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Listen in as our expert panel untangles the latest recommendations for using equations to estimate kidney function. You'll hear their insights on when and how to use creatinine, cystatin C, or both to help safely adjust medication doses in kidney disease.Special guests:Erin F. Barreto, PharmD, PhD, FCCM, FASN, BCCCPAssociate Professor of Medicine and PharmacyMayo ClinicTracy Anderson-Haag, PharmD, BCPS, BCTXPClinical Pharmacy Specialist-TransplantationResidency Program Director, PGY-2 Solid Organ TransplantHennepin HealthcareNone of the speakers have anything to disclose. This podcast is an excerpt from one of TRC's monthly live CE webinars, the full webinar originally aired in June 2026.
Witam Państwa, nazywam się Jarosław Drożdż, pracuję w Centralnym Szpitalu Klinicznym Uniwersytetu Medycznego w Łodzi, skąd nagrywam podcast Kardio Know-How. W tym odcinku omawiam zespół sercowo-nerkowo-metaboliczny.Nowe wytyczne ACC/AHA dotyczące zespołu sercowo-nerkowo-metabolicznego (CKM) rozwijają koncepcję przedstawioną wcześniej przez AHA i polskich ekspertów, traktując choroby serca, nerek i zaburzenia metaboliczne jako jedno kontinuum, a nie trzy odrębne jednostki chorobowe (https://www.ahajournals.org/doi/10.1161/CIR.0000000000001184, https://journals.viamedica.pl/nadcisnienie_tetnicze_w_praktyce/article/view/90302/68962). W praktyce oznacza to odejście od myślenia o pacjencie wyłącznie przez pryzmat niewydolności serca, cukrzycy czy przewlekłej choroby nerek na rzecz rozpoznania jednego zespołu CKM. Kluczowym markerem staje się albuminuria (UACR), która obok eGFR pozwala wcześnie wykryć uszkodzenie nerek i jednocześnie precyzyjnie ocenia ryzyko sercowo-naczyniowe. Wytyczne wyróżniają cztery stadia choroby – od nadwagi i otyłości, przez zaburzenia metaboliczne i subkliniczną chorobę serca, aż do jawnych powikłań narządowych – przy czym leczenie powinno rozpoczynać się już w stadium 1, zanim pojawią się objawy kliniczne. Największą zmianą filozofii jest przesunięcie akcentu z leczenia rozwiniętej choroby na ochronę serca i nerek poprzez wczesne zastosowanie inhibitorów SGLT2, agonistów GLP-1 oraz finerenonu u odpowiednio dobranych pacjentów. Dokument integruje wyniki najnowszych badań i proponuje spójną strategię terapii narządowej zamiast wybierania pojedynczych leków zależnie od specjalizacji. Jednocześnie pozostawia otwarte pytanie, kto powinien prowadzić takich chorych – kardiolog, nefrolog, diabetolog czy lekarz rodzinny – co w praktyce wymaga ścisłej współpracy wszystkich specjalności. Autor zwraca również uwagę na wyzwania organizacyjne, obejmujące konieczność powszechnego oznaczania UACR, wcześniejszego rozpoznawania nadwagi i otyłości oraz szerszego stosowania nowoczesnych terapii, co wiąże się ze wzrostem kosztów ochrony zdrowia. Nadal nie wiadomo, czy tak szeroki model prewencji okaże się w pełni opłacalny ekonomicznie, choć intuicyjnie zapobieganie niewydolności serca i przewlekłej chorobie nerek wydaje się korzystniejsze niż leczenie ich zaawansowanych powikłań. Zdaniem autora wytyczne wyznaczają kierunek rozwoju kardiologii, nefrologii, diabetologii i medycyny rodzinnej na najbliższe lata, a ich znaczenie pokaże również to, czy podobną filozofię przejmą kolejne wytyczne ESC dotyczące niewydolności serca, przewlekłej choroby nerek i prewencji sercowo-naczyniowej. Szczegółowy TRANSKRYPT do odcinka.Podcast jest przeznaczony wyłącznie dla osób z profesjonalnym wykształceniem medycznym.
CardioNerds (Drs. Apoorva Gangavelli, Jenna Skowronski, and Hannah Every) discuss the continuum of prevention and heart failure with Drs. Anu Lala and Martha Gulati. Grounded in a clinical case of a 55-year-old woman with uncontrolled hypertension, type 2 diabetes, and obesity who is on the trajectory toward heart failure, this episode unpacks a paradigm-shifting framework from a joint HFSA/ASPC Scientific Statement. The discussion explores how prevention should not be siloed from heart failure management but rather integrated across a patient’s lifespan—from primary prevention in at-risk individuals, to secondary prevention in those with established heart failure, to tertiary prevention in patients with advanced therapies such as LVADs and heart transplantation. The experts highlight the importance of aggressive risk factor management, biomarker-guided screening, the AHA’s Life’s Essential 8, and the need for multidisciplinary collaboration and systems-level change to shift heart failure care from reactive to proactive. Audio editing for this episode was performed by CardioNerds Intern, Dr. Julia Marques Fernandes. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here. CardioNerds Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls Systemic inflammatory diseases are associated with an elevated CVD risk that has significant implications for early detection, risk Heart failure prevention is a continuum, not a checkpoint. Prevention applies at every stage—from at-risk (Stage A) through advanced/post-transplant care—and every clinical encounter is an opportunity to intervene. The AHA’s Life’s Essential 8 (diet, physical activity, nicotine exposure, sleep, BMI, blood lipids, blood glucose, blood pressure) forms the foundation at every stage. Hypertension carries the highest population-attributable risk for heart failure of any modifiable risk factor. In the Framingham Heart Study, 91% of patients with newly diagnosed HF had pre-existing hypertension. The SPRINT trial demonstrated a 38% reduction in HF incidence with intensive blood pressure targets (30 ng/L or NT-proBNP >125 ng/L) identify individuals at heightened risk for progression to symptomatic HF. The ACC/AHA/HFSA guidelines give a Class IIa recommendation for natriuretic peptide screening in at-risk patients. Urine albumin-to-creatinine ratio (UACR) is an underutilized screening tool that provides additional insight into CKM risk. The heart failure label does not close the prevention window—it accentuates it. Secondary prevention through GDMT optimization (quadruple therapy in HFrEF) and continued risk factor management remains critical. Tertiary prevention extends to post-LVAD and post-transplant patients, where hypertension, diabetes, obesity, and CKD management remain essential to long-term outcomes. Show notes For a comprehensive review, please review the full HFSA/ASPC Joint Scientific Statement: Lala A, Beavers C, Blumer V, et al. The Continuum of Prevention and Heart Failure in Cardiovascular Medicine. J Card Fail. 2026;32:75-105. doi:10.1016/j.cardfail.2025.06.013 1. What is the “continuum of prevention” framework, and how does it differ from traditional approaches to heart failure prevention? Historically, prevention and heart failure management have been treated as separate disciplines—primary prevention handled by preventive cardiologists and treatment managed by heart failure specialists. This joint HFSA/ASPC Scientific Statement reframes prevention as a dynamic, continuous process that spans a patient’s entire lifespan, regardless of HF stage or ejection fraction. The framework maps onto the ACC/AHA HF staging system: Primary prevention targets Stage A (“at risk”) and Stage B (“pre-HF”) patients to reduce the burden of incident HF. Secondary prevention targets Stage C (symptomatic) and Stage D (advanced) patients to reduce the impact of established HF through GDMT optimization and ongoing risk factor management. Tertiary prevention encompasses risk factor management in patients with LVADs or heart transplants—populations where hypertension, diabetes, and obesity still drive outcomes. The Central Figure of the statement illustrates that Life’s Essential 8 (blood pressure and lipid control, diabetes management, exercise, sleep, smoking cessation, weight management, and diet/nutrition counseling) forms the foundation at every stage, with pharmacologic and device-based therapies layered on top as disease progresses (Figure) 2. How do traditional risk factors drive heart failure, and what should clinicians prioritize? Hypertension carries the greatest population-attributable risk for HF. In the Framingham Heart Study (N=5,143), HTN was associated with a 2- to 3-fold increased risk of HF, with a population-attributable risk of 39% in men and 59% in women. The SPRINT trial showed a 38% reduction in HF incidence and 25% reduction in the primary composite outcome with intensive BP targets (30 ng/L or NT-proBNP >125 ng/L) are associated with heightened risk for progression to symptomatic HF. In the ARIC study, incorporating NT-proBNP reclassified 20% of older adults without HF into Stage B. Factors that affect interpretation include age, sex, obesity (lower values), and CKD (higher values). High-sensitivity cardiac troponin (hs-cTn): Concentrations above the 99th percentile are now included in the definition of Stage B HF. Troponin testing may complement natriuretic peptides, particularly when BNP/NT-proBNP values are ambiguous. Risk scores: The PCP-HF equation predicts 10-year HF risk using traditional risk factors plus QRS duration. The AHA PREVENT score incorporates HF risk calculation and includes markers of kidney function (albuminuria, eGFR), though it may underestimate risk in men and Black adults. The CKM syndrome staging framework (Stages 0–4) provides a holistic approach to assessing systemic cardiovascular-kidney-metabolic risk. 4. What are the key nontraditional risk factors and cross-cutting themes in heart failure prevention? Genetics: Pathogenic cardiomyopathy variants exist in ~1 in 200 individuals in the general population. The HFSA and ACMG recommend cascade testing to identify at-risk family members. Polygenic risk scores for dilated cardiomyopathy show a 3.8-fold risk for DCM in the top 10th percentile compared with the median. Sex-specific considerations: Women have 2.8 times the odds of developing HFpEF, while men have similarly increased odds of HFrEF. A complete obstetric/gynecologic history is essential—preeclampsia is associated with a 4-fold increased risk of HF. Peripartum cardiomyopathy requires intentional screening in high-risk populations. Cardiotoxic exposures: Clinicians should be aware of medications that cause direct myocardial toxicity (e.g., anthracyclines, trastuzumab, tyrosine kinase inhibitors). A team-based approach with pharmacists can help optimize medication selection and risk factor modification. Social determinants of health: Environmental exposures (air pollution, arsenic, lead, cadmium), food insecurity, financial instability, and limited healthcare access contribute to HF risk and progression. Equity-focused, risk-based prevention strategies are needed. Psychological health: Depression is common in HF and independently associated with worse outcomes. Screening with brief questionnaires (e.g., PHQ-2) is recommended. Meditation, spirituality, and holistic wellness approaches remain underutilized. 5. What systems-level and policy changes are needed to move the needle on heart failure prevention? Multidisciplinary HF prevention clinics that bring together preventive cardiologists, HF specialists, endocrinologists, nephrologists, dietitians, pharmacists, exercise physiologists, and genetic counselors are advocated by the statement. EHR-embedded risk stratification could proactively flag patients on a trajectory toward HF—analogous to sepsis alerts or fall risk flags—enabling earlier intervention, particularly for patients who may not reach a cardiologist. Cardiac rehabilitation remains underutilized, particularly in HFrEF (Class 2b recommendation) and HFpEF (not yet covered by Medicare). The HF-ACTION trial showed quality-of-life benefits, and the REHAB-HF trial showed particular benefit in older patients with HFpEF. Policy priorities include expanding insurance coverage for preventive screening and novel therapies (SGLT2i, GLP-1 RAs, nsMRAs), reducing clinical inertia through team-based care models with closer follow-up intervals, and ensuring equitable access to evidence-based therapies across diverse populations. Digital health and AI hold promise for personalized risk prediction, remote monitoring (e.g., wearable devices, implantable PA pressure monitors), and virtual cardiac rehabilitation to overcome access barriers. Figure Lala A, Beavers C, Blumer V, et al. The continuum of prevention and heart failure in cardiovascular medicine: a joint scientific statement from the Heart Failure Society of America and the American Society for Preventive Cardiology. J Card Fail. 2026;32(1):75-105. doi:10.1016/j.cardfail.2025.06.013) References Key references are bolded. Lala A, Beavers C, Blumer V, et al. The continuum of prevention and heart failure in cardiovascular medicine: a joint scientific statement from the Heart Failure Society of America and the American Society for Preventive Cardiology. J Card Fail. 2026;32(1):75-105. doi:10.1016/j.cardfail.2025.06.013 Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA guideline for the management of heart failure: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2022;145(18):e895-e1032. doi:10.1161/CIR.0000000000001063 Lloyd-Jones DM, Allen NB, Anderson CAM, et al. Life’s Essential 8: updating and enhancing the American Heart Association’s construct of cardiovascular health: a presidential advisory from the American Heart Association. Circulation. 2022;146(5):e18-e43. doi:10.1161/CIR.0000000000001078 SPRINT Research Group, Wright JT Jr, Williamson JD, et al. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med. 2015;373(22):2103-2116. doi:10.1056/NEJMoa1511939 Levy D, Larson MG, Vasan RS, Kannel WB, Ho KK. The progression from hypertension to congestive heart failure. JAMA. 1996;275(20):1557-1562. doi:10.1001/jama.1996.03530440037034 Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic: the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). JAMA. 2002;288(23):2981-2997. doi:10.1001/jama.288.23.2981 Yusuf S, Sleight P, Pogue J, et al. