Podcasts about inhibition

Intravenous dihydropyridine calcium channel blockers can quietly worsen oxygenation by blunting hypoxic pulmonary vasoconstriction. In this episode, we break down the bedside mechanism, which agents are implicated, who's at highest risk (post-op atelectasis, obesity, pneumonia, focal ARDS, COPD), how soon it happens, and exactly what to do.The Vasopressor & Inotrope HandbookAmazon: ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠https://amzn.to/47qJZe1⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ (Affiliate Link)My Store: ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠https://eddyjoemd.myshopify.com/products/the-vasopressor-inotrope-handbook⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ (Use "podcast" to save 10%)Citations:Weir EK, López-Barneo J, Buckler KJ, Archer SL. Acute oxygen-sensing mechanisms. N Engl J Med. 2005 Nov 10;353(19):2042-55. doi: 10.1056/NEJMra050002. PMID: 16282179; PMCID: PMC2803102.Weir EK, Olschewski A. Role of ion channels in acute and chronic responses of the pulmonary vasculature to hypoxia. Cardiovasc Res. 2006 Sep 1;71(4):630-41. doi: 10.1016/j.cardiores.2006.04.014. Epub 2006 Apr 27. PMID: 16828723.Lumb AB, Slinger P. Hypoxic pulmonary vasoconstriction: physiology and anesthetic implications. Anesthesiology. 2015 Apr;122(4):932-46. doi: 10.1097/ALN.0000000000000569. PMID: 25587641.Timour G, Fréderic V, Olivier S, Shango DN. Nicardipine-induced acute respiratory failure: Case report and literature review. Clin Case Rep. 2023 May 1;11(5):e7186. doi: 10.1002/ccr3.7186. PMID: 37143457; PMCID: PMC10151601.McMurtry IF, Davidson AB, Reeves JT, Grover RF. Inhibition of hypoxic pulmonary vasoconstriction by calcium antagonists in isolated rat lungs. Circ Res. 1976 Feb;38(2):99-104. doi: 10.1161/01.RES.38.2.99. PMID: 1245025.Simonneau G, Escourrou P, Duroux P, Lockhart A. Inhibition of hypoxic pulmonary vasoconstriction by nifedipine. N Engl J Med. 1981 Jun 25;304(26):1582-5. doi: 10.1056/NEJM198106253042606. PMID: 7231503.Kennedy T, Summer W. Inhibition of hypoxic pulmonary vasoconstriction by nifedipine. Am J Cardiol. 1982 Oct;50(4):864-8. doi: 10.1016/0002-9149(82)91246-2. PMID: 7124646.Chrétien B, Decros JB, Suard F, Dolladille C, Fischer MO, Alexandre J, Descamps R. Hypoxia Associated With Dihydropyridine Calcium Channel Inhibitors: A Pharmacovigilance Study in VigiBase. Clin Pharmacol Ther. 2023 Sep;114(3):686-692. doi: 10.1002/cpt.2970. Epub 2023 Jun 29. PMID: 37309986.Burghuber OC. Nifedipine attenuates acute hypoxic pulmonary vasoconstriction in patients with chronic obstructive pulmonary disease. Respiration. 1987;52(2):86-93. doi: 10.1159/000195309. PMID: 3671896.Suard F, Mombrun M, Fischer MO, Hanouz JL, Decros JB, Derville S, Gakuba C, Al Issa G, Menard C, Chretien B, Descamps R. Oxygenation Effects of Antihypertensive Agents in Intensive Care: A Prospective Comparative Study of Nicardipine and Urapidil. Clin Pharmacol Ther. 2025 Mar;117(3):742-748. doi: 10.1002/cpt.3509. Epub 2024 Nov 27. PMID: 39604146.

