNA, and Molecular DNA of the Tumor.Basically everything else you can order on your own through Direct Patient Labs: https://www.mojohealth.org/direct-labs-mojo-panelsConnect with Julie Stevens and the MOJO Movement: Instagram: https://instagram.com/mojohealthorg TikTok: https://tiktok.com/@julie.stevens97YouTube: https://www.youtube.com/@mojohealth Facebook: https://facebook.com/mojohealthorg Website: https://www.mojohealth.org/DISCLAIMER: The views, thoughts, and opinions expressed on this podcast are the speaker's own and do not represent the views, thoughts, and opinions of MOJO Health Cooperative LLC, a Georgia Limited Liability Company, its respective officers, directors, employees, agents, or representatives. This podcast is presented by MOJO Health Cooperative, and cannot be copied or rebroadcast without consent. The material and information presented here is for general information purposes only, and not intended to supplant the expert advice and/or consultation of a medical doctor and/or a licensed physician, and/or an attorney. In short, this podcast is not intended to replace professional medical advice, nor legal advice. The "MOJO Health" name and all forms and abbreviations are the property of its owner and its use does not imply endorsement of or opposition to any specific organization, product, or service. Again, none of the content of this podcast should be considered legal advice, nor medical advice. As always, consult a lawyer and/or a licensed physician in lieu of relying upon the advice of any of the participants of this podcast. The host(s) of this podcast are not licensed lawyers, physicians, doctors of osteopath, nor medical doctors in any jurisdiction anywhere. The host(s) of this podcast do not practice medicine and do NOT profess to be able to do any of the following: (1) diagnose, heal, treat, prevent, prescribe for, or removing any physical, mental, or emotional ailment or supposed ailment of an individual; (2) engage in the end of human pregnancy; (3) treat human ailments; nor (4) perform acupuncture. MOJO Health Cooperative LLC is not responsible for any losses, damages, or liabilities that may arise from the use of this podcast.
In this JCO Precision Oncology Article Insights episode, Dr. Jiasen He summarizes JCO PO article "Synthetic Lethal Co-Mutations in DNA Damage Response Pathways Predict Response to Immunotherapy in Pan-Cancer" by Hua Zhong et al. TRANSCRIPT Jiasen He: Hello and welcome to the JCO Precision Oncology Article Insights. I am your host, Jiasen He, and today we will be discussing the JCO Precision Oncology article, "Synthetic Lethal Co-mutations in DNA Damage Response Pathway Predict Response to Immunotherapy in Pan-Cancer" by Dr. Zhang and colleagues. Immunotherapy has emerged as a groundbreaking treatment option for many types of cancer. However, the overall response rate to immunotherapy is low, around 10% to 30%. This highlights the critical need to identify which patients are most likely to benefit from immunotherapy. Two of the most extensively studied biomarkers are PD-L1 expression and tumor mutation burden (TMB). High levels of PD-L1 and TMB have been associated with better response to immune checkpoint inhibitors, which are now widely used in clinical practice. The predictive value of these markers is inconsistent across all settings. Some tumors with high PD-L1 or TMB still respond poorly to immunotherapy. One reason is that TMB reflects new antigen production, but recent studies suggest that new antigen levels do not always correlate with tumor immunogenicity. Many new antigens are not effectively recognized by T cells, limiting the immune response. Emerging evidence indicates that mutations in the DNA damage response (DDR) pathway play a critical role in moderating tumor immune interactions. Tumors harboring DDR pathways frequently exhibit increased genome instability, which may enhance their sensitivity to immune checkpoint inhibitors. While all these pathways are under active investigation, the optimal DDR pathway biomarkers for patient selection remain unclear. Notably, tumor cells with a defect in one DDR pathway may acquire greater reliance on alternative DDR pathways. Recent studies suggest that synthetic lethal co-mutations within DDR pathways are associated with immune-inflamed or hot tumor