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. N Engl J Med. 2000;342(3):145-153. doi:10.1056/NEJM200001203420301 Zinman B, Wanner C, Lachin JM, et al. Empagliflozin, cardiovascular outcomes, and mortality in type 2 diabetes. N Engl J Med. 2015;373(22):2117-2128. doi:10.1056/NEJMoa1504720 Anker SD, Butler J, Filippatos G, et al. Empagliflozin in heart failure with a preserved ejection fraction. N Engl J Med. 2021;385(16):1451-1461. doi:10.1056/NEJMoa2107038 Solomon SD, McMurray JJV, Claggett B, et al. Dapagliflozin in heart failure with mildly reduced or preserved ejection fraction. N Engl J Med. 2022;387(12):1089-1098. doi:10.1056/NEJMoa2206286 Filippatos G, Anker SD, Agarwal R, et al. Finerenone reduces risk of incident heart failure in patients with chronic kidney disease and type 2 diabetes: analyses from the FIGARO-DKD trial. Circulation. 2022;145(6):437-447. doi:10.1161/CIRCULATIONAHA.121.057983 Solomon SD, McMurray JJV, Vaduganathan M, et al. Finerenone in heart failure with mildly reduced or preserved ejection fraction. N Engl J Med. 2024;391(16):1475-1485. doi:10.1056/NEJMoa2407107 Lincoff AM, Brown-Frandsen K, Colhoun HM, et al. Semaglutide and cardiovascular outcomes in obesity without diabetes. N Engl J Med. 2023;389(24):2221-2232. doi:10.1056/NEJMoa2307563 Deanfield J, Verma S, Scirica BM, et al. Semaglutide and cardiovascular outcomes in patients with obesity and prevalent heart failure: a prespecified analysis of the SELECT trial. Lancet. 2024;404(10454):773-786. doi:10.1016/S0140-6736(24)01498-3 Kosiborod MN, Abildstrøm SZ, Borlaug BA, et al. Semaglutide in patients with heart failure with preserved ejection fraction and obesity. N Engl J Med. 2023;389(12):1069-1084. doi:10.1056/NEJMoa2306963 Ndumele CE, Neeland IJ, Tuttle KR, et al. A synopsis of the evidence for the science and clinical management of cardiovascular-kidney-metabolic (CKM) syndrome: a scientific statement from the American Heart Association. Circulation. 2023;148(20):1636-1664. doi:10.1161/CIR.0000000000001175 Khan SS, Matsushita K, Sang Y, et al. Development and validation of the American Heart Association’s PREVENT equations. Circulation. 2024;149(6):430-449. doi:10.1161/CIRCULATIONAHA.123.067626 Khan SS, Ning H, Shah SJ, et al. 10-year risk equations for incident heart failure in the general population. J Am Coll Cardiol. 2019;73(19):2388-2397. doi:10.1016/j.jacc.2019.02.057 Bozkurt B, Fonarow GC, Goldberg LR, et al. Cardiac rehabilitation for patients with heart failure: JACC expert panel. J Am Coll Cardiol. 2021;77(11):1454-1469. doi:10.1016/j.jacc.2021.01.030 Packer M. Leptin-aldosterone-neprilysin axis: identification of its distinctive role in the pathogenesis of the three phenotypes of heart failure in people with obesity. Circulation. 2018;137(15):1614-1631. doi:10.1161/CIRCULATIONAHA.117.032474 Lala A, Tayal U, Hamo CE, et al. Sex differences in heart failure. J Card Fail. 2022;28(3):477-498. doi:10.1016/j.cardfail.2021.10.006 Bozkurt B, Coats AJS, Tsutsui H, et al. Universal definition and classification of heart failure. Eur J Heart Fail. 2021;23(3):352-380. doi:10.1002/ejhf.2115 Hershberger RE, Givertz MM, Ho CY, et al. Genetic evaluation of cardiomyopathy—a Heart Failure Society of America practice guideline. J Card Fail. 2018;24(5):281-302. doi:10.1016/j.cardfail.2018.03.004 Levine GN, Cohen BE, Commodore-Mensah Y, et al. Psychological health, well-being, and the mind-heart-body connection: a scientific statement from the American Heart Association. Circulation. 2021;143(10):e763-e783. doi:10.1161/CIR.0000000000000947 Ezekowitz JA, Colin-Ramirez E, Ross H, et al. Reduction of dietary sodium to less than 100 mmol in heart failure (SODIUM-HF): an international, open-label, randomised, controlled trial. Lancet. 2022;399(10333):1391-1400. doi:10.1016/S0140-6736(22)00369-5
Featuring perspectives from Dr Sarah B Goldberg, Dr Jonathan Goldman, Dr Joel W Neal, Dr Antonio Passaro and Dr Jacob Sands, moderated by Dr Sands, including the following topics: Introduction (00:00) Evolving First-Line Treatment for Metastatic EGFR-Mutated Non-Small Cell Lung Cancer (NSCLC) — Prof Passaro (2:27) EGFR-Targeted Therapeutic Strategies for Relapsed EGFR-Mutant NSCLC — Dr Neal (36:08) Utility of TROP2-Targeted Antibody-Drug Conjugates in the Management of EGFR-Mutant NSCLC — Dr Sands (56:16) Emerging Role of Bispecific Antibody-Based Approaches for EGFR-Mutated NSCLC — Dr Goldman (1:19:08) Tolerability Considerations with the Use of Available and Emerging Therapies for EGFR-Mutated NSCLC — Dr Goldberg (1:38:46) CME information and select publications
Stop kidney decline before it starts. See how eGFR and proteinuria trends are reshaping IgA nephropathy management. Credit available for this activity expires: 7/17/27 Earn Credit / Learning Objectives & Disclosures: https://www.medscape.org/viewarticle/translating-emerging-evidence-iga-nephropathy-proteinuria-2026a1000nyb?ecd=bdc_podcast_libsyn_mscped
Have you heard of Farxiga (dapagliflozin), Jardiance (empagliflozin), Ozempic, Wegovy, Mounjaro, or finerenone, but aren't quite sure what they do or whether they're right for people living with kidney disease? In this episode of Diary of a Kidney Warrior Podcast, host Dee Moore is joined by Professor Alex, Consultant Nephrologist and researcher, for an essential conversation about some of the biggest breakthroughs in kidney medicine in recent years. Originally developed for diabetes, SGLT2 inhibitors have transformed kidney care and are now helping to protect kidney function, reduce protein in the urine and improve outcomes for many people living with chronic kidney disease (CKD). We also explore the growing role of GLP-1 receptor agonists and finerenone, and explain what patients need to know about these treatments. Whether you're living with chronic kidney disease, caring for someone who is, or you're a healthcare professional wanting a patient-friendly explanation, this episode is packed with practical, evidence-based information. In this episode, you'll learn: ✅ What SGLT2 inhibitors are and how they protect the kidneys ✅ Why medications developed for diabetes are now transforming kidney care ✅ How GLP-1 receptor agonists (including Ozempic, Wegovy and Mounjaro) may benefit kidney health ✅ What finerenone is and who may benefit from it ✅ Why your eGFR may temporarily fall after starting treatment—and why this isn't always a cause for concern ✅ The benefits and possible side effects of these medications ✅ Which kidney patients may be suitable for these treatments ✅ The latest developments in kidney research and future treatments This episode shares expert insight designed to educate, empower and inspire people living with kidney disease and those who support them.
On today's episode, Yaron Werber, John Maraganore, Sam Fazeli, and Matt Gline open with a discussion of biotech market volatility, with Matt noting that it often seems driven more by opaque factor dynamics than company-specific fundamentals. The group then turns to Eli Lilly's continued “Amazonification” and reinventing the pharma business as it acquires a variety of different companies, including this week's $2.8B upfront acquisition of Atai Beckley, a psychedelic-focused company. The conversation turns to BioCentury's reporting on Asia-to-West NewCos, prompting a debate about whether China is uniquely changing the market or simply reflects broader shifts in cheaper, faster development. On policy, the group covers BIO's response to the OMB proposal that could inject political review into federal grant decisions. The co-hosts also debate Kalshi's move to create prediction markets around clinical trial and regulatory outcomes. On pipeline updates, the group discusses Merck's approval of Lipfendra, the first oral PCSK9 drug, and the broader class implications. In CNS, Biogen and Ionis' diranersen tau ASO data spark a discussion of aconfusing dose response, ASO tolerability, tau as a target in Alzheimer's disease, and the promise of alternative modalities from Arrowhead and Alnylam. The episode closes with M&A and financing, including AstraZeneca's licensing deal with Dizal for the EGFR exon 20 inhibitor sunvozertinib andErasca's RAF data plus its $500M financing, which Sam views as a strong market signal despite a volatile biotech backdrop. This episode aired on July 17, 2026.
Send us Fan MailThe July 2026 PBS update brings a number of important changes for oncology clinicians, with several new and expanded cancer medicine listings set to improve access to cancer treatments across breast, lung, blood and biliary tract cancers.In this episode, Rachael Babin and Professor Craig Underhill discuss the clinical significance of the latest Pharmaceutical Benefits Scheme changes, including who is now eligible for treatment, what these listings mean for multidisciplinary care and why comprehensive biomarker testing continues to grow in importance.In this episode:PBS listing for pertuzumab (Perjeta®) in high-risk HER2-positive early breast cancer Listing of alectinib (Alecensa®) for ALK-positive non-small cell lung cancer Osimertinib (Tagrisso®) listing for EGFR-mutated unresectable Stage III NSCLC following chemoradiation First PBS listing of romidepsin (Romidepsin-Reach®) for relapsed peripheral T-cell lymphoma First PBS listing of futibatinib (Lytgobi®) for FGFR2-altered advanced cholangiocarcinoma What the new broad (multi-cancer) PBS listing principles for PD-(L)1 inhibitors could mean for future cancer drug fundingFollow The PBS Update for regular discussions on PBS listings and oncology policy changes affecting Australian healthcare professionals.Visit the Show Notes for links to the PBS updates discussed in this episode and to send us audio feedback or questions for future episodes.Proudly produced by The Oncology Network
Thank you for joining us for our 2nd Cabral HouseCall of the weekend! I'm looking forward to sharing with you some of our community's questions that have come in over the past few weeks… Kudisha: Hello Dr. Cabral, Thank you for all that you do. I wish you and your family many healthy years to come. Would you advise someone with an eGFR between 60 and 90 to take the Advanced Cell Force supplement? Also, what are your thoughts on Sea Moss? Thank you in advance for your guidance. Anonymous: Me again! I I am getting ready for my first detox. IM only doing a 7 day out of intimidation. I have a lot of histamine issues and I hope I don't have a bad reaction! Please give tips in case this happens to me. Also, I know the detox advertises weight loss. It seems very low calorie. I don't plan on tracking during the detox or anything, but i have read that losing weight too fast is not healthy, or sustainable as people often gain it back very quickly. I was curious if weight loss during a detox will mainly be water weight, or can I actually lose fat on a 7 day detox? Is this too fast to lose weight? And obviously besides going back to a bad diet, how is the weight loss sustainable after going back to higher calories after the detox? I would love to lose some fat while I'm doing my detox Robin: I currently have blood pressure issues and i treating it naturally it hasnt changed i need help Sarah: Hi Dr. Cabral, We appreciate you and your company and have benefited from using your supplements and protocols. I am wondering what your thoughts are on the efficacy of homeopathic remedies/constitutions and what your thoughts are if you think they truly help. I have a child with PANS-like symptoms, impulsivity, irritability, and some OCD. Using DNS, calming mag, omega 3, added zinc based on HTMA, sometimes NAC and TMG, have done some para cleanses which temporarily helped, successfully lowered heavy metals. Sometimes use PEMF, red light, rebounding, exercise/play/sunlight, chiro, etc. Also do saline nasal spray at night to promote nasal breathing, did myofunctional therapy for a little bit, etc. It is a lot. Gluten free, adequate protein, no artificial food dyes. Could homeopathy help? Laura: Hi Dr. Cabral, Let me begin by first saying that I am really enjoying your lectures. I have just joined IHP and already worked thru the diet and exercise portion. Thank you for sharing all of your valuable knowledge. I would like for you to share with me if you would, how to speed read like you talked about. I have always had difficulty reading maybe because I have dyslexia and ADD. I would like to be able to read like you do and comprehend it at the same time. Also, I would like to share with you that I have had Hypothyroidism since the age of 2 which I have been on Synthroid all of my life. I am 61 now. I have had diabetes for 11 years. I have also been told I have fatty liver. Could you make any recommendations on where I should start to get better? Thank you. Thank you for tuning into this weekend's Cabral HouseCalls and be sure to check back tomorrow for our Mindset & Motivation Monday show to get your week started off right! - - - Show Notes and Resources: StephenCabral.com/3810 - - - Get a FREE Copy of Dr. Cabral's Book: The Rain Barrel Effect - - - Join the Community & Get Your Questions Answered: CabralSupportGroup.com - - - Dr. Cabral's Most Popular At-Home Lab Tests: > Complete Minerals & Metals Test (Test for mineral imbalances & heavy metal toxicity) - - - > Complete Candida, Metabolic & Vitamins Test (Test for 75 biomarkers including yeast & bacterial gut overgrowth, as well as vitamin levels) - - - > Complete Stress, Mood & Metabolism Test (Discover your complete thyroid, adrenal, hormone, vitamin D & insulin levels) - - - > Complete Food Sensitivity Test (Find out your hidden food sensitivities) - - - > Complete Omega-3 & Inflammation Test (Discover your levels of inflammation related to your omega-6 to omega-3 levels) - - - Get Your Question Answered On An Upcoming HouseCall: StephenCabral.com/askcabral - - - Would You Take 30 Seconds To Rate & Review The Cabral Concept? The best way to help me spread our mission of true natural health is to pass on the good word, and I read and appreciate every review!
