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Good morning from Pharma Daily: the podcast that brings you the most important developments in the pharmaceutical and biotech world. Let's dive into the latest happenings shaping the landscape of this dynamic industry. The pharmaceutical and biotech sectors are navigating a complex landscape replete with scientific advancements and regulatory challenges. A significant legal development comes from Takeda, which faces an $885 million verdict in a landmark pay-for-delay antitrust case. This ruling highlights the intense scrutiny of pharmaceutical companies over antitrust regulations, with potential implications for drug pricing strategies and industry practices. The possibility of tripling damages under these laws could set a precedent affecting future business operations, as Takeda plans to appeal, underscoring the high stakes involved in such litigation. Meanwhile, on the regulatory front, the White House's decision to include 600 generic medications in the TrumpRx purchasing portal marks a strategic effort to improve drug affordability. While its overall impact remains uncertain, this initiative aims to bridge gaps in medication accessibility for cost-sensitive populations. Similarly, Roche's licensing agreement with the Medicines Patent Pool to allow generic versions of Xofluza in 129 developing countries is a noteworthy step towards enhancing global access to essential medicines. These efforts underscore ongoing attempts to address affordability and accessibility concerns on a global scale. In clinical developments, UCB's Bimzelx has shown promising results against AbbVie's Skyrizi in treating psoriatic arthritis, demonstrating a statistically significant reduction in disease activity compared to Skyrizi in a Phase 3b trial. With nearly half of the patients showing improved outcomes at week 16, Bimzelx is poised to become a competitive therapeutic option, potentially redefining treatment protocols for psoriatic arthritis. Novartis's termination of its contract with Chinese CDMO Porton Pharma Solutions due to regulatory issues underscores the challenges inherent in cross-border pharmaceutical partnerships. The $64 million legal claims looming over this decision highlight the financial and operational risks associated with international collaborations. Meanwhile, biopharmaceutical buyers are increasingly turning to artificial intelligence and local expertise to navigate rising licensing costs in China. Sanofi and Wave Life Sciences are making progress in addressing α1-antitrypsin deficiency (AATD), a genetic disorder that has witnessed limited therapeutic innovation for decades. Their efforts were highlighted at the American Thoracic Society meeting, showcasing ongoing attempts to bridge treatment gaps for rare diseases through next-generation approaches. Strategic investments continue to shape the industry, as evidenced by Lauxera Capital Partners' successful EUR520 million fundraising aimed at advancing healthcare technologies. Additionally, Merck's agreement to supply Keytruda for Exelixis' colorectal cancer trial exemplifies collaborative efforts crucial for advancing cancer research. These developments reflect an industry balancing innovation with regulatory compliance and market dynamics. Scientific progress is also evident in Relay Therapeutics' advancement with its PI3K inhibitor, which has shown promising Phase 2 data in treating blood vessel disorders. This underscores the potential of PI3K inhibitors to address unmet medical needs by targeting pathways significant in cancer and other diseases. The integration of artificial intelligence into drug discovery processes is another critical trend. Incyte's collaboration with Edison Scientific aims to enhance decision-making and streamline drug discovery, showcasing AI's potential to revolutionize R&D efficiency. However, persistent challenges remain as AI scales up but doesn't yet resolve clinical trial protocol issues fully. On the business front, Bristol Myers Squibb considers investing $1 billion in a Houston manufacturing plant, emphasizing strategic infrastructure investments crucial for meeting growing pharmaceutical demands. In drug approvals, AstraZeneca's Baxfendy has received FDA approval for treating uncontrolled hypertension by targeting aldosterone synthesis—offering a novel approach as a combination therapy. Moreover, Merck & Co.'s sacituzumab tirumotecan has achieved Phase 3 success in endometrial cancer trials, demonstrating superior survival outcomes compared to chemotherapy. This highlights the growing impact of targeted therapies in oncology and the ongoing shift towards precision medicine. Despite these positive developments, challenges persist. BioMarin Pharmaceutical's BMN 401 faced setbacks after missing key Phase 3 endpoints for skeletal healing in ENPP1 deficiency patients—highlighting complexities in rare disease drug development. In conclusion, these diverse developments reflect an industry steadfastly committed to advancing healthcare through scientific innovation while navigating regulatory hurdles and operational challenges. As these sectors evolve further, maintaining a balance between rapid innovation and rigorous oversight remains essential to ensuring impactful treatments reach patients worldwide promptly. Thank you for tuning in to Pharma Daily—stay informed and stay ahead of industry trends with us tomorrow!Support the show
Host: Charles Turck, PharmD, BCPS, BCCCP Guest: Sarah Sammons, MD Despite advances in the treatment of HR-positive HER2-negative advanced breast cancer, patients with PIK3CA-mutated disease who progress after a CDK4/6 inhibitor still face limited effective and tolerable treatment options.1 This unmet need has fueled interest in zovegalisib (formerly RLY-2608), a next generation, pan-mutant-selective PI3Kα inhibitor designed to spare wild-type protein and potentially reduce class-related toxicities.2 Dr. Sarah Sammons joins Dr. Charles Turck to review key findings from the first-in-human ReDiscover trial of zovegalisib + fulvestrant that supported initiation of the Phase 3 ReDiscover-2 study3,4, which is currently enrolling. They also discuss ReDiscover-2 eligibility criteria, along with patient selection and screening considerations, using hypothetical case scenarios. Dr. Sammons is the Associate Director of the Metastatic Breast Cancer Program at the Dana-Farber Cancer Institute in Boston, Massachusetts. References: Mishra R, Patel H, Alanazi S, Kilroy MK, Garrett JT. PI3K inhibitors in cancer: clinical implications and adverse effects. Int J Mol Sci. 2021;22(7)doi:10.3390/ijms22073464 Varkaris A, Pazolli E, Gunaydin H, et al. Discovery and clinical proof-of-concept of RLY-2608, a first-in-class mutant-selective allosteric PI3Kα inhibitor that decouples antitumor activity from hyperinsulinemia. Cancer Discovery. 2024;14(2):240–257. doi:10.1158/2159-8290.cd-23-0944 ClinicalTrials.gov. NCT06982521. Accessed April 12, 2026. https://clinicaltrials.gov/study/NCT06982521 Rugo HS, Saura C, Jhaveri K, et al. Poster PS5-08-25: …