microenvironments. Based on this rationale, Dr. Zhang is investigating if synthetic lethal co-mutations in DDR pathway response pathway can serve as a treatment biomarker for immune checkpoint inhibitors. To address this question, Dr. Zhang and colleagues first utilized SynLethDB 2.0, a comprehensive database that integrated multiple data sets. Synthetic lethal (SL) gene pairs in this resource are identified through both experimental and computational approaches, with confidence scores assigned to each pair. These SL pairs were then mapped to gene sequencing results from several clinical cohorts. SL co-mutation status was defined as positive when both genes in a synthetic lethal pair were mutated. From this, SL co-mutation pairs specifically involving DDR pathway genes were selected. Patients were classified as DDR co-mutation positive if both genes in a synthetic lethal pair, each belonging to the defined DDR pathways, were mutated. In total, 431 DDR-related SL pairs were identified and matched to sequencing data from clinical cohorts. Clinical information was extracted from the cBioPortal, while further analysis of immune infiltration was performed using DNA mutation and RNA expression data from The Cancer Genome Atlas (TCGA) pan-cancer data set. The author first examined the correlation between SL co-mutation status and response to ICI therapy. They discovered that patients with SL co-mutation showed significantly improved outcome to ICI therapy across various clinical cohorts. Notably, in patients who did not receive ICI treatment, patients with SL co-mutation showed markedly compromised overall survival. Further analysis focused on the predictive value of SL co-mutation within DDR pathway genes. The author found that patients with DDR SL co-mutation had a longer overall survival compared to those with mutations in a single DDR gene, implying that SL co-mutations may be more effective biomarkers within the DDR pathway. To explore this further, in the TMB-MSKCC cohort, the author found that patients with DDR co-mutation constituted approximately 20% of various cancer types, including non-small cell lung cancer, melanoma, and bladder cancer. These patients demonstrated significantly better survival outcomes and disease control rates when treated with ICIs compared to DDR co-mutation negative patients. Notably, the TMB level was substantially higher in patients with DDR co-mutation, a finding consistent with data from the Miao-lung cohort. Furthermore, in cohorts not treated with ICIs, patients with DDR co-mutation had a shorter overall survival compared to their counterparts. Upon stratifying by PD-L1 expression, the author observed that patients with DDR co-mutation who were also PD-L1 positive derived the greatest clinical benefit from ICI therapy. Upon analyzing the frequency of co-mutation within the DDR pathway, the authors found that patients with SL co-mutation in the CPF-CPF pathway experienced remarkable survival benefit from ICIs. Within this group, one of the most common co-mutation combinations was TP53-ATM, observed in approximately 45% of cases, which was associated with a better response to ICI therapy. Further analysis of immune cell infiltration revealed that patients with TP53-ATM co-mutation exhibited a distinct tumor immune microenvironment. As the authors stated, the study's main limitation lies in the nature of retrospective analysis, which lacked the control over confounding variables and was subject to non-random sampling. For instance, patients with both SL co-mutations and DDR SL co-mutations exhibited high TMB, and TMB was known to be associated with improved response to ICI therapy itself. So, these findings require validation through prospective studies, and immune infiltration analysis needs confirmation via laboratory experiments. In conclusion, the authors found that patients with SL co-mutations in DDR pathways showed favorable clinical response and prolonged survival following ICI therapy. They also identified TP53-ATM co-mutations as a clinically relevant biomarker for predicting ICI treatment response. Thank you for tuning in to JCO Precision Oncology Article Insights. Don't forget to subscribe and join us next time as we explore more groundbreaking research shaping the future of oncology. 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.