In today's episode, we had the pleasure of speaking with Kevin Kalinsky, MD, MS, FASCO, about the evolving treatment paradigm for hormone receptor (HR)–positive breast cancer post-CDK4/6 inhibition, as well as the need for more advanced therapies to improve patient outcomes in this setting. Dr Kalinsky is a professor and director in the Division of Medical Oncology of the Department of Hematology and Medical Oncology at Emory University School of Medicine, as well as the director of the Glenn Family Breast Center and the Louisa and Rand Glenn Family Chair in Breast Cancer Research at Winship Cancer Institute in Atlanta, Georgia. In our exclusive interview, Dr Kalinsky discussed combination therapies that have shown promise for the management of HR-positive breast cancer following endocrine therapy, factors influencing treatment selection for patients who have received prior CDK4/6 inhibition, best practices for genomic testing in this population, and breast cancer research highlights from the 2025 ESMO Congress.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/NCPD/AAPA/IPCE information, and to apply for credit, please visit us at PeerView.com/SMF865. CME/MOC/NCPD/AAPA/IPCE credit will be available until October 7, 2026.Elevating Psoriasis and Comorbidity Management With TYK2 Inhibition: Achieving and Sustaining Outcomes to Transform Care In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported through an educational grant from Bristol Myers Squibb.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/NCPD/AAPA/IPCE information, and to apply for credit, please visit us at PeerView.com/SMF865. CME/MOC/NCPD/AAPA/IPCE credit will be available until October 7, 2026.Elevating Psoriasis and Comorbidity Management With TYK2 Inhibition: Achieving and Sustaining Outcomes to Transform Care In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported through an educational grant from Bristol Myers Squibb.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/NCPD/AAPA/IPCE information, and to apply for credit, please visit us at PeerView.com/SMF865. CME/MOC/NCPD/AAPA/IPCE credit will be available until October 7, 2026.Elevating Psoriasis and Comorbidity Management With TYK2 Inhibition: Achieving and Sustaining Outcomes to Transform Care In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported through an educational grant from Bristol Myers Squibb.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/NCPD/AAPA/IPCE information, and to apply for credit, please visit us at PeerView.com/SMF865. CME/MOC/NCPD/AAPA/IPCE credit will be available until October 7, 2026.Elevating Psoriasis and Comorbidity Management With TYK2 Inhibition: Achieving and Sustaining Outcomes to Transform Care In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported through an educational grant from Bristol Myers Squibb.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/NCPD/AAPA/IPCE information, and to apply for credit, please visit us at PeerView.com/SMF865. CME/MOC/NCPD/AAPA/IPCE credit will be available until October 7, 2026.Elevating Psoriasis and Comorbidity Management With TYK2 Inhibition: Achieving and Sustaining Outcomes to Transform Care In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported through an educational grant from Bristol Myers Squibb.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/NCPD/AAPA/IPCE information, and to apply for credit, please visit us at PeerView.com/SMF865. CME/MOC/NCPD/AAPA/IPCE credit will be available until October 7, 2026.Elevating Psoriasis and Comorbidity Management With TYK2 Inhibition: Achieving and Sustaining Outcomes to Transform Care In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported through an educational grant from Bristol Myers Squibb.Disclosure information is available at the beginning of the video presentation.

Brad McGregor joins us on the heels of his #ESMO25 discussion of these important data in the NMIBC landscape.

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-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/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/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/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/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/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/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/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/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.

In today's episode, we had the pleasure of speaking with Asad Dean, MD, about treatment selection for patients with chronic lymphocytic leukemia (CLL) in the second-line setting. Dr Dean is a physician at the Texas Oncology-Fort Worth Cancer Center. In our exclusive interview, Dr Dean discussed the roles of covalent BTK inhibitors and BCL-2 inhibitors in the management of CLL. He highlighted the importance of molecular profiling for treatment rechallenge decisions and the potential for resistance mutations in this disease. He also noted the role of pirtobrutinib (Jaypirca) in overcoming treatment resistance, along with clinical signs indicating that patients may need a therapy change. Dr Dean also mentioned the high response rates seen with CAR T-cell therapy in patients with CLL and explained the possibility for combination regimens in CLL. Additionally, he expressed optimism about BTK degraders and bispecific antibodies.

Darshan H. Brahmbhatt, Podcast Editor of JACC: Advances, discusses a recently published original research paper on IL-1 Pathway Inhibition in Recurrent Pericarditis Management: Real-World Adoption of Corticosteroid Sparing in RESONANCE.