Host: Charles Turck, PharmD, BCPS, BCCCP Guest: Sarah Sammons, MD Despite advances in the treatment of HR-positive HER2-negative advanced breast cancer, patients with PIK3CA-mutated disease who progress after a CDK4/6 inhibitor still face limited effective and tolerable treatment options.1 This unmet need has fueled interest in zovegalisib (formerly RLY-2608), a next generation, pan-mutant-selective PI3Kα inhibitor designed to spare wild-type protein and potentially reduce class-related toxicities.2 Dr. Sarah Sammons joins Dr. Charles Turck to review key findings from the first-in-human ReDiscover trial of zovegalisib + fulvestrant that supported initiation of the Phase 3 ReDiscover-2 study3,4, which is currently enrolling. They also discuss ReDiscover-2 eligibility criteria, along with patient selection and screening considerations, using hypothetical case scenarios. Dr. Sammons is the Associate Director of the Metastatic Breast Cancer Program at the Dana-Farber Cancer Institute in Boston, Massachusetts. References: Mishra R, Patel H, Alanazi S, Kilroy MK, Garrett JT. PI3K inhibitors in cancer: clinical implications and adverse effects. Int J Mol Sci. 2021;22(7)doi:10.3390/ijms22073464 Varkaris A, Pazolli E, Gunaydin H, et al. Discovery and clinical proof-of-concept of RLY-2608, a first-in-class mutant-selective allosteric PI3Kα inhibitor that decouples antitumor activity from hyperinsulinemia. Cancer Discovery. 2024;14(2):240–257. doi:10.1158/2159-8290.cd-23-0944 ClinicalTrials.gov. NCT06982521. Accessed April 12, 2026. https://clinicaltrials.gov/study/NCT06982521 Rugo HS, Saura C, Jhaveri K, et al. Poster PS5-08-25: …
Go to my sponsor https://trylco.com/liveleanaging and use code liveleanaging to get 20% off select tests, including the Healthy Aging Test. Disclaimer: When my dad was diagnosed with cancer, I did what I always do, I went deep into the research to learn what I could do to lower my own risk. This video is the result of that. I'm not a doctor and this is not medical advice, but I believe this information is too important not to share. Always work with your healthcare provider. ► Free 7 Day Trial To My Workout App: https://www.liveleantv.com ► Live Lean Body Quiz: https://www.liveleantv.com/quiz ► Free 7 Day Meal Plan And Recipes: https://www.liveleantv.com/free-stuff When most men think about cancer risk, they think genetics and bad luck. But there's a metabolic side to cancer risk that almost nobody talks about, and it's largely within your control. In this video, I break down exactly how excess body fat, high insulin levels, and chronic inflammation are quietly fueling cancer risk for millions of men, and what you can actually do about it. ⏱ TIMESTAMPS 00:00 Intro 00:48 Obesity Significantly Increases Your Risk For Certain Cancers 01:38 Diabetes Significantly Increases Your Risk For Certain Cancers 02:38 How Excessive Insulin Feeds Cancer Growth 03:27 How Belly Fat Is Fueling Cancer Risk 06:34 The Cancer Risks You Can Control 07:23 The Diet That Starves Cancer Risk 08:40 Here's Your Anti-Cancer Action Plan
Metastatic Colorectal Cancer has a dearth of targetable mutations that have effective outcomes. This week, Michael and Josh see whether the wonder drug (trastruzumab deruxtecan) works in HER2-expressing colorectal cancer. Michael takes a more positive tone, with the recycling of aspirin to reduce recurrence risk for PI3K pathway cancers.Josh promised he will have the right audio this episode - thanks to our astute listener who told us last time!Studies discussed in this episode:ALASCCADestiny-CRC01For 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 a slide presentation and related discussion from Dr Seth Wander, including the following topics: Biological impact of clinically relevant biomarkers (eg, ESR1 mutations, PIK3CA/AKT1/PTEN alterations) (0:00) Methodologies for biomarker assessment in clinical practice: Tissue versus liquid biopsy (5:21) Methodologies for biomarker assessment in clinical practice: Novel platforms (13:56) Appropriate timing for assessment of ESR1 and PI3K pathway alterations (17:34) Evolving guidelines for routine biomarker evaluation (21:37) Implications of precision oncology clinical trials for future biomarker utility (25:07) Summary, key questions, future directions (33:09) CME information and select publications
Podcast with global experts discussing the role of AKT and PI3K inhibitors in patients with resistance to endocrine therapy in the adjuvant or metastatic disease settings following current guidelines, indications, and best clinical practices. Presenters: Nadia Harbeck, MD Breast Cancer Director Department of OB&GYN and Comprehensive Cancer Center Munich LMU University Hospital Munich, Germany Francois-Clement Bidard, MD, PhD Breast Medical Oncology Institut Curie & University of Versailles Paris, France Link to full program:https://bit.ly/4cFd0Xj Get access to all 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.
HelixTalk - Rosalind Franklin University's College of Pharmacy Podcast
In this episode, we discuss the most important annual updates in the American Diabetes Association Guidelines, Standards of Care 2026, particularly focusing on changes in pharmacotherapy recommendations and the supporting evidence. Key Concepts A few existing agents now have ASCVD risk reduction data in patients with existing ASCVD or high indicators for ASCVD. They are: oral semaglutide and tirzepatide. SGLT2is are still first-line in patients with diabetes and HF including HFpEF, but SC semaglutide and tirzepatide are now recommended for those with symptomatic HFpEF and obesity due to positive outcomes in this population. The GLP-1RA and dual GLP-1/GIP RA are the preferred agents for weight management in patients with T2DM, but use of GLP-1RA can be considered for weight loss in patients with T1DM. The guideline also better defines recommendations for medication-induced hyperglycemia from immune checkpoint inhibitors, PI3Kɑ (phosphoinositidylinositol 3-kinase α) inhibitors, mTOR inhibitors, and steroids. References American Diabetes Association. Standards of care in diabetes—2026. Diabetes Care. 2026;49(suppl 1):S1-S377. SOUL study. Darren K. McGuire, Marx N, Mulvagh SL, et al. Oral semaglutide and cardiovascular outcomes in high-risk type 2 diabetes. N Engl J Med. 2025;392(20):2001-2012. doi:10.1056/NEJMoa2501006. SURPASS-CVOT. Nicholls SJ, Pavo I, Bhatt DL, et al. Cardiovascular outcomes with tirzepatide versus dulaglutide in type 2 diabetes. N Engl J Med. 2025;393(24):2409-2420. doi:10.1056/NEJMoa2505928. SUMMIT. Packer M, Zile MR, Kramer CM, et al. Tirzepatide for heart failure with preserved ejection fraction and obesity. N Engl J Med. 2025;392(5):427-437. doi:10.1056/NEJMoa2410027. STEP-HFpEF. Kosiborod MN, Abildstrom 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. STEP-HFpEF DM. Kosiborod MN, Petrie MC, Borlaug BA, et al. Semaglutide in patients with obesity‑related heart failure and type 2 diabetes. N Engl J Med. 2024;390(15):1394‑1407. doi:10.1056/NEJMoa2313917.