Featuring an interview with Dr Jamie E Chaft, including the following topics: Case: A man in his early 70s with a 40 to 50 pack-year history of smoking and cT2bN1 squamous cell carcinoma of the lung with PD-L1 60% treated with induction therapy and surgery (00:00) Available clinical data with immunotherapy in the neoadjuvant, perioperative and adjuvant settings (07:45) Factors in the selection of adjuvant immunotherapy, including circulating tumor DNA (11:39) Evolving approaches to management, including systemic therapy, surgery and radiation therapy techniques (19:28) Case: A woman in her early 60s with nonmetastatic non-small cell lung cancer (NSCLC) and an EGFR exon 19 deletion who is enrolled in the NeoADAURA study (24:03) Importance of clinical trials in the adjuvant setting (33:02) Data surrounding treatment in the neoadjuvant setting; key implications of the NeoADAURA study (35:41) Case: A man in his late 60s with a history of smoking and Stage III T4N3 NSCLC not otherwise specified with low PD-L1 expression, high tumor mutation burden, microsatellite stability and an STK11 mutation (41:34) Selecting patients for the NeoADAURA study treatment approach; deciding between chemoimmunotherapy and chemoradiation therapy (51:01) CME information and select publications
En este episodio especial de BreastLink, el Dr. Juan Carlos Samamé conduce un análisis sobre las principales novedades en cáncer de mama presentadas en la reunión anual de la Sociedad Americana de Oncología Clínica. Para ello, cuenta con la participación de dos destacados referentes internacionales: el Dr. Antonio Llombart, del Hospital Arnau de Vilanova de Valencia, y el Dr. Fernando Petracci, del Instituto Alexander Fleming de Buenos Aires y presidente de la Asociación Latinoamericana de Cáncer de Mama. La discusión se centra en la evolución de los esquemas terapéuticos hacia una medicina cada vez más personalizada, destacando la consolidación de la desescalada terapéutica en enfermedad temprana y la optimización de las líneas de tratamiento en etapas avanzadas.Durante la revisión del subtipo HER2 positivo, el Dr. Llombart destaca la maduración de datos en estrategias de mantenimiento para enfermedad metastásica (estudios HER2CLIMB y PATINA), así como la exploración de la "respuesta parcial profunda" en primera línea. En el ámbito de la temprana, resalta el creciente interés en la desescalada terapéutica apoyada en estudios como PHERGain-2, que evalúa el doble bloqueo con trastuzumab y pertuzumab sin quimioterapia en tumores pequeños.Por su parte, en el panorama de los tumores luminales, el Dr. Petracci subraya la relevancia del estudio OPTIMA. Este ensayo de no inferioridad, guiado por la firma genómica PAM50, plantea un posible cambio en la práctica clínica al demostrar que es seguro omitir la quimioterapia en un subgrupo de pacientes de alto riesgo. Adicionalmente, se discuten las actualizaciones sobre los SERDs, con menciones a los estudios lidERA (giredestrant) y PERSEVERA (elacestrant).Finalmente, en el contexto del cáncer de mama triple negativo, se analizan los datos de seguimiento a largo plazo del estudio KEYNOTE-522 y el impacto real de mantener pembrolizumab en la fase adyuvante en pacientes que ya han alcanzado una respuesta completa patológica. Se exploran también resultados en enfermedad avanzada, como la combinación de sacituzumab govitecán con pembrolizumab (ASCENT-04) y la incursión de nuevos anticuerpos conjugados biespecíficos dirigidos a EGFR y HER3.El panel concluye reflexionando sobre los retos de incorporar estas plataformas moleculares, los nuevos ADC y biomarcadores emergentes, como el ctDNA en la toma de decisiones clínicas rutinarias.Referencia:Este contenido se basa en la interpretación crítica de la evidencia científica disponible, así como en la experiencia clínica del o los ponentes como profesionales de la salud en instituciones de referencia. Para profundizar en los conceptos discutidos, se recomienda al profesional de la salud consultar literatura científica vigente, guías clínicas internacionales y la normatividad aplicable en su país.
Chronic kidney disease often develops silently for years, but even early kidney damage sharply increases your risk of heart attack, stroke, heart failure, and dangerous heart rhythm problems Two common tests called eGFR and UACR reveal hidden kidney stress long before symptoms appear and provide an early warning sign that your cardiovascular system is already under strain Researchers discovered that damaged kidneys release microscopic particles into the bloodstream that directly injure heart muscle cells, weaken heart contractions, and disrupt the electrical timing of the heartbeat Chronic inflammation, fluid overload, high blood sugar, excess sodium retention and overactivation of the nervous system create a destructive cycle that damages both the kidneys and the heart simultaneously Daily habits that improve metabolic health, including stable blood sugar, regular movement, lower intake of seed oils, restorative sleep, and healthy circulation, help reduce long-term stress on both organs before irreversible damage develops
This week, Josh and Michael's ASCO 2026 coverage looks at "Agents of the Future", trials of intrigue, promise and potential beyond its status. This episode also sheds light on more orphan status cancers like head and neck cancer, basket cohort studies, resistant EGFR lung cancer, metastatic colorectal cancer and hepatocellular carcinoma.One more episode left of this arc - The Plenary! Stay tuned.Studies Discussed in this EpisodeOrigAMI-4WU-KONG28A Phase 1/2 Study of JK06, a 5T4-Targeted Antibody Drug Conjugate (ADC), In Patients with Unresectable Locally Advanced or Metastatic CancerESANOAROSETTA Lung-02Ivonescimab + FOLFOXHERIZON-CRC01CIRCULATEEMERALD-3BLUESTARGLP-1 agonist in breast cancer (Palleschi et al)For more episodes, resources and blog posts, visit www.inquisitiveonc.comPlease find us on Twitter @InquisitiveOnc!If you want us to look at a specific trial or subject, email us at inquisitiveonc@gmail.comArt courtesy of Taryn SilverMusic courtesy of AlisiaBeats: https://pixabay.com/users/alisiabeats-39461785/Disclaimer: This podcast is for educational purposes only. If you are unwell, seek medical advice.Oncology for the Inquisitive Mind is recorded with the support of education grants from our foundation partners Pfizer and Merck Pharmaceuticals. Our partners have access to the episode at the same time you do and have no editorial control over the content. Hosted on Acast. See acast.com/privacy for more information.
Featuring perspectives from Dr Jonathan Goldman and Dr Zofia Piotrowska, including the following topics: Introduction (0:00) Current Management of Metastatic EGFR-Mutated Non-Small Cell Lung Cancer (NSCLC) — Dr Goldman (0:38) Nonmetastatic EGFR-Mutated NSCLC, Exon 20 Insertion Mutations and Novel Agents — Dr Piotrowska (33:20) CME information and select publications
Link to claim CME credit: https://bit.ly/4uRr3ir In this episode, Elizabeth Krueger, NP, and Sam Vafadar, DHSc, PA-C, discuss how they optimize first-line EGFR-targeted therapy for patients with EGFR-mutated NSCLC, including: First-line treatment options available for EGFR-mutated NSCLC and the clinical trials that resulted in their approval Adverse event identification and management Generalized strategies to support patient adherence to TKIs Get access to all of our new podcasts by subscribing to the Decera Clinical Education Podcast on Apple Podcasts, YouTube Music, or Spotify Presenters: Elizabeth Krueger, NP Center for Thoracic Cancers Mass General Brigham Cancer Institute Boston, Massachusetts Sam Vafadar, DHSc, PA-C Physician Associate Department of Thoracic Oncology H. Lee Moffitt Cancer Center and Research Institute Tampa, Florida Hosted by Simplecast, an AdsWizz company. See pcm.adswizz.com for information about our collection and use of personal data for advertising.
In a special edition of Oncology On the Go, Chinmay Jani, MD, joined CancerNetwork® in the studio to speak about different research initiatives he is involved with across precision oncology. He discussed ongoing work dedicated to validating and applying artificial intelligence (AI)–based tools in clinical work as well as overcoming immunotherapy resistance among patients with lung cancer.Jani, chief fellow in Hematology and Oncology at University of Miami Sylvester Comprehensive Cancer Center, first detailed findings from a study he presented at the 2026 American Society of Clinical Oncology (ASCO) Annual Meeting evaluating AI decision support in the context of EGFR-mutated non–small cell lung cancer (NSCLC). Although AI systems aligned with expert decision-making in frontline treatment, significant divergence was observed in second-line care, highlighting a need for more rigorous validation and clinical safeguards when integrating AI into oncologic decision-making. Improving documentation and using tools more ethically, Jani said, will also be critical for future applications of AI in field.Jani also spoke about the rapidly evolving thoracic oncology field based on research he and colleagues are leading at the University of Miami. Different investigations are exploring potential advancements in precision medicine, overcoming immunotherapy resistance, and early cancer detection to help elevate outcomes among patients with lung cancer. Looking ahead, Jani emphasized how novel therapeutics like tarlatamab-dlle (Imdelltra) and the incorporation of liquid biopsy may assist with the goal of turning lung cancer into “a chronic disease” where patients can survive not just for a few month or years but for decades.According to Jani, other key concerns in the field include the evolving landscape surrounding adolescent and young adult (AYA) patients, who may require different types of molecular testing and therapeutic needs compared with adult populations. Being able to detect more fusions and alterations that may inform therapeutic strategies via circulating tumor DNA plus circulating tumor RNA or through wider minimal residual disease testing, he said, represents another ongoing goal in terms of precision medicine.ReferenceJani C, Pérez-Granado J, Kalucha A, et al. Evaluating AI decision support in a rapidly evolving therapeutic landscape: EGFR-mutant metastatic NSCLC. J Clin Oncol. 2026;44(suppl 16):1630. doi:10.1200/JCO.2026.44.16_suppl.1630
Dr. Deb Muth 00:02What if I told you that before a single drop of chemotherapy goes into a cancer patient’s body, we can take a blood sample, grow their actual living cancer cells in a lab, and test 70 different drugs against those cells, all outside the patient’s body, to find out which ones actually work. And what if I told you that the conventional oncology doesn’t routinely use this test? Well, today we’re going to talk about why that matters and we’re going to go through and I’m going to share a story that is very personal to me. It’s about a 38 year old man with a rare complex cancer diagnosis and the precision testing that is helping to keep that cancer from progressing. Stay with me. This is one that is going to change how you think about cancer treatment. Dr. Deb Muth 01:05You guys can put a little ad right in here before we start the next segment here. Hey everybody, welcome back to Let’s Talk Wellness Now. I’m Dr. Deb and today we’re going deep. I mean really deep. It’s some of the most cutting edge cancer testing I have ever seen in clinical practice. Now, normally I don’t talk about cancer. And I would not be sharing this story if it was anyone other than my own family. I do have permission to share and talk about this publicly. So I want to do this. I want to make sure that I share this message. And he is giving his blessing to share this story because we both believe that it can save lives. So his name is Cameron. He’s 38 years old. And he is my son-in-law. And two years ago, he came to me with a small lymph node underneath his arm and a bullseye rash. So of course, being the lime literate person that I am, my first inclination was to say, yeah, this makes sense. You have an enlarged lymph node because you have this bullseye rash. You got bit by the tick. Let’s keep an eye on it. If it doesn’t go away, let me know. So Fast forward a year and a half later, he comes to me and says, mom, what do you think about this? This thing is getting a little bit larger. And I said, yeah, it’s a little larger. Not sure. Let’s keep an eye on it. He wasn’t feeling anything. All his labs looked okay. And then one day he was out chopping wood and he started getting numbness in that arm and he felt it again. And it had exploded in size. And so after some evaluation with my daughter and him, we decided to do a ultrasound. And we thought what was going to come back was a fatty tumor. It felt like one looks like one responded to one. He’s 38 years old. He’s healthy. There’s nothing in our mind that’s ever thinking the result that we’re going to get back. Dr. Deb Muth 03:28Is a possible lymphoma. Needless to say, we were shocked by that ultrasound result. And we go fast forward, we have the biopsy. I requested a total excisional biopsy. I was told by the oncologist that that was old school. They don’t do that that way anymore. And I need to stay out of this. I need to let the experts take care of this because that’s what they do best. And this came from a breast surgeon here in Wisconsin. And so I stepped back for a moment. I let him do his biopsy and what came back was adenocarcinoma of an unknown origin. Had we excised the entire lymph node, we would have had more tissue to work with. I think we could have gotten a better diagnosis. So over the course of the next two and a half, three months, we have some more imaging done. We have some more testing done. They send a pathology out to Mayo Clinic. And what continues to come back is this incongruent test results. If anybody’s ever had this, it’s extremely frustrating. One test shows lymphoma. Now it shows breast cancer. Then the next week it shows estrogen receptor HER2 positive breast cancer. Two weeks later, another test comes back and it says, no, it’s not HER2, it’s triple negative breast cancer. And now it looks like it’s out of the lymph nodes. Now it looks like it’s in the lymph nodes. And we do a PET scan and they can’t find cancer anywhere except in this axilla area. But now we find a lymph node on the right side. So it must have spread.Let’s go ahead and do a biopsy on that. And so they biopsy the right side and the right side comes back with nothing other than tattoo ink. Now, all of this is kind of crazy. I am not a cancer specialist. I want to start by saying that I am not a cancer specialist. What I am sharing today is from a mother-in-law’s perspective, from a medical detective’s perspective, I do know how to do research. I do know how to find answers. And so what I’m going to share with you Dr. Deb Muth 05:54Is totally my opinion and totally my experience. And I’m not telling anybody to do anything different than what their doctors are telling them to do. But I am telling you to ask questions. So I go deep down the rabbit hole and find out that Tattoo Ink can appear like metastatic cancer on a PET scan. And we all know everybody gets tattoos today. They’re all over everyone. And yet we’re not thinking about how this tattoo ink can cause problems for us down the road, not to mention that there are heavy metals in them and it’s a toxin and it’s creating an inflammatory process in your body that your body’s constantly trying to get rid of. So the surgeon says to us, well, yes, that’s normal that that lymph nodes inflamed. It’s normal that there’s tattoo ink in it. The body’s doing what it’s supposed to do. It’s trying to get rid of a toxin. Okay. I will agree with that, but My son-in-law is covered with tattoos everywhere. And why didn’t we mention the tattoo ink that was found in the left axilla? We are only mentioning it in the right axilla. So there’s a lot of controversy, a lot of confusion. Many of you would never know any of this because A, you either don’t look at your lab results. And if you do, you don’t understand what you’re looking at. And that creates a problem for us, right? You don’t know what questions to ask. So we go into the doctor and the doctor tells us you have cancer and we’re going to swoop you in. And in the next two weeks, you’re going to be doing chemotherapy and radiation. And six months from now, we’re going to be doing surgery and there’s no time for questions and you’re scared shitless and you’re just doing what you can to survive. And I get that. And I totally understand that. And I appreciate that. But I’m telling you that If that is your choice, that is your choice. But as you’re doing that, take the time to ask the right questions. When this happened to us, there was a lot of challenging things with the oncology team. Nobody bothered to allow them to be a partner in their care. They dictated their care, but didn’t allow them to be a partner. So, Dr. Deb Muth 08:17Here’s what most oncologists do when patients get a cancer diagnosis. They look at the tumor type, they look at the stage, they look up the NCC guidelines, the National Comprehensive Cancer Network, and they follow the algorithm. Now, I have an enormous respect for conventional oncology. I really do. Working with cancer is probably one of the hardest things in medicine that anyone can do. The advances in this field over the last 10 years have been remarkable. But here’s my issue. Standard