Richard A. Lewis, MD - Navigating the Evolving CIDP Treatment Landscape: Expert Perspectives on the Therapeutic Potential of Complement Inhibition

Richard A. Lewis, MD - Navigating the Evolving CIDP Treatment Landscape: Expert Perspectives on the Therapeutic Potential of Complement Inhibition

Richard A. Lewis, MD - Navigating the Evolving CIDP Treatment Landscape: Expert Perspectives on the Therapeutic Potential of Complement Inhibition

Richard A. Lewis, MD - Navigating the Evolving CIDP Treatment Landscape: Expert Perspectives on the Therapeutic Potential of Complement Inhibition

Interview with Ehsan Rahimy, MD, author of Mammalian Target Rapamycin Inhibition as a Therapeutic Target for Prevention of Proliferative Vitreoretinopathy. Hosted by Neil Bressler, MD. Related Content: Mammalian Target Rapamycin Inhibition as a Therapeutic Target for Prevention of Proliferative Vitreoretinopathy

Interview with Ehsan Rahimy, MD, author of Mammalian Target Rapamycin Inhibition as a Therapeutic Target for Prevention of Proliferative Vitreoretinopathy. Hosted by Neil Bressler, MD. Related Content: Mammalian Target Rapamycin Inhibition as a Therapeutic Target for Prevention of Proliferative Vitreoretinopathy

In today's OncClub episode, we had the pleasure of speaking with Shailee S. Shah, MD, about a retrospective study she and colleagues conducted to understand the effect of immune checkpoint inhibitors on patients with cancer and pre-existing neurologic autoimmune diseases, including multiple sclerosis, myasthenia gravis, Guillain-Barre syndrome, and Parkinson's disease. Dr Shah is a clinical assistant professor of neurology (MS/neuroimmunology) at the Northwestern University Feinberg School of Medicine in Chicago, Illinois.  In our exclusive interview, Dr Shah discussed the design of this study, key findings, and how these results emphasize the need for multidisciplinary care and risk stratification for more effective and comprehensive patient care.  Check out the full OncClub subseries to see additional findings and insights from this research!

As we continue to learn more and more about arthrogenic muscle inhibition after ACL reconstruction surgery, we can continue to build better rehabilitation programs for our athletes.In this episode, the team discusses a recent review article on AMI and its impact on postoperative rehabilitation and return to sport decision-making.To see full show notes and more, head to: https://mikereinold.com/management-of-arthrogenic-muscle-inhibition/ Click Here to View My Online CoursesWant to learn more from me? I have a variety of online courses on my website!Disclaimer: This post contains affiliate links. If you make a purchase, I may receive a commission at no extra cost to you.Support the show_____Want to learn more? Check out my blog, podcasts, and online coursesFollow me: Instagram | Twitter | Facebook | Youtube

Join Professor Iain McInnes as he discusses the top publications in the world of RA. This month, the conversation covered the ‘dual JAK and ROCK inhibition with CPL'116 in patients with RA with inadequate response to MTX' and ‘the benefit–risk analysis of UPA versus adalimumab in patients with RA and higher or lower risk of cardiovascular disease'

If you've ever asked yourself, “Where should I treat first,” this is the episode for you.This episode of the Unreal Results podcast, is all about one of my favorite tools that's simple to implement and wildly effective at uncovering what's actually driving pain: inhibition tests.You've probably heard me reference inhibition tests in past episodes and today I'm breaking them down into what they are, how they work, and why they can be a game-changer in identifying hidden drivers of pain, mobility limitations, and strength loss.  You'll hear me talk about what makes a good inhibition test, why so many people get it wrong, and how this approach can take you from guessing to knowing exactly where to start treatment.Whether you'rve been using the LTAP™ for some time or just starting to question traditional orthopedic thinking, this episode will show you how to listen to the body in a whole new way and get those jaw-dropping “holy cow!” moments in your sessions.Resources Mentioned In This Episode2025 Birthday Sale! Get the savings HEREEpisode 6: The Mysterious, Misunderstood, and Mistreated SI JointEpisode 9: Left Sided Sciatica or Right Sided Shoulder Pain?Episode 16: Why The Shoulder Comes LastEpisode 54: A Better Way To Assess The SI JointEpisode 77: The Controversy of the Gillet SI Joint TestGet the book Visceral Manipulation II by Jean-Pierre BarralLearn the LTAP™ In-Person in one of my upcoming coursesThe annual birthday sale is here! From July 29th-August 1st you can save up to 60% on self-paced online education courses and the Regen library.Get the birthday sale savings HERE=================================================Watch the podcast on YouTube and subscribe!Join the MovementREV email list to stay up to date on the Unreal Results Podcast and MovementREV education. Be social and follow me:Instagram | Facebook | Twitter | YouTube