After 20 years of platform building and resets, Arrowhead Pharmaceuticals is making a bid to become a large-cap biotech. On the latest BioCentury This Week podcast, BioCentury's analysts discuss how the company has built a pipeline and set of enabling technologies that could enable a steep period of value creation based on RNAi.The team then analyzes the $2 billion deal between Synnovation and Novartis for a pan-mutant-selective PI3Kα inhibitor. The analysts also assess where AI is integrating into the biotech venture funnel and provide insights into ultra-rare disease advocacy, FDA's search for a successor to CBER Director Vinay Prasad, and the Trump administration's most-favored nation (MFN) drug pricing policy.View full story: https://www.biocentury.com/article/658892#RNAiTherapeutics #BiotechMA #PI3KAlpha #AIDrugDiscovery #DrugPricingPolicy00:00 - Introduction01:14 - Bio€quity Europe05:33 - Arrowhead16:49 - Synnovation Novartis20:00 - AI in Biotech Venture27:07 - Rare Disease Advocacy31:22 - MFN Pricing PolicyTo submit a question to BioCentury's editors, email the BioCentury This Week team at podcasts@biocentury.com.Reach us by sending a text
Good morning from Pharma Daily: the podcast that brings you the most important developments in the pharmaceutical and biotech world. Today, we delve into a series of transformative events that are shaping the industry and its trajectory.Novo Nordisk's Wegovy HD has successfully navigated the FDA's National Priority Voucher Program, strengthening its foothold in the obesity treatment market. This achievement follows the earlier success of its GLP-1 drug, Wegovy. As obesity rates rise globally, this approval underscores the vital role of innovative weight management therapies. It positions Novo Nordisk to better compete in this increasingly crowded field. In India, the expiration of patents for Novo Nordisk's semaglutide-based drugs paves the way for over 40 companies to introduce affordable generics of Ozempic and Wegovy. This is likely to reshape pricing dynamics and improve accessibility in diabetes and obesity management. Further highlighting the focus on obesity treatments, Rhythm Pharmaceuticals' Imcivree has received FDA approval for acquired hypothalamic obesity. This is significant as it addresses an unmet need for patients with brain-damage-related obesity, showcasing the potential of targeted therapies for complex neurological conditions.In other developments, CSL Behring has raised concerns about potential supply issues for Hemgenix, its gene therapy for hemophilia. As a one-time treatment option, Hemgenix represents a significant breakthrough; thus, ensuring a steady supply is essential to maintain patient trust and therapeutic efficacy.Turning to oncology, Novartis has made a strategic move with a $2 billion acquisition of Synnovation Therapeutics' pan-mutant-selective PI3Kα inhibitor program. This acquisition bolsters Novartis' breast cancer portfolio and provides a competitive edge against rivals like Eli Lilly. Such strategic acquisitions highlight efforts by major pharmaceutical companies to enhance their pipelines amidst intensifying competition.AstraZeneca's commitment to expanding its presence in China is evident with its investment in a cell therapy manufacturing hub and R&D center in Shanghai. This move aligns with their broader $15 billion investment strategy in China, reflecting the growing importance of cell therapies and the strategic role of the Chinese market in global biopharmaceutical innovation. Strategic investments continue transforming industry landscapes, with increased demand for cell therapies within oncology sectors.On another front, Verily is making strides with a $300 million fundraising round aimed at boosting its AI initiatives within precision health. This underscores a broader industry trend towards integrating AI technologies into drug development processes—a transition poised to enhance therapeutic outcomes through data-driven approaches. Additionally, Fauna Bio and Eli Lilly's collaboration using AI for obesity research exemplifies how technology accelerates innovation in complex conditions like obesity.Pfizer is streamlining its R&D focus by discontinuing an early-phase antibody-drug conjugate targeting solid tumors. This decision fits into Pfizer's strategy to allocate resources towards projects with higher clinical and commercial potential. In clinical trials, Pfizer's Talzenna combined with Xtandi shows promise for metastatic castration-sensitive prostate cancer—demonstrating the potential of PARP inhibitors in enhancing therapeutic efficacy.Regulatory landscapes are also evolving, as seen with China's approval of its first commercial brain-computer interface—a groundbreaking advancement offering new possibilities for treating neurological disorders. Regulatory advancements also make headlines as GSK's Lynavoy receives FDA approval for treating cholestatic pruritus in primary biliary cholangitis patients.In governance-related news, recent confusion surrounding the CDC's vaccine advisory panel highlights Support the show
In today's episode, Neil Iyengar, MD, moderated an OncLive Insights discussion about adverse effect management when using breast cancer therapies targeting the PI3K, AKT, and mTOR pathways. Dr Iyengar is an associate professor in the Department of Hematology and Medical Oncology and co-director of Breast Medical Oncology in the Department of Hematology and Medical Oncology at Emory University School of Medicine; as well as director of Survivorship Services at the Winship Cancer Institute of Emory University in Atlanta, Georgia. He was joined by Heather Moore, CPP, PharmD, a clinical pharmacist practitioner at the Duke Cancer Center Breast Clinic in Durham, North Carolina; and Sarah Donahue, MPH, NP, a nurse practitioner at the University of California San Francisco Health. In our exclusive discussion, the experts highlighted the importance of early and comprehensive testing (using both tissue and liquid biopsies) for genetic alterations to guide treatment decisions. They also noted strategies for managing diarrhea, including patient education on diet, proactive use of loperamide, and regular monitoring. They also explained that hyperglycemia management should hinge on prophylactic use of metformin or SGLT2 inhibitors, dietary restrictions, and frequent glucose monitoring. Their conversation on rash management included insights about prophylactic antihistamines, patient education on skin care, and involving dermatology for severe cases. Overall, the experts spotlighted the importance of multidisciplinary collaboration and proactive patient education when treating patients with breast cancer.