treatment assumes your cancer is the same as the cancer in the clinical trial that created the guidelines. It’s assuming that you and your cancer are the exact same as everyone else. You are the unique fingerprint, not the cancer. And this is the problem because your cancer is unique, just as unique as if you had your fingerprint taken, the mutations driving your tumor, the drugs your cancer cells are sensitive to, the metabolic vulnerabilities of your cancer. These are all different from the person sitting next to you in the chemo suite that has the same triple negative breast cancer or HER2 positive breast cancer or prostate cancer or colon cancer that you have. So what do do about that? Well, in my world, in the integrative medicine world, we test precisely, intelligently with the tools that most oncologists have never heard of. Or if they have, they haven’t incorporated it into their treatment modality for a variety of reasons. Either it’s not acceptable by the organization that they work for, they don’t understand it, They’re not going to be able to change their protocol anyway because they have to follow the NCCN protocol. So they don’t do it or they use a portion of it and they don’t do anything outside the protocol. So today I want to cover three things with you, three tools that we used that I think every cancer patient should be asking for when they start treatment or wherever you are in treatment at this point. Dr. Deb Muth 10:44you need to have these tests done. I don’t have any affiliation with any of these companies. I don’t get paid to tell you any of this. So let me just start by saying that I understand the chemistry behind these and how important it is to give you precision cancer treatment. And that’s why I’m talking about them today. The first one we’re going to talk about is the North Star response. This is your cancer surveillance score in the blood. How much cancer is circulating in the blood. The North Star Select, your cancer’s genomic blueprint from a blood draw. And the Datar Cancer Genetic Chemoscale, the live cell drug sensitivity test that tells us which drugs actually kill your cancer. So let’s go. Let’s dive into this. Let me just take a drink here. I’m going to cough a little bit. I apologize. I have this horrible tickle. It just never seems to go away, but that is not for today to discuss. So what is all of this? OK, the North Star response is a test that was developed by a company called Billion to One. And yes, that name is intentional because of the precision involved. It’s a next generation sequencing test, meaning it reads DNA at an incredibly detailed level. And it looks at something called methylated circulating tumor DNA or methylated CT DNA. Now let me break this down in plain English for you, because this can get a little overwhelming. When the cancer cells die or shed, they release tiny fragments of DNA into your bloodstream. We call this cell-free DNA or CFDNA, and it’s hidden within that cell-free DNA. And there are fragments that come from tumor cells. We call those CT DNA or circulating tumor DNA. Here’s what makes North Star’s response different. Rather than just looking for mutations in that tumor DNA, which is what most liquid biopsies do, and a liquid biopsy is just a blood test, Dr. Deb Muth 13:03This test looks at something called methylation patterns. Think of methylation like a dimmer switch on a gene. In healthy cells, certain genes are switched on and off in a very predictable way. In cancer cells, those dimmer switches go haywire. And cancer DNA has a characteristic hypermethylation, meaning switches are turning on and should be off or off and they should be on. And these patterns are essentially a cancer fingerprint in the blood. Now the North Star response scans more than 2000 locations in the genome for these cancer specific methylation patterns. And then it adds them all up into a single number called the tumor methylation score or TMS. So for Cameron, Cameron’s blood which was drawn on April 20th, 2026, his baseline tumor methylation score came back at 13. Now here’s the critical thing, to understand this was his baseline test, his starting point. And the real power of this test is in serial monitoring, meaning we run it again and again and again over time. And if that number goes up, the cancer activity is likely increasing. If it goes down, we’re likely suppressing the tumor activity. And if it stays flat or falls, that’s telling us that the disease is responding. So this is now in the blood. We have an actual fingerprint and every test from here forward will be compared to this number. Now let’s talk a little bit about this because I was not familiar with this test at all. I wasn’t sure what to expect. I wasn’t sure what to do with it. I did not order this test. He’s working with Inveda Medical and they are fabulous over there. I will tell you that from the beginning. This is coming from a practitioner and from a mother-in-law. They were absolutely wonderful to us. So when I saw this North Star, I didn’t know, should it be zero? Should it be a hundred? And when I talked to the doctor, he said, Dr. Deb Muth 15:29This number is actually really good. An average person walking around who’s never been diagnosed with cancer, who doesn’t have cancer, their number will be between 75 and 100. Cameron’s was 13. I think that’s fantastic. But what was the first question that went through my head? It’s probably the same question that you guys are doing. How can he have cancer with a number of 13 when it’s less than the normal average? And if we’re supposed to use this to track what’s happening with his cancer, how are we going to do that once we remove the cancer? Is this number going to go to zero? And it could possibly do that. And we may not be able to use this to track whether or not the disease is actually gone. But what we can do is use this to track over the course of his lifetime to see if the cancer cells are coming back long before we detect them on imaging. And that’s the huge part of this.So this is not a test that just anybody should go out and get because you’re worried about cancer. It is a test that should be done in somebody that is already diagnosed with cancer. So let’s start by making sure we explain that, okay? So imagine if every time your cancer cells are active and they’re shedding and they’re multiplying and they’re fighting back, they’re leaving a signature in your blood not just any signature, but a specific chemical tag that says, cancer’s here. That’s what the North Star Response Test reads. Those tags across thousands of locations and gives us a single score. So we track that score over time like a thermometer for your tumor. If it goes up, we get concerned. If it stays stable or goes down, we celebrate. And we can catch a change in the blood often months before it will show up on a scan. Pretty important when we’re talking about surveilling somebody for cancer returning, when we’re worried about it, and everybody knows the cancer patient is always worried after they get that clean bill health that something’s gonna come back, and most of the time they’re told that there is no way for them to determine that or know that from a blood test. And here is the blood test that can tell us, yes, it can. Dr. Deb Muth 17:51So I would really encourage you guys to talk to your oncologist about this. If you can’t find an oncologist that will do this, talk to an integrative cancer doctor. They will most likely be familiar with it. If not, ask them to find it for you and order it for you. So next, let’s talk about that genetic blueprint because North Star Select is a different test also by billion to one run on the same blood draw, but this one is doing something completely different. This is a comprehensive genomic liquid biopsy. Liquid biopsy just means blood tusks, meaning it’s looking for specific mutations in 84 cancer related genes, all from a blood sample, no biopsy needle, no surgery, just a blood draw. It looks for CNVS, single nucleotide variants, tiny one-letter typos in the DNA code. It looks for indels, small insertions or deletions in the DNA. It looks for copy number changes, the sections of the genomes that are duplicated or deleted. It looks at fusions. So when two genes incorrectly link together to create a dangerous hybrid, MSI status, micro satellite instability, which tells us whether immunotherapy is likely to work. And it has extraordinary sensitivity. It can detect a mutation that represents as little as 0.15 % of cell free DNA in the bloodstream. That is an almost impossibly small signal in the ocean of genetic noise. So what did this show for Cameron? This is where Cameron’s case gets clinically fascinating and where it tells the story of how his cancer is being held in check. Two major mutations were identified as actionable. One was called CRAS G12C. Dr. Deb Muth 20:11And it’s a variant-ELI fraction at 0.1%. Now, CRAS, if you’ve spent any time in integrative oncology, you’ve heard this name. CRAS is one of the most well-known oncogenes in cancer biology. Think of it like an accelerator pedal in the car. In a healthy cell, CRAS pushes the cell to grow when it receives the signal to do so. And then it stops. In cancer, crass gets stuck in the go position, like on the accelerator, foot on the accelerator, to the floor, going as fast as you can around that track, right? But it’s stuck there permanently. It doesn’t turn off and it’s supposed to be turning off. The G12C variant specifically is a mutation at a very precise location. Position 12 of the CRAS protein, where a glycine is replaced by cysteine. And this matters because CRAS G12C is now a drugable target. There are FDA approved drugs specifically designed to lock this mutation into its inactive state, essentially putting a foot on the brake. Now those are drugs like, and I’m gonna slaughter these names, Sordisib, a brand name is Lumacras, and Atacras, the brand name is Crastol. Neither is yet FDA approved for breast cancer, but they are approved for lung and colorectal cancer with CrasG2C. And Cameron’s tests identified 10 active clinical trials within a region that he could potentially qualify for with this mutation. The fact that his CRAS G12C is circulating at only 0.1%. That is a very low fraction. We call that a VAF, V-A-F, very low fraction. And it tells us something important. It means that this mutation is present in a small subclone of the tumor. It’s not the overall tumor burden. So either way, when we identify, we know it’s there. Dr. Deb Muth 22:37We can catch it and we can watch it. Now, here’s another interesting thing that we saw. His TP53 was at 0.23%. This is a tumor suppressor gene, the guardian of genome. And this gene is responsible for telling damaged cells to either repair themselves or self-destruct. And when it mutates as it is here in the position R196Q, that guardian goes off duty. The cell no longer has a reliable mechanism to prevent uncontrolled growth. So TP53 mutations are present in roughly 50 % of all human cancers. And there’s currently no FDA approved drug directly targeting the TP53 but there are clinical implications. TP53 mutant tumors may respond differently to chemotherapy and several investigational approaches, including TP53 vaccines and aurora kinase inhibitors are under active investigation. So we are seeing things happen in this part of cancer right now. Now there’s something called the VUS list and we are watching This is what we’re watching. beyond those two actionable mutations, NORSTAR Select identified what we call variants of an unknown significance, VUS, adenocarcinoma of an unknown significance, ACUP. These are mutations where we don’t yet have enough clinical evidence to determine whether they’re driving cancer or not, but we watch them. So on our mutation list was CDH1, a gene linked to hereditary gastric and lobular breast cancer, CDKN2A, a tumor suppressor cell cycle regulator, CDK12, involved in DNA repair, EGFR, ERBB, this is HER2 receptor, tyrosine kinases. Dr. Deb Muth 24:55I thought this one was pretty interesting since he had an IHC that showed a three plus HER2, but then when we confirmed it with FISH, FISH showed that was negative, but now we’re actually seeing genes expressing this HER2. So is there a HER2? Is there not a HER2? This is really important because if we don’t get these diagnoses right in cancer the first time, people will spend months and years treating the wrong type of cancer with the wrong type of medication. And this may be in part why some people do better than others. If we get it right out of the gate, they do good. If we don’t get it right out of the gate, they don’t do so good. Very important to have the actual genetic makeup of the tumor that’s growing in somebody. Now last, we have something called Notch C1, NRAS and RAF1. These are key pathway components. Now all of these were at very low baffs under 0.5%. These are just whispers, not shouts, but whispers that this cancer is excreting, but your body is listening. We have to be listening. We have to be able to watch these things and monitor these. Now here’s another note of clinical interest. It was an androgen receptor positive cancer. So also detected as a VUS.We know from tissue pathology that Cameron’s tumor was androgen receptor positive. So seeing this in circulation confirms that this AR expression of the cells are present in the bloodstream and that an anti-androgen approach remains worth considering. What that means is suppressing the testosterone. What all of you know I’m about ready to say is that I hate ever suppressing hormones, especially in a 38 year old male. That is not necessarily a good thing. So before we go suppressing hormones willy-nilly, we have to know that it’s the right thing to do. And we have to be able to combat all of the complications that are going to result of that. A 38-year-old male with no testosterone could lead to heart disease down the road, could lead to bone loss, could lead to dementia, Alzheimer’s. Not to mention the sexual side effects that are going to be present. And in a man that is very, very Dr. Deb Muth 27:20Difficult for someone to manage. So you have to be very specific and you want to be very, very diligent about what you’re doing in these cases like this. Now the MSI status was not detected. This tells us that cancer is not a microsatellite instability high, meaning that standard monotherapy may have a lower baseline response of probability and the strategic integration that we’re working with with in Vita could create an immunogenesis genicity becomes even more critical. So immunotherapy is going to be very critical in a cancer case like this and working with somebody that understands that and can carefully navigate that, especially if you have an autoimmune disease like Hashimoto’s or lupus, this is all very, very pristine and has to be looked at very carefully and done very diligently in order for somebody to do this without overstimulating that immune system and causing more problems. So when we looked at the blood and found this DNA fingerprint of the cancer cells circulating in the body, from that, what we see exactly is the genetic switches that are stuck on. They’re stuck on in the wrong position. This tells us which drugs were designed to fix exactly that problem. And it opens the door to clinical trials built for these specific mutations. It also gives us a list of things to watch for over time. And if one of those tiny little signals starts to grow, we know that cancer is gaining a ground in that area. And if it shrinks or disappears, we know we’re winning. This is like, I cannot tell you how exciting this is in the cancer world and the medical world because this is really pristine cancer therapy that we’re dealing with here. And to be able to have this is just so important to life saving events in treating cancer. So. Dr. Deb Muth 29:41Let’s talk about something called the Dittar Chemoscale. This is the battle before the battle. Okay, so I’ve saved the most remarkable test for last, and this is one from a company called Dittar Cancer Genetics. They’re based out of the UK. They are CAP and CLIA certified, which means it meets the rigorous standards required for clinical laboratory testing in the US. And this test is called the ChemoScale. And it is a live cell chemosensitivity assay. So let me explain exactly what that means because it sounds complex, but the concept is actually quite elegant. When we drew the blood from Cameron, the Dittar’s laboratory isolated what are called circulating tumor associated cells or CTACs. And these are actually living cancer cells and they’re associated cells that are traveling through his bloodstream. Excuse me. So let’s think about that for a moment. Real live cancer cells isolated from a blood draw. Those living cancer cells were placed into a lab environment and exposed to over 70 different drugs, both conventional chemotherapy agents and what we call repurposed drugs. I’ll talk more about those in a minute. The lab then measured how many of those cancer cells were killed by each drug expressed as a percentage of cell death. So the scale runs from zero to a hundred and below 25%, that drug doesn’t work well against any type of cancer in that person. Might work great in somebody else, but in that particular person’s cancer that they have, it’s not gonna work so great. Anything that’s 25 to 50 % is intermediate and above 50 % is a high response. And that’s really where