Drs. M. Ali Khan and Ajay Kuriyan join to discuss the current sentiment in the retina community regarding geographic atrophy treatment, specifically complement inhibition. Relevant Financial Disclosures: Dr. Sridhar has consulted for both Apellis and Iveric Bio in the past 3 years. You can claim CME credits for prior episodes via the AAO website. Visit https://www.aao.org/browse-multimedia?filter=Audi

Ashkan Shoamanesh, MD, FRCPC - Can We Find a New Way Forward in Secondary Stroke Prevention? Exploring the Rationale and Potential Roles for Factor XIa Inhibition

In today's episode, supported by Coherus BioSciences, we had the pleasure of speaking with Michael Dennis, MD, about recent updates to the nasopharyngeal carcinoma treatment paradigm. Dr Dennis is a physician at Dana-Farber Cancer Institute; as well as an instructor in medicine at Harvard Medical School, both in Boston, Massachusetts. In our exclusive interview, Dr Dennis discussed the latest National Comprehensive Cancer Center guideline updates for the treatment of patients with nasopharyngeal carcinoma; practice-informing data from the phase 3 JUPITER-02 trial (NCT03581786), which investigated first-line toripalimab-tpzi (Loqtorzi) plus chemotherapy in patients with recurrent or metastatic nasopharyngeal carcinoma; and ongoing developments in the locally advanced treatment setting.

Emma Guttman-Yassky, MD, PhD - Atopic Dermatitis and the 0X40 Pathway: Understanding the Therapeutic Potential of OX40 Inhibition in Atopic Dermatitis

In our exclusive interview, Dr Morgans detailed the evolving role of AR inhibitors in the mHSPC setting, including the recent expanded approval for darolutamide (Nubeqa) for this population. She discussed treatment considerations for determining whether to give docetaxel along with darolutamide; other factors to remember with AR inhibition; and the need to continue driving consensus across practices in the management of prostate cancer.

What if you could decrease your pain by covering one eye? In this episode, I speak with my podcast producer, Tony, about inhibition tools and how removing stimulus can actually be the key to success when it comes to decreasing pain and improving movement. I talk about overactivity in different systems of the brain, and why sometimes staying in that elevated state of activity can lead to pain, anxiety, lack of focus, training imbalances, and more. By inhibiting some parts of the nervous system, we can focus our training away from areas that are increasing threat, or are simply doing too much of the work so that we can target a weaker system that isn't properly doing it's job. I relay the stories of several clients that benefited from inhibition tools, and give concrete examples of tools that you can easily purchase or make at home. This is a powerful concept that can be useful for those who keep trying to "train" their problems without success, or have "tried everything" and nothing works. Thank you to my podcast idea man and coach, Tony Fowler (Instagram: @tone_reverie) for helping me put together this episode! Free Resources: Join our mailing list HERE to stay up to date on the latest updates from Kruse Elite Join our free Neuro Masterclass here to get a taste of how neurology impacts your movement and pain issues Subscribe to our YouTube HERE for in-depth educational videos and tutorials Whenever you're ready here's how we can help you: Become an expert in problem solving movement and pain issues with our beginner neuro course, Neuro Foundations Master applied neurology so you can feel confident you can help anyone who walks through your door by joining our advanced neuro course, The Neuro Dojo