In this episode we catch up with Zack Round. Zack is known as the Tumor Warrior and does a lot for others who suffer from brain tumors like Zack had. We get to catch up and talk about his re-branding in this episode. Support for the Segment Podcast are brought to you by:THE SEGMENT / DISCOUNT CODES / SUPPORTERSYT Industrieshttps://us.yt-industries.com/Etnies MTB Shoes: Promocode TheSegment30https://etnies.com/collections/bike-mtb Versus Tires: www.versustires.comTASCO MTB Apparel 15% offhttps://tasco-mtb-2.kckb.st/3bb12b05Promo Code: SEGMENT24 Spy Optic: https://www.spyoptic.com/Promo code SEGMENT20 20% off your purchaseKapu CoffeePurchase "The Sender" here: https://kapucoffee.com/pages/segment25% of the proceeds help the charity "Making Spirits Bright" which helps get kids outside and on bikes.https://msbfoundation.org/Kali Protectiveshttps://kaliprotectives.com/collections/full-face/products/dh-invader?variant=41188142481502Promo Code Segment25Mother Earth Brew Company: https://www.motherearthbrewco.com/PelliBikeCare: https://www.pellibikecare.com/Strong Coffee: 15% off https://strongcoffeecompany.com/?ref=Segment30Or use promo code SEGMENT15 at checkout. To become a Podcaster for Free try this link: https://streamyard.com/pal/c/4674191405613056PHAT Lids: https://www.phatlids.com/Use promo code SEGMENT to get 10% off at checkout. SALTSTICK https://aletenutrition.com/pages/saltstick Use promo code SEGMENT20 to get 20% off
The only way to follow up last week's milestone is with the rarest of the rare medical cases. Fun. — Support and sponsor this show! Venmo Tip Jar: @wellthatsinteresting Instagram: @wellthatsinterestingpod Bluesky: @wtipod Threads: @wellthatsinterestingpod Twitter: @wti_pod Listen on YouTube!! Oh, BTW. You're interesting. Email YOUR facts, stories, experiences... Nothing is too big or too small. I'll read it on the show: wellthatsinterestingpod@gmail.com WTI is a part of the Airwave Media podcast network! Visit AirwaveMedia.com to listen and subscribe to other incredible shows. Want to advertise your glorious product on WTI? Email me: wellthatsinterestingpod@gmail.com Learn more about your ad choices. Visit megaphone.fm/adchoices
Send us a textDr Kate Lund is a psychologist, TEDx speaker, and podcast host of The Optimized Mind, and she spends her days helping people turn those "what now?" Moments into genuine resilience.. Her work centers on translating over 20 years of research into simple, science-backed habits that real humans can use during in their hardest of times, whether they're navigating parenthood, setbacks, or that feeling of life falling apart.Dr Kate talks about her early childhood with hydrocephalus, (she explains what that is!!) and subsequent tumor diagnosis, and how that set her apart as different than her peers and at the same time fostered a sense of resilience and possibility beyond the challenges. As a best selling author, she has seen firsthand how messy, imperfect resilience can change someone's story. Her book, ‘Step Away: The Keys to Resilient Parenting', is out in October 2025. Book: https://a.co/d/4CaffaCSite: Www.katelundspeaks.com TedX: https://www.youtube.com/watch?v=-p6YcTsWySU&t=14sThe Dom Sub Living BDSM and Kink PodcastCurious about Dominance & submission? Real stories, real fun, really kinky.Listen on: Apple Podcasts SpotifySupport the show
In this episode of Blood Cancer Talks, hosts Eddie, Ashwin, and Raj welcome two distinguished experts to explore the cutting-edge field of circulating tumor DNA (ctDNA) in B-cell lymphomas. Dr. David Russler-Germain, a lymphoma clinician from Siteman Cancer Centre at Washington University in St. Louis, returns as a familiar voice to the podcast audience. Joining him is Dr. Ash Alizadeh, the Moghadam Family Professor of Medicine, Oncology, and Hematology at Stanford University and leader of the Cancer Genomics Program at Stanford Cancer Institute. Dr. Alizadeh has been instrumental in advancing our understanding of lymphomagenesis and lymphoma genetics over the past two decades, pioneering multiple ctDNA techniques that are revolutionizing cancer care. Together, they discuss the transformative potential of ctDNA technology in B-cell lymphomas, particularly DLBCL, covering everything from the technical evolution of biomarker detection to groundbreaking clinical data that may reshape how we monitor and treat these aggressive cancers. Key Discussion Topics1. Genetic Heterogeneity in B-Cell LymphomasComplex genetic landscape of DLBCLImplications for treatment strategiesNeed for personalized approaches 2. Clinical Need for ctDNA in LymphomaWhy ctDNA is needed in aggressive lymphomas:Curative vs. non-curative treatment settingsLimitations of current PET imagingAdditional prognostic information beyond imagingRisk stratification capabilitiesPotential to avoid overtreatmentTherapy adaptation opportunities 3. Challenges in Lymphoma MRD AssessmentWhy lymphoma MRD is more complex than other hematologic malignancies:Differences from acute leukemias, CLL, and myelomaTechnical challenges specific to lymphoid tumorsLower circulating tumor burden compared to liquid tumors 4. ClonoSEQ TechnologyMechanism: Immunoglobulin sequencing approachAdvantages: Established platform with regulatory approvalDisadvantages: Limited sensitivity in peripheral blood, requires adequate tumor sample 