Dr. Deb Muth 31:43we want to be. We want to see anything higher than 50 % because that’s a great medication that can be used to kill the cancer. This is not a theoretical test. This is not based on tumor’s genetic sequence and the computer algorithm that predicts the drug response. This is a HIS actual tumor cell being killed or not being killed in real time. That is the difference. So in traditional chemotherapy, we have our protocols. If you have triple negative breast cancer, if you have HER2 positive breast cancer, if you have prostate cancer, if you have colon cancer, here’s the protocol that you’re going to use because that’s the type of cancer you have. That’s what’s been studied. Now, the problem is most of these cancers have mutated over time, especially depending on how long they’ve been in your body, because that’s what they do to try to survive. They have to change so they can survive because your immune system’s constantly trying to kill them. And so this is a really important thing. And if we don’t take an individual into response or into our thought process when we’re creating these protocols, we may give a drug that doesn’t work at all towards that cancer and you just wasted seven cycles of chemotherapy with a drug that never would have worked in the first place or had such low resistance to it that it’s now just created side effects for you but did nothing to the cancer. And then we pull out another drug and we try that. And then we pull out another drug and we try that. Instead of us knowing precisely what we can use and what we can do. And this goes for both the conventional world and the alternative world. In the alternative world of cancer, we use things like IV vitamin C and tumeric and lately ivermectin and fenbendazole and mendendazole and all kinds of other things. And if we are not truly aware that this is going to do anything, we could be wasting somebody’s time and money. So I love that this test is available. I want to walk you through a little bit about what Dr. Deb Muth 34:01we are what we saw in our case, because I think this can make a big impact on people to ask the right questions. So this particular blood test looked at several different drugs. Cameron had sensitivity from 44 % up to 61 % on different medications. Now he was really lucky. The three main drugs that they would use to treat his cancer he had greater than a 50 % response to. So that was great. However, the drugs that were recommended for him to use out of the gate had less than 50 % activity. So he would have had one drug that was really good, one drug that was not so good. And we don’t know what the outcome would have been, right? So I think this is such an incredible, incredible test to have done. This is critical friends. I’m telling you if his oncologist had chosen the two drugs based on the general guidelines for his tumor, his cells would have largely not survived. But because we ran this test, we know. So we know to avoid the drugs that won’t work and we focus on the firepower where it really counts. So I want to also talk about this repurposed drug result because this is where it gets integrated for us. Now, this section is what I want everyone in our community, our Let’s Talk Wellness community, our members to understand. This is where conventional medicine and integrative medicine intersect in a peer-reviewed clinical validated way. So the Dittar test looks at live cancer cells against what they call repurposed drugs, meaning pharmaceuticals and natural compounds that were developed for the purposes, for other purposes, like it could be an antibiotic, it could be an herbal medicine, it could be all kinds of things, vitamins, whatever. But they have demonstrated anti-cancer activity in research. And when we’re talking about integrative medicine, this is a lot of where we get Dr. Deb Muth 36:26The integrative protocols from because these particular drug compounds are known for having anti-cancer benefits. And so that’s how integrative protocols get developed. But again, it could be just like medication, like cancer drugs. If your body doesn’t have a susceptibility to it, then you’re using a product that’s not necessarily going to work. And we all know we cannot take everything that somebody recommends just simply because it has an anti-benefit to whatever it is we’re treating. There’s only so many supplements you can take. There’s only so many things you can do before you get burnt out on taking it. We call it supplement fatigue. And so we want to be very precise with what we’re doing and target this very specific area. So one of the things that showed up really, really well for our case was artemisium, sweet wormwood. It’s an anti-malarial drug that has very potent anti-cancer effects. Now I found this extremely interesting in Cameron’s case because he does have a positive tick-borne illness called Babesia. And this is one of the things that we use to treat Babesia. The other thing I think is very interesting in this case is we are studying how parasites affect cancer these days. And that’s how Ivermectin, Fenbendazole, and Menbendazole have all gotten thrown into the treatment of cancer. And so for this drug or this herb to be sensitive to this type of cancer is really intriguing to me in the world of parasites and how parasites are truly decreasing the body’s immune system and causing cancer to grow. Another thing that worked, showed up really well for him was Valprolac acid. It’s an anti-seizure drug with HDAC inhibitor properties, and this disrupts cancer cell gene expression. There was a soy formula that showed up really well. Naltrexone, you guys have heard me talk about low dose naltrexone, LDN. This actually stimulates an endogenous opioid immune response feeling, and this drug actually showed up really well. Dr. Deb Muth 38:49Something as simple as quercetin. It’s an anti-inflammatory. This is a crass inhibitor in some studies. So this is really important. I’m sure most of you have heard about the benefits of green tea and green tea also actually has anti-angiogenic or anti-cancer benefits to it. Hydroxychloroquine, very popular drug. It’s another anti-malarial drug. So again, now we have two anti-malarial drugs that are susceptible to this type of cancer. And on top of it, he has a positive babesia test. So just saying, you got to connect the dots sometimes. You got to think outside the box sometimes. Metformin is very well known as a anti-proliferative in cancer. We use it to suppress the sugar because sugar feeds cancer. Nobody should be eating sugar if they have cancer. So this one showed up as well. And then CBD, we all know of the benefits of THC, the Rick Simpson oil, and CBD can be tested to see if that is beneficial to a particular cancer cell. This is different than THC. THC works very differently in cancer. CBD is your healthy component of it. It’s the part of the marijuana plant that does not make you high. So very important here. So now let me be very clear, because I always try to be very clear. This is not FDA approved. I’m going to repeat that. This is not FDA approved. This test is a laboratory developed test, not FDA cleared. These results represent in vitro testing, meaning in a lab, not inside the human body. And the results can differ in what we call in vivo, inside the body. And this is why I always say work with a qualified clinician who can interpret these results in full clinical context. But here’s why this matters. We now have evidence, live evidence of a cancer cell that shows sensitivities to compounds that are accessible, relatively safe, and some of which he may already be using, which some of them we were. Dr. Deb Muth 41:13We were already using some of them, which made us sit back and say, this cancer has been in there for two years. If it’s a triple negative breast cancer, it’s supposed to be an aggressive breast cancer that should have spread to a different organ already after two years. It is not, it has stayed in one spot. Also interesting in this case is that there is no breast tumor that they could find anywhere. This was all confined to the axilla into the lymph node. So to have this growing for this period of time with such a small tumor marker number, that 13 that we talked about in the North Star test originally, and to see some mutations, there’s a lot of questions to this particular case. And there are lots of questions to everybody’s cancer case. They are not all straightforward cancer cases. So this is what’s important to understand this fingerprint of these cancer cells so that you can identify exactly, exactly what’s going on and treat it exactly the correct way. Super important. So this kind of information gives us the direction in an integrative protocol. It’s not guessing. This is not eat more tumor, I can hope for the best. This is personalized tumor specific precision guided integrative oncology. It is very precise. There are several countries, several clinics like this around the country that offer this type of therapy. If it’s something that you’re interested in doing, I would encourage you to look at in Vita Medical. Hope for Cancer is another great facility. There are several great facilities around the country. Like I said, that could put together an integrative approach for you if this is something that you are thinking about doing. If you’re looking for answers, if you’re in stage four or stage three and you are not getting the results that you want to get, you want to look at a different approach. You want to do a combo approach of integrative medicine and traditional medicine and alternative medicine. Dr. Deb Muth 43:37I think this is so important to look at and have experts on your team. You know, in our case, Cameron’s cancer is very complex. It’s genomically aggressive in its presentation, yet it’s not progressing to distant areas, which is so wonderful. And I want to be careful here. I can’t tell you with certainty that this is any one thing. Biology is complex. Cancer is adaptive. It’s trying to survive. That’s what it is supposed to do. It is changing its shape. It’s changing its genetic structure. It’s changing everything to try to survive and try to hide against your immune system. Now we are not even close to the finish line in our journey, but what I can tell you is that what the integrative precision approach has done that standard care alone might not do. I can tell you that today and I will share our journey along the way for any of you that are going through this that want to look at a different approach as well because I think it’s important to have this information. So first of all, we know the tumor’s fingerprint. North Star response gives us that TMS score. so we can track it over time. And if the cancer tries to gain ground, we’ll see it in the blood before a scan, we’ll show it. We know the cancer’s genetic vulnerability. We know how to handle the DNA now. We know the watch list of things to look for. And when those signals start to grow, we have a roadmap of how to address it next, how to change it. We know which drugs will automatically work against the tumor cells. We’re not guessing based on a tumor type. We tested the cells. We know how many drugs in the commercial world and in the repurposed world will and will not work. And this is going to guide the treatment protocol that we walk forward with. So we’re not giving him drugs that won’t work or have a low response. Dr. Deb Muth 45:55We’re avoiding them completely and that matters because every ineffective drug is a dose of toxicity with no benefit. There is no lie to this. Chemotherapeutic drugs are toxic. That’s how they kill the cells, but they kill the good cells and the bad cells. And if we can avoid using a drug that’s not going to work, that is so important. And then we’re layering in those repurposed and natural compounds with proven activity against specific cells. This is not complementary fluff. This is biologically active tumor tested precision medicine. Very, very important. So here is what I need you all to know and what I want you to walk away with today. If you or someone you love is facing a cancer diagnosis before treatment starts, before the first infusion goes in, I want you to ask these questions so quick. Go grab something to write with. Pause this if you need to, because this is really, really important for you to do that. And we’re going to take a break for just a second while you guys go and do that. We’re going to give you a word from our sponsor, and then we’re going to come back. And I’m going to give you the four questions that I want you to ask specifically of your medical team so that you have the answers and the ammunition that you need to work with. So we’ll be right back. Dr. Deb Muth 47:29All right, everybody, welcome back. I hope you got your pencil, your paper, your pen, your phone, whatever you’re going to take notes with because this is important. So I’m to give you four questions that I want you to ask your medical team before you get started. Question one, can we do a chemo sensitivity test before we choose a chemotherapy regime? Ask specifically about DATAR, D-A-T-A-R. cancer genetics, Oncostat Plus, or a similar functional chemosensitivity platform. Very, very important to ask those specific things. All right, question two. Can we do a comprehensive liquid biopsy to identify actionable mutations and monitor tumor burden? Ask about North Star Select, Billion to One, Guardian 360, or Foundation One Liquid CDX? I’m gonna say those for you one more time, because I said them kind of fast. North Star Select by Billion to One, Guardian 360 or Foundation One Liquid CDX? Okay, question three. Can we establish a baseline tumor methylation score, TMS, so we have a surveillance marker to track over time? and ask specifically about the North Star Response Test. All right, question four. Is there an integrative oncology center that can layer precision guided natural compounds alongside conventional treatment? Research institutes like Inveda Medical Center, CTA CA Integrative Medicine, or Hope for Cancer, these people are doing integrative medical miracles. Let me tell you, I have researched every one of them. I have spoken to each of them individually before we made our decision of who we were going to work with. They are all fantastic. You want to work with an integrative nurse practitioner who understands oncology. And if you’re working with an integrative practitioner, you want to ask them these same questions about this test so that you can get the best outcome. Dr. Deb Muth 49:56For what you’re dealing with. You are allowed to ask these questions. You are allowed to want more information from that protocol that was designed for the average patient. You’re not average and your cancer is not average either. And your care doesn’t have to be. You do not have to settle for the same thing that the person sitting next to you in the IV suite is dealing with when you both have different cancers excreting different genetic material. This is so incredibly important. want to make sure you understand precision medicine is what changes the lives for people every single day, every single day. So I started this episode by telling you about a 38 year old man with a cancer that baffled conventional medicine and integrative medicine, an occult primary that was not found complex genetic genomic profile, a presentation that in many hands might have resulted in a one size fits all treatment protocol and a prayer. And instead we ran the tests, we mapped the fingerprint, we watched the cells, we guided the protocol, and we are still fighting with precision, with data, with intelligence. This is what Let’s Talk Wellness is all about not giving up. This is what not accepting we don’t know as a final answer and demanding the level of scrutiny and personalization that every cancer patient deserves. So if this episode resonates with you, please share it because somewhere out there, there is a person who is about to get the wrong chemotherapy because no one ran the right test. And maybe, just maybe, that This episode will be the reason someone asks the right question at the right moment. If you’re going through something like this, you need a group, you need somebody to connect with, please join our free Facebook group called Seen At Last. It is where we support one another, we share this information, we share knowledge, and we help people for free support and ask the right questions. Dr. Deb Muth 52:23And if you’re inclined in your heart to pray, pray for Cameron, we could use every ounce of prayer. If you are in a position where you can help support this journey financially, we do have a fund going in free funder. I can post the link below. Every little bit helps. If you have $5, $500, it doesn’t matter. We’re raising money for this treatment. And along the way, I am documenting every step of what we’re going through so I can provide more episodes like this for you guys to share the outcome and share what our journey is like so that it can help the next person along. I really always believe that whatever happens to us happens to us because we’re meant to share it. That’s why I’ve shared my personal journey. I’m sharing his personal journey and we want to help other people. So until next time, I’m Dr. Deb. Keep asking questions, keep advocating, and never ever accept being unseen.The post Episode 274 – Stop Guessing on Chemotherapy: The Live Cell Test Most Doctors Miss first appeared on Let's Talk Wellness Now.