Welcome to the Oncology Brothers podcast! In this episode, we welcomed Dr. Neil Iyengar and Dr. Emily Gallagher, to dive deep into the world of PIK3CA and AKT pathway inhibitors for hormone receptor-positive (HR+) metastatic breast cancer. We discussed the latest approvals, including Inavolisib, Alpelisib, and Capivasertib, and explored their common side effects such as hyperglycemia, rash, and gastrointestinal issues. Our experts shared practical management strategies, dosing considerations, and the importance of patient education to ensure safe and effective treatment. Key topics covered in this episode: • Overview of PIK3CA and AKT inhibitors • Common side effects and their management • The significance of proactive patient education • Dosing strategies and when to consider dose modifications • Insights on managing hyperglycemia and gastrointestinal symptoms This episode is packed with valuable information to enhance your understanding of these important therapies in the breast cancer world. Don't forget to subscribe for more episodes on treatment algorithms, toxicities, and the latest in oncology! #PI3Kinhibitors #BreastCancer #Hyperglycemia #ToxCheck #MetastaticBC #OncologyBrothers #TargetedTherapy
Featuring an interview from Dr John Strickler, including the following topics: Prognostic value of molecular residual disease (MRD) as detected by circulating tumor DNA (ctDNA) and optimal incorporation of MRD assays into the care of patients with colorectal cancer (0:00) Potential use of MRD assays for patients with microsatellite instability (MSI)-high localized colorectal cancer or those with delayed progression or metastatic disease (16:09) Tumor-informed MRD assays under clinical development (20:36) Predictive role of ctDNA in Stage III colon cancer treated with celecoxib; effect of low-dose aspirin on response to celecoxib in patients with PI3K pathway alterations (24:19) Case: A man in his late 50s with resected Stage IIA colon cancer (30:06) Case: A woman in her late 40s with Lynch syndrome and MSI-H colon cancer with a solitary, small hepatic metastasis (34:57) MRD as a future clinical trial endpoint for solid tumors; increasing incidence of colorectal cancer in younger people (40:24) Antibody-drug conjugates in the treatment of colorectal cancer (45:13) Perspectives on promising areas of clinical research in colorectal cancer (48:23) CME information and select publications
Featuring a slide presentation and related discussion from Dr John Strickler, including the following topics: Defining molecular residual disease (MRD); tumor-informed and tumor-naïve methods for assessing (0:00) GALAXY and BESPOKE CRC studies of a tumor-informed MRD assay to identify patients with localized colorectal cancer who have an increased risk of recurrence and those who are likely to benefit from adjuvant chemotherapy (6:56) Sustained circulating tumor DNA (ctDNA) clearance and disease-free survival outcomes for patients with localized colorectal cancer (13:21) DYNAMIC study of a ctDNA-guided approach to adjuvant chemotherapy for patients with Stage II colorectal cancer (16:17) ctDNA positivity and radiographic evidence of colorectal cancer (18:48) ctDNA-guided approaches to escalating or de-escalating adjuvant chemotherapy for patients with localized colorectal cancer (21:24) Predictive role of ctDNA assay results in Stage III colon cancer treated with celecoxib; low-dose aspirin for patients with Stage II to III colorectal cancer with a PI3K pathway alteration (26:02) CME information and select publications
Host: Charles Turck, PharmD, BCPS, BCCCP Guest: Sarah Sammons, MD About 40 percent of patients with metastatic HR+/HER2- breast cancer have an activating mutation in the PIK3CA gene,1,2 which plays a key role not only in tumor growth, but also in driving resistance to endocrine therapy.3-5 And while there are several FDA-approved PI3K pathway-targeted agents for patients with PIK3CA tumor mutations,6-8 they come with challenges, like modest efficacy and on-pathway effects.9-12 Given this unmet need, the ReDiscover trial evaluated the investigational agent RLY-2608 in combination with fulvestrant in in patients with PIK3CA-mutated HR+/HER2- aBC previously treated with a CDK4/6 inhibitor.13 Joining Dr. Charles Turck to share updated safety and efficacy data from the trial is Dr. Sarah Sammons, a Senior Physician at the Dana-Farber Cancer Institute and an Assistant Professor of Medicine at Harvard Medical School in Boston. References: Vasan N, Cantley LC, Vasan N, Cantley LC. At a crossroads: how to translate the roles of PI3K in oncogenic and metabolic signalling into improvements in cancer therapy. Nat Rev Clin Oncol. 2022;19(7):471-485. doi:10.1038/s41571-022-00633-1 Network TCGA. Comprehensive molecular portraits of human breast tumours. Nature. 2012;490(7418):61-70. doi:10.1038/nature11412 Saal LH, Johansson P, Holm K, et al. Poor prognosis in carcinoma is associated with a gene expression signature of aberrant PTEN tumor suppressor …
CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/The-Future-of-PI3K-Inhibition-in-HR-HER2-Breast-Cancer/37339/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.
CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/The-Future-of-PI3K-Inhibition-in-HR-HER2-Breast-Cancer/37339/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.
CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/PI3K-Pathway-Inhibitors-Safety-and-Tolerability-Profiles/37338/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.
CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/Case-in-Point-Applying-PI3K-Combinations-in-Early-Recurrent-HR-HER2-mBC/37336/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.
CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/Triple-Threat-Key-Data-on-Simultaneous-Estrogen-CDK4-6-and-PI3K-Inhibition-in-mBC/37335/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.
CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/Double-Take-Pivotal-Data-Evaluating-PI3K-Inhibitor-Endocrine-Therapy-Regimens-in-mBC/37333/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.
CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/Comprehensive-Biomarker-Testing-in-mBC-Informs-Clinical-Decision-Making/37332/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.
CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/PI3K-Pathway-inhibition-in-HR-HER2-mBC-Mechanistic-Insights/37329/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.
CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/Understanding-Endocrine-Resistance-in-HR-HER2-mBC/37323/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.
CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/PI3K-Pathway-Inhibitors-Safety-and-Tolerability-Profiles/37338/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.
CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/Case-in-Point-Applying-PI3K-Combinations-in-Early-Recurrent-HR-HER2-mBC/37336/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.
CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/Triple-Threat-Key-Data-on-Simultaneous-Estrogen-CDK4-6-and-PI3K-Inhibition-in-mBC/37335/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.
CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/Double-Take-Pivotal-Data-Evaluating-PI3K-Inhibitor-Endocrine-Therapy-Regimens-in-mBC/37333/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.
CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/Comprehensive-Biomarker-Testing-in-mBC-Informs-Clinical-Decision-Making/37332/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.
CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/PI3K-Pathway-inhibition-in-HR-HER2-mBC-Mechanistic-Insights/37329/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.
CME credits: 0.75 Valid until: 07-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/Understanding-Endocrine-Resistance-in-HR-HER2-mBC/37323/ The PI3K-AKT-mTOR pathway is a crucial signaling network dysregulated in many cancers, promoting cell survival, growth, and proliferation, and often implicated in resistance to cancer therapies. Inhibition of this pathway by PI3K inhibitors disrupts a complex network of cellular processes that contribute to breast cancer, markedly reducing cell proliferation, promoting apoptosis, inhibiting angiogenesis, and ultimately preventing tumor formation and progression. In hormone receptor–positive (HR+), activating PIK3CA mutations occur in approximately 35% to 40% of patients and a variable prevalence across BC subtypes. Testing is thus crucial to ensure appropriate treatment selection. The development of PI3K-targeted agents may revolutionize the treatment landscape for HR+, HER2- metastatic breast cancer (mBC, and due to the recent approval of inavolisib, clinicians must be apprised of both the clinical evidence and best practices regarding the use of this agent. This activity has been designed to review the role of the PI3K-AKT-mTOR pathway in breast cancer, the importance of testing when making clinical decisions, and the role of PI3K-targeted therapies in HR+, HER- mBC.