5. CAPP-Seq TechnologyFull Name: Cancer Personalized Profiling by Deep SequencingInnovation: Developed ~10 years ago by Dr. Alizadeh's groupMechanism: Targeted sequencing of cancer-specific mutationsAdvantages: High sensitivity, personalized approach 6. PhasED-Seq TechnologyEvolution: Next-generation advancement of CAPP-SeqKey Improvements: Enhanced sensitivity and specificityTechnical Advances: Phased variant detection Clinical Data Highlights1. Remission Assessment by ctDNA in LBCL on 5 prospective studies of frontline anthracycline-based chemo-immunotherapy: https://pubmed.ncbi.nlm.nih.gov/40802906/2. Prospective validation of end of treatment ctDNA-MRD by PhasED-Seq in DLBCL patients from HOVON-902 clinical trial: https://ascopubs.org/doi/10.1200/JCO.2025.43.16_suppl.70003. Korean data on prognostic utility of ctDNA: https://ashpublications.org/blood/article/142/Supplement%201/69/501573
BUFFALO, NY - September 24, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on September 22, 2025, titled “Loss of Trp53 results in a hypoactive T cell phenotype accompanied by reduced pro-inflammatory signaling in a syngeneic orthotopic mouse model of ovarian high-grade serous carcinoma.” In this study, led by first author Jacob Haagsma and corresponding author Trevor G. Shepherd from the Verspeeten Family Cancer Centre and Western University, Canada, researchers investigated how the loss of Trp53 – a critical tumor suppressor gene – affects immune responses in ovarian cancer. The team found that deleting Trp53 led to more aggressive tumor growth and a weaker immune response. These findings help explain why some ovarian tumors may be resistant to immunotherapy and point to new ways to improve treatment. High-grade serous ovarian carcinoma (HGSC) is a deadly cancer that is often diagnosed at a late stage. Immunotherapy, which enhances the body's immune system to fight cancer, has shown limited effectiveness in treating this type of cancer. To better understand why, the researchers developed a mouse model that closely mimics human HGSC. They injected ovarian epithelial cells, with and without Trp53, into the fallopian tubes, the origin site of most ovarian cancers. “In this study, we developed a syngeneic model reflecting both the site of origin and the genotype of early HGSC disease by deleting Trp53 in mouse oviductal epithelial (OVE) cells.” Mice injected with cells lacking Trp53 developed faster-growing and more invasive tumors, reflecting how the disease typically progresses in humans. These tumors also had fewer active T cells, which are immune cells responsible for attacking cancer. Moreover, the T cells that were present appeared less capable of responding to the tumor, creating an immune environment that allowed cancer to grow uncontrolled. Further analysis revealed that tumor cells without Trp53 had reduced activity in genes related to inflammation. These changes were associated with lower levels of key proteins that normally help immune cells detect and attack tumor cells. When the researchers collected tumor cells from the abdominal fluid of the mice—a condition that simulates advanced-stage disease—they observed even lower immune signaling than before. This suggests that as the tumor spreads, it becomes better at evading the immune system. This study highlights how early genetic mutations can shape the interaction between tumors and the immune system. In particular, the loss of Trp53 appears to trigger a chain of events that weakens immune surveillance and accelerates tumor progression. These findings emphasize the need to consider both genetic mutations and the tumor environment when designing immunotherapies for ovarian cancer. Understanding how genes like Trp53 influence immune behavior may lead to more effective treatments and help identify which patients are most likely to benefit from immunotherapy. DOI - https://doi.org/10.18632/oncotarget.28768 Correspondence to - Trevor G. Shepherd - tshephe6@uwo.ca Abstract video - https://www.youtube.com/watch?v=WFQw0psuC3M Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28768 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM
Colorectal cancer is one of the most common—and deadliest—cancers worldwide. Once it spreads and reaches the metastatic stage, treatment becomes far more difficult. Tumors can also behave very differently from one patient to another, especially after multiple rounds of therapy. Precision oncology is helping to overcome these challenges by enabling clinicians to analyze each tumor's unique genetic profile and tailor treatment accordingly. This approach was recently highlighted in a case study published in Volume 16 of Oncotarget. The report detailed how a 62-year-old man with advanced colorectal cancer received a highly personalized treatment plan, developed by an international panel of experts, after completing all standard treatment options. Full blog - https://www.oncotarget.org/2025/09/24/precision-oncology-in-metastatic-colorectal-cancer-a-real-world-case-study/ Paper DOI - https://doi.org/10.18632/oncotarget.28744 Correspondence to - Shai Magidi - shai.magidi@winconsortium.org Abstract video - https://www.youtube.com/watch?v=uWDtWNgpK7A Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28744 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, precision oncology, molecular tumor board, colorectal carcinoma, cancer management To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM
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Stupid News 9-23-2025 8am …Dumbest Lawsuit of the Year …He somehow got His Head Stuck inside a Traffic Light …It is a Tumor
Fr. Eric Nielsen joins Patrick to discuss Miracles: Padre Pio Who was Padre Pio and what miracles did he do? (14:03) Why do some people get miracles and others don’t? (17:19) Juliette - My father was in a bad accident. He is on a ventilator. Tried to remove it. Did not succeed. 84 years old. At what point is it too much. Miracle he survived. I feel like there have been some answered prayers. Is that a miracle in itself that he was able to communicate his wishes? (22:05) Break 1 (23:45) Helen - When my daughter was 3, my daughter had a brain tumor. She had tumor removed. Came back. Went through surgery again, I prayed and asked that she not suffer if she was going to be taken. Tumor disappeared and now she's 39 years old. She's my miracle baby. Does God allow bargaining? Dan - I worked as a hospice chaplain, and one of the greatest pieces of advice...sometimes we just need to get out of God's way and let God do what he needs to do. The miracle of bringing a soul to heaven is the ultimate miracle. (32:53) Brenda - My cousin heard mass by Padre Pio. Was part of my conversion to Catholicism. (37:10) Break 2 Barbara - Miracle when I was baptized. I was instantly delivered from smoking cigarettes. 45-year smoker. (41:59) Eileen - The priest who got me into my faith was leading a colorful life. Padre Pio told him he would become a priest one day. Love the story that he told him he would become a priest. Father shares an email about how can we pray when God doesn’t answer our prayer? (46:13) Brenda - Years after my mom passed, I was thinking about her and praying and walked to the living room and noticed a little star out of nowhere. I think it was a sign and miracle that she was there. Had this happen several other times. Miracle think it was the Lord saying 'I have them.'
There is a new treatment option available now that can precisely target prostate lesions with electrical pulses, while helping preserve sexual function and urinary control. Whether you or a loved one has prostate disease, or you are a urologist considering this technology for your practice, you will not want to miss today's discussion on this innovative new option. September is Prostate Cancer Awareness Month, so we have a special episode today to kick it off. We are excited to welcome the distinguished urologist, Dr. Spencer Krane, to the Prostate Health Podcast. Dr. Krane is the Chief of Urology at the US Department of Veterans Affairs in New Orleans, Louisiana. He specializes in personalized medicine for patients with urologic malignancies, aiming to use new biomarkers, genomic classifications, epigenetic signatures, and advanced imaging modalities, including MRI-guided prostate biopsies, to offer his patients individualized care that improves cancer outcomes while minimizing therapy side effects. Dr. Krane has published extensively in urologic journals, and his work was selected to provide guidelines for urologic care. He has 50 peer-reviewed articles in national and international journals and has presented his work internationally, from Chile and Rome to Taiwan, as well as across the United States. We are excited to welcome him today to share his experience with the innovative new NanoKnife system as a treatment option for men with prostate tumors. It is exciting to see ongoing innovation in the technology we have available for men with prostate tumors. For the appropriate candidates, this minimally invasive option offers precise targeting of the lesion while helping preserve both sexual function and urinary control. Pertinent disclosure for today's episode – Dr. Krane is a paid consultant for AngioDynamics, Inc., which manufactures and sells the NanoKnife System. The views, information, and opinions expressed in this podcast are solely those of Dr. Krane, and does not necessarily represent those of AngioDynamics, Inc., its affiliates, or subsidiaries. Show Highlights: Dr. Krane reviews the concept of targeted focal therapy and explains what the NanoKnife system is Who is an ideal candidate for irreversible electroporation with the NanoKnife system? The advantages and features of the NanoKnife system Does prostate size or shape limit the candidacy for IRE with the NanoKnife system? Would prostate anatomies on the MRI or biopsy exclude a patient from NanoKnife therapy? Dr. Krane explains how long it takes to resolve the initial decrease in sexual ability after NanoKnife therapy. Why many patients experience improved urinary function in the long term after having NanoKnife therapy Dr. Krane clarifies the time it takes to resolve the initial decrease in sexual ability after being treated with NanoKnife therapy. Links: Follow Dr. Pohlman on Twitter and Instagram - @gpohlmanmd. Get your free What To Expect Guide (or find the link on our podcast website) Join our Facebook group Follow Dr. Pohlman on X and Instagram Sign up for the Prostate Health Academy You can access Dr. Pohlman's free mini-webinar, where he discusses his top three tips to promote men's prostate health, longevity, and quality of life here.