In Part 2 of Thinking Thoracic's annual review of the year's most influential thoracic oncology research, Drs. Jeff Yang and Linda Martin examine practice-changing studies in perioperative care, lung cancer treatment, and multidisciplinary cancer management. The discussion covers emerging evidence on cryoanalgesia, preoperative fasting, targeted therapies for EGFR-mutated lung cancer, and other key clinical trials and consensus recommendations that are influencing patient care today.
This episode discusses the urgency for pharmacists to transition from using Cockcroft-Gault eCrCL to non-race based estimated glomerular filtration rate (eGFR) to improve medication-related decision-making in persons with reduced kidney function. Listeners will learn how to transition from C-G eCrCL to eGFR adjusted for body surface area to improve medication effectiveness and safety in persons with chronic kidney disease. The information presented during the podcast reflects solely the opinions of the presenter. The information and materials are not, and are not intended as, a comprehensive source of drug information on this topic. The contents of the podcast have not been reviewed by ASHP, and should neither be interpreted as the official policies of ASHP, nor an endorsement of any product(s), nor should they be considered as a substitute for the professional judgment of the pharmacist or physician.
A guide to diagnosing, imaging, and managing acute renal colic and nephrolithiasis in the ED. Hosts: Brian Gilberti, MD Avir Mitra, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Nephrolithiasis.mp3 Download Leave a Comment Tags: Kidney Stones, Urology Show Notes 1. CLINICAL CORE & PHYSIOLOGIC FRAMEWORK Epidemiologic Risk Profiles Lifetime incidence parameters hover around 1 in 11, presenting with a prominent male sex skew. Peak demographic manifestation concentrated within the 30–60 age band. High-yield temporal parameter: 50% recurrence vector within a 5-year post-initial-insult window. Mineralogical Composition Vectors Calcium oxalate crystals represent the predominant structural matrix. Struvite configurations (magnesium ammonium phosphate matrix) account for 1–2% of cohorts. Struvite stones function explicitly as infection-driven configurations secondary to upper tract proliferation; higher distribution index noted in female cohorts. Etiological & Modifiable Relational Dynamics Profound systemic dehydration or low baseline fluid throughput states. High-sodium diet structures and heavy animal-protein consumption loads. Positive genetic/familial history variables. Relative risk modulation: Each variable independently operates to expand baseline risk by a factor of 2x to 3x. Pathophysiologic Symptom Complexes Acute, sudden-onset, maximum-intensity (10/10) unilateral flank pain. Classic structural radiation vector tracking downward toward the ipsilateral groin/genitourinary dermatomes. Distinctive behavioral marker: Renal colic pacing/writhing behavior with zero antalgic position availability. Concomitant autonomic triggers: Nausea and emesis manifest in 50% of acute presentations. Physical Exam Discordance Metrics Severe subjective distress contrasted with a characteristically soft, completely non-tender abdominal palpation exam. CVA tenderness is completely variable and lacks reliable negative predictive value. Atypical Presentation Classifications Vague, poorly localized abdominal pain presentations occurring in up to 20% of active cases. Isolated lower urinary tract irritative signs including acute frequency or severe urgency. Incidental & Asymptomatic Dynamics Silent intrarenal or ureteral stones found incidentally. Longitudinal tracking demonstrates up to 33.3% of initially asymptomatic cohorts convert to fully symptomatic renal colic within a multi-year tracking window. 2. EXCLUSION DIAGNOSES & CRITICAL PATHWAY RED FLAGS Vascular Mimics: AAA rupture/expansion. This is a mandatory exclusion pathway in elderly cohorts presenting with acute flank or back pain. Physical tracking requires active exploration for an expansile, pulsatile abdominal mass. Gynecologic Emergencies: Ruptured ectopic pregnancy. Demands universal screening protocols via rapid beta-hCG testing in all female patients of childbearing potential presenting with lower abdominal/pelvic localization. Infectious Upper Tract Decompensation: Acute uncomplicated pyelonephritis. Differentiated via persistent high spikes, high fevers, systemic shaking chills, and profound pyuria. Genitourinary Structural Crises: Acute testicular torsion. Mandates a thorough, explicit scrotal/testicular structural exam if the flank pain radiates into the scrotum. Gastrointestinal and Adnexal Torsional Confounds: Acute appendicitis variants, acute mesenteric/bowel ischemia, and ovarian torsion syndromes. 3. LABORATORY TESTING & PHYSIOLOGIC EVALUATION Urinalysis Interpretation Nuances Microscopic or gross hematuria presents in approximately 66% to 90% of acute cases. Critical Pathological Caveat: Complete absence of hematuria documented in 20% to 33.3% of confirmed, acute obstructing ureteral stones. Diagnostic rule: A pristine urinalysis with zero red blood cells is entirely insufficient to exclude acute ureterolithiasis. Urinary pH as a Composition Clue Consistently low urinary pH parameters (pH < 5.5) point strongly toward a uric acid crystalline composition. Elevated urinary pH parameters (pH > 7.5) indicate the presence of urease-producing microbial pathogens, pointing toward a struvite infection stone. Infectious Screening Metrics Active tracking for marked pyuria, positive leukocyte esterase, and bacterial nitrites to rule out an obstructed, infected upper urinary tract system. BMP Immediate quantification of baseline serum creatinine to establish accurate eGFR values. Targeting detection of post-renal AKI from bilateral obstruction, unilateral obstruction in a single functioning kidney, or severe volume depletion. CBC Evaluation for marked leukocytosis. Physiologic Nuance: Mild-to-moderate white blood cell count elevations frequently represent non-specific stress demargination driven by severe pain and repetitive vomiting. High-grade white blood cell shifts demand immediate exclusion of systemic bacteremia or an infected, obstructed urinary system. Adjunctive Lab Pathways Rapid qualitative urine hCG testing. Reflex urine culture execution whenever urinalysis metrics display significant inflammatory profiles or clinical suspicion of UTI is high. 4. IMAGING MODALITIES & ALGORITHMIC CLINICAL SELECTION Non-Contrast CT Diagnostics Gold standard; diagnostic sensitivity and specificity parameters exceed 95% for stones >2 mm. Provides precise quantification of stone diameter (mm), exact localization (proximal, mid, or distal ureter), and degree of secondary hydronephrosis. Excellent structural visualization for detecting or ruling out alternate retroperitoneal, vascular, or intra-abdominal pathologies. Contrast-Enhanced CT Protocols Indicated when alternative intra-abdominal surgical pathology is highly suspected over isolated renal colic. Retains diagnostic capability to identify urinary tract stones >3 mm even within contrast-enhanced phases. NCCT Structural Architecture Limitations Standard stone protocol CT scans are executed in a prone position without IV contrast enhancement. It does not opacify the ureteral lumen. Presents a cumulative radiation exposure penalty when utilized serially across recurrent ED presentations. POCUS / Radiology Ultrasound Direct stone visualization capabilities are modest, operating at approximately 50% to 60% sensitivity, and is highly dependent on anatomical positioning at the extreme proximal ureter or the UVJ. Secondary obstruction tracking: Demonstration of hydronephrosis operates at a high sensitivity of approximately 80%. POCUS Clinical Utility Metrics Eliminates ionizing radiation exposure and allows immediate, rapid real-time execution directly at the patient’s bedside. Confirmation of significant hydronephrosis within a classic clinical presentation yields high post-test probability for stone presence while lowering suspicion for vascular catastrophes like a AAA. KUB Radiography Extremely poor overall diagnostic sensitivity, hovering around 57%. Fails to image radiolucent configurations (pure uric acid matrices) or small stones measuring
In this episode of the Oncology Brothers podcast, we discussed challenging cases focused on metastatic non-small cell lung cancer (NSCLC) with common EGFR mutations. Joined by experts Dr. Shirish Gadgeel from the Emory University and Dr. Wade Iams from Tennessee Oncology, the discussion revolved around two real-life patient cases. The first case featured a 54-year-old gentleman with active tobacco use and diffusely metastatic NSCLC, including an isolated brain lesion. The panel explored treatment options, including single-agent osimertinib versus dual combinations of amivantamab-lazertinib and osimertinib-chemotherapy, emphasizing the importance of shared decision-making and considering co-mutations and patient demographics. In the second case, the conversation shifted to supportive care and managing side effects, particularly focusing on skin toxicity associated with amivantamab. The experts shared their proactive approaches to patient education and the significance of monitoring and adjusting treatment plans to enhance patient quality of life. Key Points: In EGFR-mutated NSCLC with CNS metastases, treatment selection between single-agent osimertinib and combination amivantamab-lazertinib vs. osimertinib-chemotherapy requires individualized consideration of age, co-mutations, extent of disease, and patient preference rather than mutation status alone. Younger patients with CNS disease may benefit from more aggressive upfront combination therapy, while shared decision-making remains central to navigating the expanded efficacy versus increased toxicity trade-off. Dermatologic toxicities associated with amivantamab requires proactive management including supportive care regimen, early dose adjustments and close patient monitoring to maintain treatment continuity. Providing the best available upfront therapy in metastatic EGFR-mutated NSCLC is critical, as sequencing options become more limited at progression. Join us for an insightful discussion on the latest treatment algorithms, the importance of personalized care, and the evolving landscape of NSCLC management. Listen us on: Spotify: https://open.spotify.com/show/31BXhY9FM4gPWG10WgE11o Apple Podcast: https://podcasts.apple.com/us/podcast/oncology-brothers-practice-changing-cancer-discussions/id1653340966 Follow us on social media: X/Twitter: https://twitter.com/oncbrothers Instagram: https://www.instagram.com/oncbrothers Website: https://oncbrothers.com/ Don't forget to subscribe for more episodes featuring conference highlights and challenging cases in oncology! #EGFRMutated, #LungCancer, #ThoracicOncology, #PersonalizedMedicine, #OncologyBrothers
Thank you for joining us for our 2nd Cabral HouseCall of the weekend! I'm looking forward to sharing with you some of our community's questions that have come in over the past few weeks… Thank you for tuning into this weekend's Cabral HouseCalls and be sure to check back tomorrow for our Mindset & Motivation Monday show to get your week started off right! Kim: What would cause my son to cough hard for hours after eating? He has done this for a year. He is 28 and said he is to the point where he just does not want to eat. Should he do the CBO protocol? Anonymous: Hi Dr Cabral, I came across your podcast a few months ago and have been listening daily to catch up on past episodes for general health education. Thank you for the valuable information you share. I would appreciate your guidance on diet and lifestyle for the following situation. My partner, a 31-year-old male, recently had an eGFR test done, and his result increased from 70 to 77. His father passed away in his 40s due to kidney failure, so this is a concern for us. We live in the Caribbean, where it is humid year-round. He strength trains 3–4 times per week and plays basketball once weekly, but I'm unsure if his cardio levels are sufficient for long-term kidney and overall health. Christine: Hi Dr. Cabral, Thank you so much for everything you do! Your IHP program and your podcast have been life changing for me. I have a question about creatine. I've noticed when I take it, my appetite completely plummets and food does not even taste good. And when I cut out creatine, the appetite comes back within a day. I take around 1g for reference, and I'm 5'1 and 115 lbs if that needs to be taken into consideration. What could be the possible reasons for this? Thank you! Christine Tricia: Good morning, Dr Cabral - hope you are well! I take many of your supplements with some being from the longevity line. I'm wondering if it is okay to take these ongoing for years or should we take a few weeks break from time to time? Are they as effective when used long term? The supplements I'm taking are your renewal system, eye health, hair supplements. Thank you for your guidance! Matt: Hi Dr Cabral, I'm a healthy 45yo, strength train 3x per and 2 days of jiujitsu. I had my first ever episode of AFIB and it occurred about 5 min after taking a growth hormone peptide Tesamorelin. I went to the ER the next day and came out of it on my own within 14 hours of when it started and haven't had an episode since. They ran all kinds of blood work, EKG, CT w contrast for blood clots and all came up clear. They seemed to think it was from excessive caffeine use (300-500mg daily) and bad sleep but weren't really sure on the peptide as there's not enough research. Seems to me that's what triggered it. I stopped caffeine&peptides immediately and have really been trying to dial in my sleep for the past two weeks. Could this be a one off thing or am I more likely to have it happen again? - - - Show Notes and Resources: StephenCabral.com/3775 - - - Get a FREE Copy of Dr. Cabral's Book: The Rain Barrel Effect - - - Join the Community & Get Your Questions Answered: CabralSupportGroup.com - - - Dr. Cabral's Most Popular At-Home Lab Tests: > Complete Minerals & Metals Test (Test for mineral imbalances & heavy metal toxicity) - - - > Complete Candida, Metabolic & Vitamins Test (Test for 75 biomarkers including yeast & bacterial gut overgrowth, as well as vitamin levels) - - - > Complete Stress, Mood & Metabolism Test (Discover your complete thyroid, adrenal, hormone, vitamin D & insulin levels) - - - > Complete Food Sensitivity Test (Find out your hidden food sensitivities) - - - > Complete Omega-3 & Inflammation Test (Discover your levels of inflammation related to your omega-6 to omega-3 levels) - - - Get Your Question Answered On An Upcoming HouseCall: StephenCabral.com/askcabral - - - Would You Take 30 Seconds To Rate & Review The Cabral Concept? The best way to help me spread our mission of true natural health is to pass on the good word, and I read and appreciate every review!