In this week's episode, we' ll learn about how TET3 has a key role in GVHD. In mice, a deficiency of Tet3 in donor T cells inhibited pathogenic immunoglobulin class switching and suppressed lung fibrosis. Accordingly, TET3 may be a new therapeutic target in chronic GVHD. After that: rilzabrutinib, a BTK inhibitor for ITP. In a randomized, placebo-controlled trial, treatment produced rapid and durable platelet responses, with acceptable safety, in adults with immune thrombocytopenia who had failed multiple previous therapies. Finally: exploring pre-TCR surface expression patterns in T-cell ALL. Co-inhibition of the interleukin-7 receptor and pre-T cell receptor pathways may play a therapeutic role for a subset of T-lymphoblastic leukemias.Featured Articles: Deficiency of T follicular helper cell Tet3 DNA demethylation inhibits pathogenic IgG2c class switching and chronic GVHDSafety and efficacy of rilzabrutinib vs placebo in adults with immune thrombocytopenia: the phase 3 LUNA3 studySurface pTα expression predicts LCK activation and preclinical synergy of LCK and JAK coinhibition in adult T-ALL

In this episode, Dr. Valentin Fuster explores groundbreaking research on long-acting Factor XI inhibitors, highlighting their potential to reduce bleeding risks during invasive procedures in patients with atrial fibrillation. Experts discuss the promising safety profile and the ongoing quest to balance effective anticoagulation without increased bleeding.

In this episode, entitled “JAK Inhibition for Treatment of Vitiligo,” expert dermatologists, Dr Andrew Alexis, MD, MPH and Dr Erik Domingues, MD, FAAD, discuss the following topics: ·       Changing the culture of vitiligo care ·       Diagnosing vitiligo and associated comorbidities ·       Strategies for managing vitiligo and educating patients about treatment options ·       Setting patient expectations for the treatment process

Featuring perspectives from Dr Ian E Krop and Dr Sara M Tolaney, including the following topics: Introduction: Adjuvant CDK4/6 Inhibition (0:00) HER2-Positive Disease (11:13) PARP Inhibition (27:34) Antibody-Drug Conjugates (34:12) Up-Front Treatment of HR-Positive Metastatic Disease (46:28) CME information and select publications

In this episode of The Moss Report, Ben Moss speaks with Dr. Ralph Moss about a little-known natural compound that may have big implications: Modified Citrus Pectin (MCP). A recent clinical trial in Israel found that MCP helped slow PSA doubling time in men with recurrent prostate cancer—suggesting it may offer real, measurable support for patients after treatment. Ben and Ralph trace the story from its origins in the 1990s through modern-day research, digging into how MCP works by targeting Galectin-3, a molecule tied to inflammation and cancer spread. Along the way, they highlight the researchers who kept this idea alive, including Dr. Kenneth Pienta and Dr. Isaac Eliaz, and ask why this research isn't more widely known. It's an honest, science-based conversation about where evidence and action meet—and how natural approaches might still be flying under the radar. Link to the full article with transcript, slide presentation, links and cited studies. https://www.themossreport.com/mcp-podcast/ Products mentioned in this podcast: Pectasol-C – https://econugenics.com/?a_aid=TMR Mycolife – The Moss Method Mushroom Formula – https://mycolife.us/product/the-moss-method-mushroom-formula/ Links and Resources:

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/AAPA information, and to apply for credit, please visit us at PeerView.com/QVF865. CME/MOC/AAPA credit will be available until April 28, 2026.Achieving Next-Level HCM Care and Outcomes With Cardiac Myosin Inhibition: From Long-Term Clinical Evidence to Real-World Data In support of improving patient care, this activity has been planned and implemented by PVI, PeerView Institute for Medical Education, and The Mended Hearts, Inc. PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant from Bristol Myers Squibb.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/AAPA information, and to apply for credit, please visit us at PeerView.com/QVF865. CME/MOC/AAPA credit will be available until April 28, 2026.Achieving Next-Level HCM Care and Outcomes With Cardiac Myosin Inhibition: From Long-Term Clinical Evidence to Real-World Data In support of improving patient care, this activity has been planned and implemented by PVI, PeerView Institute for Medical Education, and The Mended Hearts, Inc. PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant from Bristol Myers Squibb.Disclosure information is available at the beginning of the video presentation.