Featuring articles on PI3K-altered colorectal cancer, type 2 diabetes, oral semaglutide, and proportional-assist ventilation; a review article on tumor lysis syndrome; a case report of a girl with chest pain and bone and liver lesions; and Perspectives on integrating pharmacotherapy into tobacco control, on Medicaid enrollees with chronic conditions, and on ultraprocessed food.
Featuring perspectives from Dr Ana C Garrido-Castro and Prof Peter Schmid, including the following topics: Introduction: Legendary Figures in Breast Cancer Research (0:00) Case: A woman in her early 80s, a current smoker with a history of myocardial infarction and stroke, who develops recurrent triple-negative breast cancer (TNBC) — Justin Favaro, MD, PhD (6:44) Case: A woman in her late 60s with metastatic TNBC and a PD-L1 level of 20% who receives chemotherapy/pembrolizumab followed by sacituzumab govitecan — Priya Rudolph, MD, PhD (25:08) Case: A woman in her late 60s with localized TNBC who develops myocarditis while receiving neoadjuvant chemotherapy/pembrolizumab — Richard Zelkowitz, MD (33:53) Case: A woman in her mid 60s with recurrent ER-negative, HER2-low, PI3K-mutant TNBC — Ranju Gupta, MD (37:49) Case: A woman in her early 60s with recurrent TNBC confined to contralateral neck nodes — Eric H Lee, MD, PhD (42:10) Case: A woman in her early 40s with metastatic TNBC who receives sacituzumab govitecan after multiple lines of chemotherapy — Estelamari Rodriguez, MD, MPH (48:10) Case: A woman in her mid 70s with ER-negative, HER2-low breast cancer who develops an isolated brain metastasis — Dr Gupta (55:02) CME information and select publications
Host: Charles Turck, PharmD, BCPS, BCCCP Guest: Hope S. Rugo, MD, FASCO Not only is PI3Kα the most common mutation seen in patients with HR+/HER2- advanced breast cancer, but it's also associated with endocrine therapy resistance and more aggressive cancer growth. Given its prevalence and impact on outcomes, it's important to know how and when to test for this mutation and how emerging targeted therapies might change our approach in clinical practice. Joining Dr. Charles Turck to share her insights on PI3Kα testing and targeted therapies for HR+/HER2- advanced breast cancer is Dr. Hope Rugo, Director of the Women's Cancers Program, Division Chief of Breast Medical Oncology and Professor of the Department of Medical Oncology and Therapeutics Research at City of Hope Comprehensive Cancer Center.
Host: Charles Turck, PharmD, BCPS, BCCCP Guest: Neil M. Iyengar, MD Guest: Komal Jhaveri, MD, FACP The second-line treatment of HR+/HER2-advanced breast cancer has evolved in recent years, particularly with the rise of biomarker-driven strategies targeting PI3Kα and other mutations. But given these advances, there's a lot we need to think about when selecting therapy, like the differences between selective and non-selective inhibitors, toxicity profiles, and shared decision-making. Joining Dr. Charles Turck to share their insights on those key considerations and how we can personalize care for patients with PI3Kα-mutated HR+/HER2- advanced breast cancer are Drs. Komal Jhaveri and Neil Iyengar. Dr. Jhaveri is the section head for the Endocrine Therapy Research Program in the Breast Medicine Service at Memorial Sloan Kettering Cancer Center, and Dr. Iyengar is the Co-Director of the Breast Oncology Program at the Winship Cancer Institute at Emory University.
Host: Charles Turck, PharmD, BCPS, BCCCP Guest: Neil M. Iyengar, MD Due to their wild-type inhibition, first-generation PIK3CA inhibitors for HR+/HER2- advanced breast cancer were limited by significant toxicities, including hyperglycemia, rash, and diarrhea. But now, mutation-specific PIK3CA inhibitors could help improve tolerability and adherence as well as simplify dosing strategies—all while maintaining efficacy. To learn more about the efficacy and safety of current and emerging PIK3CA-targeted therapies, Dr. Charles Turck speaks with Dr. Neil Iyengar, Co-Director of the Breast Oncology Program and Director of Cancer Survivorship Service at Winship Cancer Institute at Emory University.
Host: Charles Turck, PharmD, BCPS, BCCCP Guest: Hope S. Rugo, MD, FASCO Not only is PI3Kα the most common mutation seen in patients with HR+/HER2- advanced breast cancer, but it's also associated with endocrine therapy resistance and more aggressive cancer growth. Given its prevalence and impact on outcomes, it's important to know how and when to test for this mutation and how emerging targeted therapies might change our approach in clinical practice. Joining Dr. Charles Turck to share her insights on PI3Kα testing and targeted therapies for HR+/HER2- advanced breast cancer is Dr. Hope Rugo, Director of the Women's Cancers Program, Division Chief of Breast Medical Oncology and Professor of the Department of Medical Oncology and Therapeutics Research at City of Hope Comprehensive Cancer Center.
Host: Charles Turck, PharmD, BCPS, BCCCP Guest: Neil M. Iyengar, MD Due to their wild-type inhibition, first-generation PIK3CA inhibitors for HR+/HER2- advanced breast cancer were limited by significant toxicities, including hyperglycemia, rash, and diarrhea. But now, mutation-specific PIK3CA inhibitors could help improve tolerability and adherence as well as simplify dosing strategies—all while maintaining efficacy. To learn more about the efficacy and safety of current and emerging PIK3CA-targeted therapies, Dr. Charles Turck speaks with Dr. Neil Iyengar, Co-Director of the Breast Oncology Program and Director of Cancer Survivorship Service at Winship Cancer Institute at Emory University.
Host: Charles Turck, PharmD, BCPS, BCCCP Guest: Neil M. Iyengar, MD Guest: Komal Jhaveri, MD, FACP The second-line treatment of HR+/HER2-advanced breast cancer has evolved in recent years, particularly with the rise of biomarker-driven strategies targeting PI3Kα and other mutations. But given these advances, there's a lot we need to think about when selecting therapy, like the differences between selective and non-selective inhibitors, toxicity profiles, and shared decision-making. Joining Dr. Charles Turck to share their insights on those key considerations and how we can personalize care for patients with PI3Kα-mutated HR+/HER2- advanced breast cancer are Drs. Komal Jhaveri and Neil Iyengar. Dr. Jhaveri is the section head for the Endocrine Therapy Research Program in the Breast Medicine Service at Memorial Sloan Kettering Cancer Center, and Dr. Iyengar is the Co-Director of the Breast Oncology Program at the Winship Cancer Institute at Emory University.