Welcome back to the Oncology Brothers podcast! In this episode, we were joined by Dr. Isabel Preeshagul from Memorial Sloan-Kettering to discuss the latest advancements in lung cancer presented at ASCO 2026. Listen us on: Spotify: https://open.spotify.com/show/31BXhY9FM4gPWG10WgE11o Apple Podcast: https://podcasts.apple.com/us/podcast/oncology-brothers-practice-changing-cancer-discussions/id1653340966 Follow us on social media: X/Twitter: https://twitter.com/oncbrothers Instagram: https://www.instagram.com/oncbrothers Website: https://oncbrothers.com/ We dived into four key studies that could change clinical practice: LIBRETTO-432: exploring the promising event-free survival data with selpercatinib in RET-positive disease and its implications for adjuvant therapy. CROWN 7yr Update: seven-year progression-free survival results with lorlatinib in ALK-positive non-small cell lung cancer and the associated side effects. CHRYSALIS-2: exciting findings regarding amivantamab for atypical EGFR mutations and its potential to become the new standard of care. HARMONi-6: dual-headed drug ivonescimab combined with chemotherapy in metastatic squamous cell lung cancer and its intriguing results. We also touched on the importance of molecular testing for all patients, regardless of stage or histology, and highlighted the latest updates on tarlatamab in small cell lung cancer. Tune in for an insightful discussion that aims to keep our oncology community informed and engaged with the latest research and treatment options! Don't forget to like, subscribe, and check out our other episodes for more insights on oncology treatments, conference highlights, and FDA approvals. #ASCO2026, #LungCancer, #ALKPositive, #RETPositive, #OncologyBrothers
In this Part 1 of 2 ASCO 2026 Highlights episodes, hosts Dr. Narjust Florez and Dr. Stephen Liu are joined by Dr. Alice Shaw and Dr. Jonathan Goldman to review some of the most impactful targeted therapy data presented at the 2026 ASCO Annual Meeting. The discussion explores the practice-changing LIBRETTO-432 trial in early-stage RET-positive NSCLC, long-term outcomes with lorlatinib in ALK-positive disease, emerging data for neladalkib, and promising results for sunvozertinib in EGFR exon 20 insertion–positive NSCLC, highlighting how these findings may influence treatment decisions across disease stages. Guests: Dr. Alice Shaw. is a Professor of Medicine at Harvard Medical School, Chair of Medical Oncology, and a thoracic oncologist at Dana Farber Cancer Institute. She is widely recognized as a pioneer in the field of ALK-positive non-small cell lung cancer, having led landmark clinical trials that established crizotinib, ceritinib, and lorlatinib as standards of care. Dr. Jonathan W. Goldman is a Professor of Medicine and thoracic oncologist at the UCLA David Geffen School of Medicine, where he serves as a principal investigator in the Phase I drug development program. Dr. Goldman has been at the forefront of early-phase oncology trials across multiple tumor types, with a particular focus on novel therapeutics in lung cancer, and he was the presenting author of Libretto 432 at the plenary session at the 2026 ASCO
In this episode, Dr. Paul Wheatley-Price speaks to Dr. Ross Camidge, our guest in this increidbly unique episode of "Perspectives", sharing his leading clinical expertise on the treatment of EGFR-positive lung cancer as Director of the Thoracic Oncology at the University of Colorado Cancer Center. On the other hand, being diagnosed with the same disease himself at stage 4 in 2022, Dr. Camidge shares his perspective and journey from the patient lens, walking in the same shoes that he'd built his career upon. Don't miss this unique episode!
Good morning from Pharma Daily: the podcast that brings you the most important developments in the pharmaceutical and biotech world. Today, we'll explore a landscape teeming with strategic partnerships, groundbreaking clinical trial results, regulatory shifts, and innovative therapeutic approaches that are redefining patient care and drug development. Pfizer's monumental $10 billion collaboration with Innovent Biologics stands out as a testament to the shifting dynamics of the oncology sector. This partnership aims to develop 12 antibody-drug conjugate (ADC) and multispecific antibody programs, spotlighting these therapies' growing significance in oncology. The precision of antibodies in delivering cytotoxic agents directly to cancer cells offers a new frontier in minimizing collateral damage to healthy tissues—a crucial advancement in cancer treatment. The deal not only highlights Pfizer's commitment to expanding its oncology pipeline but also underscores the strategic importance of leveraging China's accelerated drug development ecosystem. In regulatory news, AstraZeneca's Imfinzi has garnered FDA approval for BCG-naive high-risk non-muscle-invasive bladder cancer. This milestone for PD-L1 inhibitors reflects the evolving landscape of immunotherapy. By harnessing monoclonal antibodies in combination therapies, the potential for enhanced anticancer efficacy is significant. With few therapeutic alternatives available, this approval presents a lifeline for many bladder cancer patients. Clinical trial outcomes also continue to capture attention. Eli Lilly's Nectin-4 targeting ADC showed promising results in advanced urothelial cancer, positioning itself as a potential competitor to Padcev. This innovation in ADC technology demonstrates the industry's relentless pursuit of targeted therapies that can revolutionize treatment paradigms. Bristol Myers Squibb's mezigdomide offers another example by showing a 52% reduction in progression risk for relapsed or refractory multiple myeloma patients, emphasizing the focus on addressing specific molecular pathways. In the realm of bispecific antibodies, Phanes Therapeutics' CLDN18.2/CD47 targeting therapy reported encouraging Phase 2 results in metastatic pancreatic ductal adenocarcinoma. These antibodies' ability to simultaneously engage multiple targets enhances their therapeutic efficacy against stubborn cancers, broadening the horizon for treatment possibilities. Meanwhile, Replimune's resubmission of its RP1 melanoma Biologics License Application (BLA) highlights the intricate dance between drug development and regulatory processes amid organizational shifts at the FDA. Such efforts reflect the continual adaptation required within the industry to navigate complex regulatory landscapes. On the funding front, Psilera's successful $8.8 million seed round indicates growing interest in psychedelic therapies for neurological conditions. Similarly, Reprogram Biosciences raised $6 million for its AI-driven cell reprogramming oncology platform, illustrating how artificial intelligence is becoming integral to advancing drug discovery and development. However, not all updates were positive. Agios Pharmaceuticals faced setbacks as their pyruvate kinase activator failed a Phase 2b trial for lower-risk myelodysplastic syndromes, serving as a sobering reminder of the inherent risks involved in drug development. Dizal Pharma emerges as a beacon of hope in lung cancer treatment following Takeda's EGFR exon 20 drug setback. By challenging existing treatments with promising small molecule data, Dizal exemplifies precision medicine's role in redefining oncology protocols—offering personalized patient options that could set new standards in treatment efficacy. The issue of drug pricing remains contentious, particularly highlighted by an AARP analysis showing an 81% increase post-launch prices stateside compared to a 13% decrease abroad. This disparity raises critical questions about achieving equitable access across markets amid Medicare negotiations and global pricing strategies like "most favored nation" policies. Regulatory updates continue with Johnson & Johnson's Tremfya label expansion stateside and AbbVie's EU extension for Venclyxto—moves that reflect efforts to maximize therapeutic reach and commercial viability across diverse geographies. Finally, Gilead Sciences' decision to discontinue its lead rheumatoid arthritis drug from MiroBio underscores ongoing challenges within emerging fields like BTLA agonists—a reminder of both innovation's promise and its perilous nature when faced with unproven therapeutic avenues. As these varied developments unfold, they collectively signal an era characterized by rapid scientific innovation and strategic collaborations across geographies alongside evolving regulatory landscapes—all driving towards enhanced patient care through more effective treatments globally. This concludes today's insights from Pharma Daily—a world where dynamic change continues reshaping healthcare delivery standards towards unprecedented possibilities for patient outcomes worldwide. Thank you for joining us; stay tuned for more updates on tomorrow's horizon-shaping advancements.Support the show
In this episode, Aarti Bhatia, MD, MPH, and Deborah J. Wong, MD, PhD, discuss the rapidly evolving treatment landscape for recurrent, metastatic, and locally advanced head and neck squamous cell carcinoma (HNSCC), including the growing role of immune checkpoint inhibitors, perioperative treatment strategies, EGFR-targeted bispecific antibodies, antibody–drug conjugates, HPV-targeted vaccines, and novel radiosensitizers. The discussion also explores emerging phase III clinical trials, treatment sequencing considerations, and future precision oncology approaches for HPV-positive and HPV-negative patients with head and neck cancer. Presenters: Aarti Bhatia, MD, MPH Associate Professor of Medicine (Medical Oncology) Clinical Research Team Leader, Head and Neck Cancers Program Yale Cancer Center New Haven, Connecticut Deborah J. Wong, MD, PhD Director, Head and Neck Medical Oncology Program Associate Clinical Professor of Medicine Division of Hematology/Oncology University of California, Los Angeles (UCLA) Los Angeles, California Link to full program: https://bit.ly/49kViqg Get access to all of our new podcasts by subscribing to the Decera Clinical Education Oncology Podcast on Apple Podcasts, YouTube Music, or Spotify. Hosted by Simplecast, an AdsWizz company. See pcm.adswizz.com for information about our collection and use of personal data for advertising.
Sickle cell disease causes accelerated kidney function decline, yet proven GFR-preserving therapies remain elusive. In this study of adults with sickle cell disease, RASi use was not associated with a significant difference in the rate of eGFR decline.
In this JCO PO Article Insights episode, host Jordan Goldstein summarizes the article, "EXONERATE-TRaCE: A Liquid Biopsy for Tracking Response to Anti–Epidermal Growth Factor Receptor–Based Therapy in Metastatic Colorectal Cancer" byTakahashi, et al. LINK TO FULL TRANSCRIPT
Dr. Joshua Reuss returns to the podcast to discuss the update to the living guideline on stage IV NSCLC with driver alterations. The conversation focuses on new cancer treatment strategies for patients with advanced NSCLC and EGFR mutations, including classical EGFR alterations (exon 19 deletions, exon 21 L858R substitution) and rarer alterations (exon 20 insertion mutations). Dr. Reuss discusses results from clinical trials, including MARIPOSA and CHRYSALIS-2 and how these impacted first-line and subsequent line treatment recommendations. He looks to the future on what new evidence and potential updates are in the pipeline for this living guideline. Read the full living guideline "Therapy for Stage IV Non-Small Cell Lung Cancer with Driver Alterations, ASCO Living Guideline Version 2026.3.1" LINK TO FULL TRANSCRIPT
Your eyes can give powerful clues about your kidney health. It's critical to catch kidney disease before it hits stage 4, and eye changes are among the first kidney warning signs. Learn to spot the signs early.
In this episode of the Oncology Brothers podcast, we dived into the world of anti-EGFR therapies in non-small cell lung cancer (NSCLC). Joined by Dr. Joshua Sabari from NYU Langone Health and Dr. Azam Farooqui from Ironwood Cancer and Research Center, we discussed the latest advancements in treatment options, including the use of osimertinib, afatinib, and the combination therapy of amivantamab and lazertinib. Listen us on: Spotify: https://open.spotify.com/show/31BXhY9FM4gPWG10WgE11o Apple Podcast: https://podcasts.apple.com/us/podcast/oncology-brothers-practice-changing-cancer-discussions/id1653340966 Follow us on social media: X/Twitter: https://twitter.com/oncbrothers Instagram: https://www.instagram.com/oncbrothers Website: https://oncbrothers.com/ Key topics include: The role of afatinib in treating uncommon EGFR mutations and its associated toxicities The well-tolerated profile of osimertinib and its common side effects, including rash, diarrhea, and the rare risk of pneumonitis Insights into the combination therapy of amivantamab and lazertinib, including management of skin toxicity and the importance of prophylactic anticoagulation to mitigate VTE risks The episode emphasized the importance of maintaining quality of life for patients while ensuring they can stay on effective therapies for longer periods. Tune in for valuable clinical pearls and strategies to optimize patient care in the community setting. Don't forget to like, subscribe, and check out our other episodes for more insights on treatment algorithms and conference highlights! #LungCancer, #NSCLC, #EGFR, #TargetedTherapy, #OncologyBrothers
JACCP associate editor and host, Erica Ernst, interviews Drs. Wendy St. Peter and Barbara Zarowitz discuss adopting race-free estimated GFR (CKD-EPI) for medication-related kidney function assessment in older adults and other patient populations, as well as moving away from the Cockcroft–Gault equation. The discussion highlights deficiencies and variabilityin Cockcroft–Gault use, emerging studies where BSA-adjusted eGFR better predicts drug clearance, barriers to cystatin C access and Medicare coverage, and the need for further research, electronic health record integration, and advocacy across organizations. Read the original article and series of letters published in JACCP.
As part of IASLC's ongoing series of podcasts in world languages, Dr. Alfredo Addeo moderates a Virtual Tumor Board discussion with Dr. Andrea Fillipi and Dr. Piergiorgio Solli. The tumor board focuses on the management of resectable EGFR-mutant NSCLC. Host: • Alfredo Addeo, MD Head of Oncology Service University Hospital Geneva Guests: Andrea R. Filippi, MD Head of Radiation Oncology, Fondazione Istituto Nazionale dei Tumori, Milan Associate Professor, Radiation Therapy Department of Oncology, University of Milan Piergiorgio Solli, MD, PhD Head of Thoracic Surgery IRCCS Fondazione Istituto Nazionale dei Tumori, Milan
Many clinical algorithms, including the eGFR test for kidney function, have actually had race baked into them and produce different results for Black patients. Most of us assume these algorithms are based on science, but what if the science is wrong? A full transcript of this episode is available at https://www.nejm.org/doi/full/10.1056/NEJMp2601974.
ASN Executive Vice President and Chief Executive Officer Tod Ibrahim explores the history of eGFR with Andrew Levey, MD, Tom Hostetter, MD, and Crystal Gadegbeku, MD. Hear how policy, equity, and care have evolved, and what future assessments demand.
ASN Executive Vice President and Chief Executive Officer Tod Ibrahim explores the history of eGFR with Tom Hostetter, MD, Crystal Gadegbeku, MD, and Andrew Levey, MD, founding director of the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI).