Doctors often use euphemisms to dance around the 'C' word. But for oncologist Dr Ranjana Srivastava, how you talk to someone with cancer goes beyond "shadows, lumps and lesions". It's all about compassion and clarity, even when honesty is difficult.Ranjana Srivastava was a young doctor in regional Australia, accompanying her consultant on his late night rounds when she heard a patient say something that stopped Ranjana in her tracks.It was in that moment that she finally knew what her speciality was going to be: oncology. Ranjana now works in Melbourne as an oncologist and an author.She often writes about the need for clarity and compassion in doctor-patient conversations, to deliver good news, bad news and everything that falls between.Ranjana had her own experience of being at the receiving end of devastating news when she was pregnant with twins.Ranjana has carried the lesson she received from her own doctor forward, into her work as an oncologist, where bearing witness to the attitudes of her patients has changed the way she sees the world and has helped put her own life in perspective.Further informationRanjana's latest book, Every Word Matters, is published by Simon & Schuster.She has published seven books about cancer and end of life care, including A Better Death, Tell Me the Truth, Dying for a Chat, So It's Cancer: Now What, and After Cancer: A Guide to Living Well.Ranjana also writes a regular column for The Guardian.In 2017, Ranjana was awarded an Order of Australia medal for her work as an oncologist and in improving doctor-patient communication.This episode of Conversations was produced by Meggie Morris. Executive producer is Nicola Harrison.It explores cancer, oncology, the big C, cancerland, breast cancer, bowel cancer, how to survive cancer, incurable cancer, end of life care, palliative care, honest doctors, refusing treatment, chemotherapy, radiation, how to be honest with patients, doctor patient relationship, geriatric oncology, India, migration, motherhood, late term miscarriage, pregnancy, writing, books, origin story, journalism.To binge even more great episodes of the Conversations podcast with Richard Fidler and Sarah Kanowski go the ABC listen app (Australia) or wherever you get your podcasts. There you'll find hundreds of the best thought-provoking interviews with authors, writers, artists, politicians, psychologists, musicians, and celebrities.
Dr. Morse Q&A - Infertility - Burns - Uterine Cancer - Thyroid Tumor #792 00:00:00 - Intro 00:03:58 - Infertility 00:26:40 - Growths - Dying Tooth - Brittle Nails - Breastfeeding 00:58:26 - Burns 01:07:52 - Uterine Cancer - Non-Stop Period/Bleeding - Unbearable Cramps - Pain - Weight Loss 01:26:36 - Thyroid Tumor - Balding - Tinnitus - Rashes - High Bilirubin - High Testosterone 00:03:58 - Infertility The supposed cause was hydrosalpinx (fluid-filled fallopian tubes). 00:26:40 - Growths - Dying Tooth - Brittle Nails -Breastfeeding I gave birth eleven months ago and feel I haven't fully healed since. 00:58:26 - Burns Can you give exact information on healing severe burns? 01:07:52 - Uterine Cancer - Non-Stop Period/Bleeding - Unbearable Cramps - Pain - Weight Loss The Doctor did a biopsy, told me I had 2 masses in my vagina. 01:26:36 - Thyroid Tumor - Balding - Tinnitus - Rashes - High Bilirubin - High Testosterone Tumor is really big, like the size of a ping-pong ball.