Featuring an interview with Dr Rinath M Jesselsohn, including the following topics: Evaluating first-line treatment of metastatic ER-positive, HER2-positive breast cancer: heredERA Breast Cancer study (0:00) Kuemmel S et al. heredERA Breast Cancer: A phase III, randomized, open-label study evaluating the efficacy and safety of giredestrant plus the fixed-dose combination of pertuzumab and trastuzumab for subcutaneous injection in patients with previously untreated HER2-positive, estrogen receptor-positive locally advanced or metastatic breast cancer. BMC Cancer 2024;24(1):641. Abstract Treatment outcomes with CDK4/6 inhibitors and with elacestrant in real-world studies (4:13) Lloyd MR et al. CDK4/6 inhibitor efficacy in ESR1-mutant metastatic breast cancer. NEJM Evid 2024;3(5). Abstract Lloyd M et al. Impact of prior treatment, ESR1 mutational (ESR1m) landscape, and co-occurring PI3K pathway status on real-world (RW) elacestrant outcomes in patients (pts) with hormone receptor-positive (HR+)/HER2-negative advanced breast cancer (aBC). San Antonio Breast Cancer Symposium 2024;Abstract PS7-05. Evaluating the CNS activity of imlunestrant, an oral selective estrogen receptor degrader (SERD) (8:06) VandeKopple M et al. Preclinical characterization of imlunestrant, an oral brain-penetrant selective estrogen receptor degrader with activity in a brain metastasis (BM) model. ESMO Breast 2023;Abstract 41P. Selective review of trials of oral SERDs in the adjuvant setting (11:27) A study of imlunestrant versus standard endocrine therapy in participants with early breast cancer (EMBER-4). NCT05514054 CME information and select publications
Send us a textWelcome to our Season 10 opening episode! Today we're discussing some of the big updates in metastatic breast cancer research from the 2024 San Antonio Breast Cancer Symposium (SABCS). Joining us today is Dr. Debu Tripathy, breast oncologist at The University of Texas MD Anderson Cancer Center who will break down into understandable terms some of the most impactful findings shared at SABCS, from advances in endocrine therapy and HER2-targeted treatments to exciting developments in PI3K inhibition and nausea control.
In today's episode, supported by Genentech, we had the pleasure of speaking with Komal Jhaveri, MD, FACP, about the clinical use of inavolisib (Itovebi) for patients with hormone receptor (HR)–positive, PIK3CA-mutated, locally advanced or metastatic breast cancer. Dr Jhaveri is section head of the Endocrine Therapy Research Program, clinical director of the Early Drug Development Service, and the Patricia and James Cayne Chair for Junior Faculty at Memorial Sloan Kettering Cancer Center in New York, New York. In our exclusive interview, Dr Jhaveri discussed the importance of having a PI3K inhibitor available for the treatment of patients with HR-positive metastatic breast cancer, advice for managing inavolisib-related adverse effects, and best practices for early biomarker testing in patients with breast cancer.
Welcome to another episode of the Oncology Brothers podcast! In this episode, Drs. Rahul and Rohit Gosain are joined by Dr. Alok Khorana, a GI medical oncologist from the Cleveland Clinic, to discuss the latest highlights from the GI ASCO 2025 conference. We dive into four key studies that are practice-informing and potentially practice-changing: 1. BREAKWATER: We explore the implications of using Encorafenib and Cetuximab in combination with FOLFOX for patients with BRAF V600E mutations, which are associated with poor prognosis. 2. CheckMate-8HW: This study investigates whether dual checkpoint inhibition is more effective than single-agent immunotherapy for MSI-high patients, revealing promising results in progression-free survival. 3. Aspirin in Adjuvant Settings: We discuss the role of low-dose aspirin in reducing recurrence rates for patients with PI3K alterations, highlighting its potential as a practice-changing intervention. 4. STARTER-NET: Finally, we review the findings from the study on Everolimus combined with Lanreotide for neuroendocrine tumors, noting the lack of overall survival benefit. Tune in for an insightful discussion on these important topics in oncology, and learn how these findings could impact treatment strategies in your practice. Don't forget to like, subscribe, and check out our other episodes for more conference highlights and treatment discussions! YouTube: https://youtu.be/YOToz3hKYTg Follow us on social media: • X/Twitter: https://twitter.com/oncbrothers • Instagram: https://www.instagram.com/oncbrothers #OncologyBrothers #GIASCO2025 #ColorectalCancer #Immunotherapy #NeuroendocrineTumors #CancerResearch #Podcast
The J.P. Morgan Healthcare Conference kicked off Monday with a flood of high-value deals, reinvigorating sentiment across the biopharma industry. Johnson & Johnson made the biggest splash, acquiring neurology leader Intra-Cellular Therapies for $14.6 billion, while GSK picked up precision therapy specialist IDRx for $1B upfront and Eli Lilly laid down up to $2.5 billion for Scorpion's PI3Kα inhibitor program. Meanwhile, the immunology and inflammation space continues to fire on all cylinders as Gilead invests up to $1.7 billion for LEO Pharma's preclinical oral small molecule STAT6 program. And those are only the deals accepted by both parties. Prior to the conference, Biogen offered to acquire its struggling neuro partner Sage Therapeutics for around $469M. The proposal follows a catastrophic run for Sage, which has seen its shares fall more than 90% in the past two years. 2024 sales and earnings forecasts have also generated attention this week, with Sarepta reporting that Duchenne muscular dystrophy gene therapy Elevidys beat analysts' expectations in the fourth quarter, and Eli Lilly projecting a full-year revenue miss driven largely by lower-than-expected sales of GLP-1 blockbusters Zepbound and Mounjaro. As expected, obesity has been a hot topic at JPM, with Pfizer CEO Albert Bourla announcing that his company is going “all in” in the space. This follows new FDA guidance revealed last week recommending a minimum weight loss threshold for drug developers. Among the many companies taking notice is newcomer Verdiva Bio, which launched last week with more than $410 million in opening funds. Also debuting last week was Kardigan, which raised $300 million to tackle heart disease. Kadigan joins a resurgent cardiovascular space, where several companies—including those developing gene therapies—are targeting myriad diseases. Finally, BioSpace senior editor Annalee Armstrong caught up with Daphne Zohar, CEO of BioSpace NextGen 2025 company Seaport Therapeutics Daphne Zohar, who offered her thoughts on the current state of the neuropsychiatric space.
Featuring articles on semaglutide in persons with obesity and knee osteoarthritis, the addition of PI3K inhibition in breast cancer, treatments in older patients with myeloma, and total hip replacement for hip osteoarthritis; a review article on lead poisoning; a case report of a man with dyspnea after old myocardial infarction; and Perspectives on large language models and the medical record, on measuring AI against the health care we have, on the failing U.S. health system, and on the contemporary rise of pronatalism.