Welcome to another episode of the Oncology Brothers podcast! In this episode, hosts Rahul and Rohit Gosain dive deep into the treatment algorithms for early-stage non-small cell lung cancer (NSCLC) with curative intent. Joined by leading thoracic medical oncologist Dr. Sanjay Popat from London, they discussed the critical role of next-generation sequencing (NGS) in treatment planning, the importance of proper staging, and the implications of actionable mutations. Listen us on: Spotify: https://open.spotify.com/show/31BXhY9FM4gPWG10WgE11o Apple Podcast: https://podcasts.apple.com/us/podcast/oncology-brothers-practice-changing-cancer-discussions/id1653340966 Follow us on social media: X/Twitter: https://twitter.com/oncbrothers Instagram: https://www.instagram.com/oncbrothers Website: https://oncbrothers.com/ Key topics covered included: The significance of NGS testing and its impact on treatment decisions. Insights from the CHECKMATE 816 trial, highlighting the benefits of neoadjuvant chemoimmunotherapy. The complexities of post-operative immunotherapy and patient-shared decision-making. The role of adjuvant chemotherapy in patients with actionable mutations like EGFR and ALK. The latest data on osimertinib and alectinib in the adjuvant setting. The standard of care for unresectable disease based on the PACIFIC trial and the implications of PD-L1 status. Join us for an informative discussion that unpacks the latest advancements in NSCLC treatment and emphasizes the importance of personalized care. Don't forget to subscribe for more episodes in our treatment algorithm series! #EarlyStageNSCLC, #CHECKMATE816, #NeoadjuvantTherapy, #PrecisionMedicine, #OncologyBrothers
Chronic kidney disease (CKD) affects an estimated 37 million Americans, yet most cases go undiagnosed until the disease has significantly progressed. A urine albumin-to-creatinine ratio (uACR) test can detect kidney damage years before a decline in the estimated glomerular filtration rate (eGFR), but it remains underutilized. In the first episode of Beyond the Silo: Integrated Care Across the CRM Continuum, a podcast series from The American Journal of Managed Care®, Marc P. Bonaca, MD, MPH, moderates a discussion with Josephine Harrington, MD, on why uACR has not yet become a standard of care, how CKD fits into the broader cardio-renal-metabolic (CRM) disease continuum, and what changes are needed across specialties, systems, and workflows. Bonaca is a cardiologist and vascular medicine specialist at the University of Colorado Anschutz and the executive director of CPC Clinical Research. Harrington is also a cardiologist, specializing in advanced heart failure and transplant cardiology at UCHealth's Heart and Vascular Center at the University of Colorado Hospital. Throughout the conversation, they emphasize that CKD is an early integral part of the CRM continuum, as it is both a driver and consequence of cardiovascular risk, with uACR elevation often appearing before eGFR decline and signaling increased risk even at mild levels. Despite strong guideline support, uACR screening remains underused due to structural barriers. Therefore, the experts explained that the primary barrier is not the test itself but the lack of streamlined workflows that make screening routine and results actionable without adding clinician burden. They concluded that early detection is critical because it enables the timely use of therapies such as SGLT2 inhibitors, glucagon-like peptide-1 receptor agonists, and finerenone, which improve outcomes. To close the gap, the experts noted that uACR should be treated as a routine vital sign for cardiometabolic risk and embedded into health system quality metrics to ensure consistent, accountable use.
Welcome to the third episode of our three-part series on colorectal cancer! In this episode of the Oncology Brothers we are joined by Dr. Rona Yaeger, a medical oncologist from the Memorial Sloan Kettering Cancer Center. Together, we dived into the management of common side effects associated with systemic treatments for colorectal cancer. Listen us on: Spotify: https://open.spotify.com/show/31BXhY9FM4gPWG10WgE11o Apple Podcast: https://podcasts.apple.com/us/podcast/oncology-brothers-practice-changing-cancer-discussions/id1653340966 Follow us on social media: • X/Twitter: https://twitter.com/oncbrothers • Instagram: https://www.instagram.com/oncbrothers • Website: https://oncbrothers.com/ Episode Highlights: • Overview of 5-FU and capecitabine, including the importance of DPYD mutation testing and side effects like cytopenia, mucositis, and cardiac toxicity. • Discussion on the use of 5-FU bolus in both metastatic and adjuvant settings. • Insights into managing oxaliplatin-induced neuropathy and the potential benefits of oral cryotherapy. • Clinical pearls for irinotecan, including the management of diarrhea and cholinergic effects. • Considerations for using Bevacizumab, including risks of hypertension, proteinuria, and blood clots. • Tips for managing side effects of anti-EGFR agents like Cetuximab and Panitumumab, including rash and infusion reactions. • An overview of oral agents such as encorafenib, TAS-102, and Regorafenib, with a focus on dosing strategies and side effect management. Join us as we explore these critical topics and provide valuable insights for healthcare professionals managing colorectal cancer treatments. Don't forget to subscribe for more episodes! #ColorectalCancer, #SideEffectManagement, #DPYDtesting, #ChemotherapyToxicity, #SupportiveCare
Year in Review: Clinical Investigator Perspectives on the Most Relevant New Datasets and Advances in EGFR-Mutant Non-Small Cell Lung Cancer | Faculty Presentation 1: Management of Metastatic EGFR-Mutant Non-Small Cell Lung Cancer (NSCLC) — Helena Yu, MD CME information and select publications
Year in Review: Clinical Investigator Perspectives on the Most Relevant New Datasets and Advances in EGFR-Mutant Non-Small Cell Lung Cancer | Faculty Presentation 2: Other Relevant Topics in EGFR-Mutant NSCLC (eg, Nonmetastatic Disease, Exon 20 Insertion Mutations, Novel Agents) — Suresh S Ramalingam, MD CME information and select publications
Featuring perspectives from Dr Suresh S Ramalingam and Dr Helena Yu, including the following topics: Introduction: Genomics of EGFR (and HER2) (0:00) Metastatic Disease (9:30) Localized Disease (30:22) EGFR Exon 20 Insertion Mutations (46:57) New Agents (54:20) CME information and select publications
In this episode of the IDEA Collider, host Mike Rea sits down with Marianne De Backer, CEO of Vir Biotechnology, to explore how she is leading one of biotech's most complex transformations. After the rapid rise and decline of COVID-19 revenues tied to sotrovimab, Marianne stepped into Vir Bio in 2023 and led a bold strategic reset—refocusing the company on immuno-oncology, infectious disease, and platform-driven innovation. The conversation dives into Vir Bio's next chapter, including its masked T-cell engager (TCE) pipeline and the PRO-XTEN® masking platform, which is designed to overcome the safety challenges of TCEs in the treatment of solid tumors by shielding therapies until they reach the tumor microenvironment. They also discuss Vir Bio's advancing hepatitis delta program, currently in registrational Phase 3 trials, and the company's growing pipeline leveraging the synergy of its AI-driven discovery, protein engineering capabilities, and universal PRO-XTEN® masking technology. Marianne shares what it takes to lead through a biotech downturn—from restructuring and capital discipline to rebuilding culture, integrating new teams, and positioning for long-term growth. This episode is a deep dive into biotech turnaround strategy, next-generation cancer therapies, and leadership in times of uncertainty. Episode Timestamps 00:00 – Introduction and Vir's transformation story 00:40 – Marianne De Backer's 30+ year pharma journey 02:42 – Vir's origins and post-COVID strategic pivot 04:42 – Taking over as CEO during a crisis 06:33 – Lessons from the biotech downturn (“biotech winter”) 08:56 – Astellas partnership and T-cell engager strategy 09:52 – ProXtend platform: masked T-cell engagers explained 13:24 – Clinical data, safety, and tumor targeting 15:32 – Integrating new teams and scientific expertise 17:38 – Expanding the pipeline (HER2, EGFR, oncology) 19:50 – Hepatitis delta program and commercialization plans 22:11 – Funding strategy and biotech market outlook 25:37 – FDA interactions and regulatory perspective 28:13 – AI in drug discovery and clinical trials (Daisy platform) 31:34 – Culture: grit, ingenuity, collaboration, authenticity 34:21 – Personal reflections and leadership mindset 35:46 – Closing thoughts Don't forget to Like, Share, Subscribe, Rate, and Review! Keep up with Marianne De Backer; LinkedIn: https://www.linkedin.com/in/marianne-d-de-backer-msc-phd-mba-73403411/ Website: https://www.vir.bio/ Follow IDEA Pharma On; Website: https://www.ideapharma.com/ LinkedIn: https://www.linkedin.com/company/idea-pharma Listen to more fantastic podcast episodes: https://ideacollider.simplecast.com/
What is an EGFR mutation — and could you pass it down to your children? Patient advocate Lysa Buonanno asks the questions every EGFR-positive lung cancer patient wants answered. Dr. Alice Berger, a lung cancer researcher at Fred Hutch Cancer Center, explains how EGFR mutations develop, why they are rarely inherited, and what targeted treatments — including exciting new FDA-approved options — mean for patients today. Whether you are newly diagnosed or supporting a loved one, this conversation will help you understand your biomarker results, know what to ask your doctor, and feel empowered by the science moving forward on your behalf. Topics covered: · What EGFR mutations are and how they develop · Whether EGFR mutations can be passed to children · The role of family history and genetic testing · Risk factors including radon, pollution, and smoking · Targeted therapies like osimertinib (Tagrisso) · New FDA-approved treatments for EGFR exon 20 mutations · Ongoing research into hereditary lung cancer risk Guests: Lysa Buonanno, Patient Advocate Dr. Alice Berger, Associate Professor, Fred Hutch Cancer Center Show Notes - https://lcfamerica.org/wp-content/uploads/2026/04/LCFA-EGFR-Positive-Lung-Cancer-Show-Notes.pdf Transcript - https://lcfamerica.org/wp-content/uploads/2026/04/LCFA-HWA-EGFR-Positive-Lung-Cancer-Transcript.pdf Watch Video - https://youtu.be/izHAxxwZVL4 Subscribe to Hope With Answers: Living With Lung Cancer podcast for future episodes on your favorite listening platform. Join LCFA's social media communities for support and information. Facebook | Twitter | Instagram | YouTube
In this episode of the Oncology Brothers podcast, we kicked off a three-part series on colorectal cancer, starting with the current treatment algorithm. They are joined by Dr. Smitha Krishnamurthi, a GI medical oncologist from the Cleveland Clinic, who walks through the evolving standard of care from early-stage disease all the way to refractory metastatic settings. Listen us on: Spotify: https://open.spotify.com/show/31BXhY9FM4gPWG10WgE11o Apple Podcast: https://podcasts.apple.com/us/podcast/oncology-brothers-practice-changing-cancer-discussions/id1653340966 Follow us on social media: • X/Twitter: https://twitter.com/oncbrothers • Instagram: https://www.instagram.com/oncbrothers • Website: https://oncbrothers.com/ Key topics discussed included: • The evolving role of ctDNA as both a prognostic and predictive tool in stage two and three colon cancer, including its utility in oligometastatic disease surveillance. • Neoadjuvant versus adjuvant immunotherapy in MSI-high resectable colon cancer, comparing the NICHE-2 and ATOMIC trial approaches and when to use each. • Single-agent versus dual checkpoint inhibition with Nivo-Ipi for MSI-high metastatic disease, based on CHECKMATE-8HW data showing a PFS hazard ratio of 0.21. • Sequencing strategies in RAS-mutant and RAS wild-type metastatic colorectal cancer, including the role of sidedness, anti-EGFR therapy, and refractory options like fruquintinib, TAS-102, and regorafenib. Join us for this comprehensive discussion on colorectal cancer management in 2026. Don't forget to like, subscribe, and check out our other episodes for more insights on oncology! #ColorectalCancer, #MSIHigh, #BRAFV600E, #ctDNA, #GIOncology, #OncologyBrothers
Featuring an interview with Dr Natalie Vokes, including the following topics: Perioperative minimal residual disease (MRD) detected by circulating tumor DNA (ctDNA) testing in patients with lung cancer (0:00) Ohara S et al. Clinical significance of perioperative MRD detected by ctDNA in patients with lung cancer with a long follow-up data: An exploratory study. JTO Clin Res Rep 2024;6(3):100762. Abstract Masuda K et al. MRDSEEKER (JCOG2111A): A prospective study to evaluate MRD and its association with prognosis in curative-intent NSCLC. World Conference on Lung Cancer 2025;Abstract P3.18.04. Zhou C et al. IMpower010: Biomarkers of disease-free survival in a phase 3 study of atezolizumab vs best supportive care after adjuvant chemotherapy in stage IB-IIIA NSCLC. ESMO IO 2021;Abstract 2O. MRD analysis of adjuvant therapy with osimertinib for resected EGFR-mutated Stage IB to IIIA non-small cell lung cancer (NSCLC) (8:28) Herbst RS et al. Molecular residual disease analysis of adjuvant osimertinib in resected EGFR-mutated stage IB-IIIA non-small-cell lung cancer. Nat Med 2025;31(6):1958-68. Abstract MRD analyses of perioperative chemoimmunotherapy for resected NSCLC (15:12) Forde PM et al. Overall survival with neoadjuvant nivolumab plus chemotherapy in lung cancer. N Engl J Med 2025;393(8):741-52. Abstract ctDNA dynamics in advanced NSCLC treated with immunotherapy (20:56) Vokes NI et al. Circulating tumor DNA (ctDNA) dynamics and survival outcomes in patients (pts) with advanced non-small cell lung cancer (aNSCLC) and high (>50%) programmed cell death ligand 1 (PD-L1) expression, randomized to cemiplimab (cemi) vs chemotherapy (chemo). ASCO 2023;Abstract 9022. Anagnostou V et al. ctDNA response after pembrolizumab in non-small cell lung cancer: Phase 2 adaptive trial results. Nat Med 2023;29(10):2559-69. Abstract Anagnostou V et al. A biomarker-directed, multi-center phase II/III study of ctDNA molecular response adaptive immuno-chemotherapy in patients with non-small cell lung cancer (BR.36). ASCO 2025;Abstract TPS8669. CME information and select publications
Empower yourself by understanding functional vs. medical blood work. In class 1 of 3, Dr. Vaughn shares how comprehensive, “natural” blood work can reveal early imbalances long before a diagnosis... And how you can partner with God's design to restore your health.You'll learn:✅ What makes functional/comprehensive blood work different from standard labs
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