BUFFALO, NY- October 30, 2024 – A new #research paper was #published in Oncotarget's Volume 15 on October 11, 2024, entitled “Initiation of tumor dormancy by the lymphovascular embolus.” Researchers Yin Ye, Justin Wang, Michael G. Izban, Billy R. Ballard, and Sanford H. Barsky from Meharry Medical College in Nashville, TN, and Scripps Mercy Hospital in San Diego, CA, uncovered critical mechanisms that lead to tumor dormancy in breast cancer. This study sheds light on how certain cancer cells can remain dormant for years before potentially reawakening as metastatic tumors. Using breast cancer patient-derived organoids and tumor samples, the research team discovered that tumor dormancy in breast cancer can be triggered by specific signaling changes within small cell clusters, called tumor emboli, which detach from the primary tumor and travel through the bloodstream. These emboli can remain inactive, sometimes for years, before reawakening in other parts of the body. Key changes include reduced activity of mTOR, a metabolic regulator, and structural shifts in E-cadherin, a molecule involved in cell adhesion. This study also suggests these changes are regulated by the PI3K pathway and occur within the unique three-dimensional structure of tumor spheroids, shedding light on the interactions within dormant cell clusters. As a conclusion, this work not only identifies mTOR and E-cadherin as key components in maintaining dormancy but also offers a promising roadmap for future therapies. By targeting these pathways, there may be potential to keep cancer cells in a dormant state, reducing the risk of late-stage recurrence and improving patient outcomes. DOI - https://doi.org/10.18632/oncotarget.28658 Correspondence to - Sanford H. Barsky - sbarsky@mmc.edu Video short - https://www.youtube.com/watch?v=z6ex7Yl8r5Q Sign up for free Altmetric alerts about this article: https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28658 Subscribe for free publication alerts from Oncotarget: https://www.oncotarget.com/subscribe/ Keywords - cancer, dormancy, lymphovascular embolus, mTOR, E-cadherin proteolysis About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science). To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM
Unlock the hidden truths about sugar's role in cancer as we sit down with chemist Dr. Lewis Cantley, whose work on the PI3K enzyme has revolutionized our understanding of this sweet substance's dark side. Picture a world where sugar isn't just a harmless treat but a trigger for one of today's leading health adversaries. This episode takes you on a journey through Dr. Cantley's personal dietary choices, stemming from his own health experiences, to his groundbreaking research that connects the dots between sugar intake, insulin spikes, and cancer cell proliferation. It's a narrative that not only sheds light on the molecular mechanisms of the Warburg effect but also opens the door to potential dietary interventions in chronic disease management.As we navigate the complexities of insulin resistance and its implications for both diabetes and cancer, we discover the pivotal discoveries in Dr. Cantley's lab. Here, the connection between high insulin levels and cancer risk emerges with startling clarity, as does the life-changing impact of insulin's discovery on diabetes treatment. This episode doesn't just leave you with alarming insights; it arms you with the knowledge needed to challenge dietary norms and embrace a path to longevity through informed nutrition. Join us as we dissect the profound impact of lifestyle choices on cancer risks, and learn how a simple decision at the dinner table could drastically alter your health's trajectory.Florence's courses & coaching programs can be found at:www.FlorenceChristophers.comConnect with Florence on:FACEBOOK | TWITTER | INSTAGRAM | YOUTUBE
In this podcast, our faculty discuss some newer treatment approaches for patients with HR-positive breast cancer including PI3K inhibition, AKT inhibition, and oral selective estrogen receptor down regulators. Visit www.morningcommutepodcast.com/HRPositiveBreast1 to view the activity and CME/CE information, download the transcript, and complete the post-test and evaluation to earn CME/CE credit.
VIDEOS : WES2022 | Yuval Noah Harari and Vanessa Nakate in conversation (3:19) Why Colleges Are Becoming Cults [Full Series] | Dr. Lyell Asher (15:00 to 43:42 Gary Null Speaking Out at the NYS Assembly Hearing (25:00) Astragulus found to inhibit breast cancer cell proliferation Fujian University of Traditional Medicine (China), September 8, 2022 Huang qi (Astragalus) is one of the fundamental herbs in traditional Chinese medicine, with earliest records of its use dating back over 2,000 years ago. Now, a study in BMC Complementary and Alternative Medicine has found that astragulus is also able to prevent the spread of breast cancer cells in the body. In the study, researchers from the Fujian University of Traditional Chinese Medicine in China looked at how astragulus extract can affect breast cancer cells and the process behind this biological effect. They also looked at the primary isoflavones in the extract, as well as its anti-proliferative activity on three breast cancer lines: MCF-7 (ER+), SK-BR-3 (HER2+) and MDA-MB-231 (triple-negative). They did this by exposing these breast cancer cells to the extract for 48 hours. In addition, they examined the effect of astragulus extract on phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathways, a primary intracellular signaling pathway that contributes to cell proliferation, growth, migration, metabolism, and apoptosis. The results of the study showed that the treatment of astragulus exhibited anti-proliferative activity on breast cancer cells. Furthermore, the therapy promoted the death of breast cancer cells. These suggested that it's ability to inhibit breast cancer cell growth was linked to its ability to inhibit PI3K/Akt/mTOR activity. Moreover, the researchers found that the Huang qi extract contains four types of isoflavones, such as campanulin, ononin, calycosin, and formononetin, which contributed to the inhibitory effect of Huang qi extract on breast cancer cells proliferation. Vitamin D supplementation could help critically ill patients University Hospital Würzburg (Germany) September 12 2022. Findings from a review and meta-analysis reported in Critical Care suggest that providing critically ill patients with vitamin D supplements may improve some clinical outcomes, including survival. “Upon ICU admission, the majority of patients have significantly reduced 25-hydroxyvitamin D levels, which remain significantly reduced over the entire ICU length of stay,” Johannes Menger and colleagues wrote. “In these patients, significantly reduced vitamin D (25-hydroxyvitamin D) serum levels are frequent and independently associated with higher incidence and severity of sepsis.” Sixteen randomized, controlled trials that evaluated vitamin D supplementation's association with mortality were identified. Vitamin D supplementation was associated with a 22% lower risk of overall mortality in comparison with a placebo or standard care. Among studies that reported 28-day mortality, vitamin D supplementation was associated with a trend toward lower a lower risk. Receiving vitamin D by injection or intravenously had the strongest effect. Patients who received vitamin D spent an average of 3.13 days less in the ICU and 5 fewer days on a ventilator than those who received a placebo. “The results of this systematic review and meta-analysis suggest that vitamin D supplementation may be associated with reduced overall mortality in critically ill patients,” they concluded. Natural compound could reduce breast cancer risk in some women Luteolin may inhibit growth of human breast cancer cells in postmenopausal women taking hormone replacement therapy University of Missouri-Columbia, September 9, 2022 More than 100 women die from breast cancer every day in the United States. The odds increase in postmenopausal women who have taken a combined estrogen and progestin hormone replacement therapy; these women also have an increased risk of developing progestin-accelerated breast tumors. Now, University of Missouri researchers have found that luteolin, a natural compound found in herbs such as thyme and parsley as well as vegetables such as celery and broccoli, could reduce the cancer risk for women who have taken hormone replacement therapy. “Most older women normally have benign lesions in breast tissue,” Hyder said. “These lesions typically don't form tumors until they receive the ‘trigger'– in this case, progestin–that attracts blood vessels to cells essentially feeding the lesions causing them to expand.” His newest study shows that when the supplement luteolin is administered to human breast cancer cells in the lab, benefits can be observed including the reduction of those vessels “feeding” the cancer cells causing cancer cell death. Hyder's lab has found that as human breast cancer cells develop, they tend to take on stem cell-like properties, which can make them harder to kill. Here, luteolin was used to monitor stem cell-like characteristics of breast cancer cells and his team saw a vast reduction in this phenomenon, further proving that the natural compound exerts its anti-tumor effects in a variety of ways. “We feel that luteolin can be effective when injected directly into the bloodstream, so IV supplements may still be a possibility,” Hyder said. “But, until the supplement is tested for safety and commercialized, which we hope will happen after further testing and clinical trials, women should continue consuming a healthy diet with fresh fruits and vegetables.” CBD shows health benefits in estrogen-deficient mice that model postmenopause Rutgers University, September 14, 2022 A Rutgers study points to cannabidiol (CBD), a major component of hemp and medical marijuana used to treat conditions such as chronic pain, inflammation, migraines, epilepsy, autoimmune diseases, depression, and anxiety, as a possible treatment for postmenopausal women whose ovaries no longer make estrogen. In a study published in Frontiers in Pharmacology, scientists reported that when estrogen-deficient mice were fed CBD, a non-intoxicating compound extracted from hemp, they showed marked improvement in several areas. Their bloodstreams more readily disposed of glucose, and they burned more energy. In addition, their bone density improved, they had less inflammation in gut and bone tissues and they possessed higher levels of beneficial gut bacteria. “This preclinical study is the first to suggest the therapeutic potential of CBD for alleviating symptoms of estrogen deficiency,” said Diana Roopchand, an assistant professor in the Department of Food Science of the Rutgers School of Environmental and Biological Sciences (SEBS) and senior author on the study. “There is much anecdotal evidence of CBD's health benefits for menopausal and postmenopausal women, but our study is the first to investigate some of the claims in an established preclinical model of postmenopause.” Over 18 weeks, researchers fed the estrogen-deficient mice a steady diet of either tiny, CBD-laced peanut butter balls or peanut butter balls without CBD. The untreated estrogen-deficient mice developed symptoms that resembled those of postmenopausal human females, such as metabolic dysfunction, evidence of inflammation, lower bone density, and lower levels of beneficial gut bacteria. However, in mice that ingested CBD, these conditions were significantly improved. Mediterranean diet and depression among older individuals Harokopio University (Greece), September 9, 2022 According to news originating from Athens, Greece,research stated, “In Europe, depression is one of the most frequent mental disorders across all age groups, but particularly in people aged 65 years and over, and higher depressive symptoms have been reported among individuals with chronic diseases (e.g., diabetes and heart disease).” Research from Harokopio University stated, “To evaluate the role of adherence to the Mediterranean diet (MedDiet) in depression in a sample of older people living in the Mediterranean basin. Standard procedures were used to determine socio-demographic, lifestyle, and clinical characteristics of the participants, as well as their dietary habits, and depressive symptoms were evaluated using the Geriatric Depression Scale (GDS). Participants classified as having mild or severe depression were less educated and physically active, and more diabetic, and they reported less adherence to the MedDiet. Adherence to the MedDiet was associated with the absence of depression [(OR, 95% CI): 0.65, 0.50 – 0.85]. In addition, daily tea drinking was also related to the absence of depression [(OR, 95% CI): 0.51, 0.40 – 0.65].” According to the news editors, the research concluded: “Greater adherence to the MedDiet and daily tea drinking seem to have a beneficial effect on depressive symptoms in older adults.” High cholesterol leads to long-term liver scarring and immune cell dysfunction in lab study University of Southern California, September 15, 2022 There's a long-established link between a high-fat, high-sugar diet and fatty liver disease, which can lead to life-threatening conditions such as cirrhosis and liver cancer. Now, new research from the Keck School of Medicine of USC adds some detail and dimension to this picture. The lab study, published in Frontiers in Immunology, is the first-ever to focus on how different amounts of cholesterol as part of a diet high in fat and sugar affect fatty liver disease progression. Modeling the disease in mice, the investigators demonstrated that high cholesterol intake can make fatty liver disease worse—driving inflammation and scarring—and that, importantly, scar tissuecan persist even after switching to a diet low in cholesterol. The findings also indicated that a high-cholesterol diet can create long-lasting dysfunction in a specific population of immune cells previously shown to play a role in fatty liver disease. “We saw that you may have a high-fat and high-sugar diet, but when you add high cholesterol to that, it will accelerate the process that causes inflammation in your liver,” said corresponding author Ana Maretti-Mira, Ph.D., an assistant research professor of medicine at USC. “People focus on high cholesterol as a risk for heart disease, but we showed that your liver may also be affected, causing inflammation, scarring and, potentially, cirrhosis.” High cholesterol makes fatty liver disease worse The researchers fed mice a high-fat, high-sugar diet shown to cause a form of advanced fatty liver disease similar to human illness. The mice were split into three groups that received different amounts of cholesterol in their food for 20 weeks—midlife for the animals. The low-cholesterol group received one-quarter the cholesterol compared to medium; the high-cholesterol group received 25 times more than the low-cholesterol group. After 20 weeks, the livers of mice from all three groups showed accumulation of fat, a benign feature of fatty liver disease, but the high-cholesterol group had more advanced disease, with increased inflammation and scar tissue. For the following 10 weeks, mice from all three groups received low cholesterol as part of a diet that remained high in fat and sugar. At the end of that time, that change in diet had reversed inflammation in the original high-cholesterol mice, but had not reduced scar tissue. This finding shows that damage caused by high cholesterol can be hard to undo. The high-fat, high-sugar diet given to mice in the study has unfortunate similarities to the typical Western diet in humans. “Our daily diet has lots of carbohydrates, such as sugary drinks, bread, rice and pasta,” Maretti-Mira said. “Then there's high fat, since everybody likes deep fried foods. At the same time, we don't have the same active life we used to, so we end up eating much more than our body needs.”