Podcasts about tumors

Brothers Rakesh Popat, PhD, multiple myeloma expert, and Sanjay Popat, PhD, thoracic oncologist, join the show for a special discourse on surrogate endpoints and patient benefit. The conversation fluctuates between the “assumption” that surrogate endpoints translate to better survival; breakdowns of the utility and association with overall survival of PFS, ORR, and MRD in the latest literature; reimbursement intricacies and issues surrounding surrogate endpoint criteria; and the need for stronger confirmatory trials after accelerated approvals, along with plenty more important points for consideration. Check out Chadi's website for all Healthcare Unfiltered episodes and other content. www.chadinabhan.com/ Watch all Healthcare Unfiltered episodes on Youtube. www.youtube.com/channel/UCjiJPTpIJdIiukcq0UaMFsA

Brain tumors don't get the same amount of attention as the other types of cancers. But they are still very important to talk about. My guest today is Dr. Daniel F. Kelly, a neurosurgeon and founder of Pacific Neuroscience Institute. Listen in to learn about Daniel's non-linear path to becoming a neurosurgeon. You'll also hear how the Pacific Neuroscience Institute uses keyhole surgery to reduce the amount of time patients need to stay in the hospital.   What You'll Learn: We learn about Dr. Daniel F. Kelly and his background. (2:00) Daniel explains his non-linear path to becoming a neurosurgeon. (3:40) I recount some of my experiences with neurosurgeons.  (5:30) Seeing a gap in specialized neuro-oncology at St. John's Cancer Institute, Daniel helped found the Pacific Neuroscience Institute.  (6:00) Daniel describes the types of tumors he sees most and how that's changed over time. (8:15) We hear how Daniel got interested in pituitary tumors. (10:20) Pacific Neuroscience Institute uses a lot of collaboration to give the patient the best care (13:05) We hear how patients' pathways may differ when treated by Daniel. (14:26) Not every brain tumor patient requires surgery. (17:20) The essence of keyhole surgery is to sneak in and sneak out. (18:36) Daniel explains how surgery has evolved throughout his career. (21:30) Not every neurosurgeon specializes in keyhole surgery. (22:00) The COVID-19 pandemic reduced the amount of time neuro-patients stayed in hospitals post surgery. (24:30) Neuro-patients are incredibly brave and resilient. (27:16) Daniel explains how he collaborates with different specialists. (30:00) There are some exciting advances happening in neurosurgery. (32:00) Pacific Neuroscience Institute is looking for a cure for Glioblastoma. (35:05) Psychedelic assisted therapy is currently having a renaissance. (36:30) Daniel describes various studies on psychedelic assisted therapy. (39:14) We discuss the Netflix show 'How to Change Your Mind'. (44:00)   Ideas worth sharing: "Not everyone who has a brain tumor needs surgery." - Dr. Daniel F. Kelly   "The essence of Keyhole Surgery is to sneak in and sneak out with minimum collateral damage." - Dr. Daniel F. Kelly   "Managing patient expectations is important for all areas of oncology." - Dr. Rosalyn Morrell   "All of my patients teach me so much. We think we're teaching them and educating them -- but a lot of times it's the other way around." - Dr. Rosalyn Morrell   Resources: Dr. June Wiley: USC Pacific Neuroscience Institute: Website Dr. Daniel F. Kelly: Email

Thank you for joining us for our 2nd Cabral HouseCall of the weekend! I'm looking forward to sharing with you some of our community's questions that have come in over the past few weeks…   Donna: Hi Dr Cabral! I was recently diagnosed with a renal AML of 1.3cms and focal nodular neoplasm on my liver was noticed on my ultrasound. I need to now do an MRI to further investigate. I can't find any archived podcasts on these issues. Some background info: I was on “Yas” birth control pill for 8 years from 14-22 years old, and in the last 2 years I took antibiotics 8 times for UTIs. I'm someone who normally NEVER takes medication. I eat well, don't drink or smoke, but I've undergone a lot of stress since becoming a mom 4 years ago and feel like it's been since that time that my health has started to deteriorate as I try to juggle motherhood with running my own growing business. I'll be running the big 5 labs in 2 weeks, as I'm convinced they will shed more light on my health. Any input from you would help! Will these tumors ever go away in your experience? Thank you so much, I value your consideration and time!   Maria: Hi Dr Cabral! I would love to hear your thoughts on lecithin as a supplement. Do you recommend it? If so, how does it support the body and what benefits are there? I've heard it connected to cognitive functions, nerves, skin, cholesterol etc. Could it be helpful for someone who has signs of dementia? What about when there's loss of sensitivity, tingling and numbness in lower parts of the legs and feet? Or is there anyone is particular that is at risk of being low in lecithin? Many many thanks for all you do, your podcast is like my encyclopedia on all health related matters.   Jesseca: Hi Dr. Cabral, Thank you so much for all of the education you share. I've learned so much from you and am so grateful to have resources like yours to empower myself and my family to live happy, healthy lives. I have two separate questions that I asked in the Facebook support group, and they don't appear to have been answered before: 1) What is your opinion on chemical peels and products like retinol as part of a regular skin care routine? As I understand it, both make your skin very sensitive to the sun (requiring very diligent SPF application), which raises some red flags for me. What do you think? 2) What is your opinion on using mushrooms like lions mane, chaga, and cordyceps while pregnant? I'm planning on getting pregnant in the next year and am thinking about how to replace my morning coffee. When I've decided to give up caffeine in the past, I found mushrooms like this (e.g. FourSigmatic's functional creamer) to work really well as an alternative. I know you recommend reducing herbs while pregnant. Would mushrooms like this fall in the same category? Thank you! Jesseca   Tina: You are amazing, and thanks for all you do! My 13-year-old son was just diagnosed with severe swelling in his sinuses, a deviated septum, and sinus polyps. I have him on daily omegas, daily activated mullti, periodic balanced zinc, daily probiotic, 3 HistPro 2 X per day, and I just ordered the alkalizing vitamin c (all Equilife products). I was forced to start him on Flonase, but I also have him on the nutribiotic GSE nasal spray. They want to do surgery, but they agreed to see if his nose improved after three months on the Flonase. So, three questions: 1-How much alkalizing vitamin c should he take? 2- Is it fine to keep him on all of these other things, and for how long? 3-Is there anything else I could be doing before this follow-up visit to help him so that his nose improves and they don't want to push us into the surgery? He's just over 100 pounds and very fit and active. He has all of the seasonal allergies and allergies to peanuts, tree-nuts, and sesame. I know it will take a while for you to answer, and I did ask on Facebook as well, but I know this will be an ongoing issue, so I wanted to get your opinion since I really value it.   Jackie: My practitioner has recommended the Candida and Bacterial Optimizer (CBO) protocol. He is not an expert on Small Intestinal Bacterial Overgrowth, however. He has noted that my good bacteria diversity is really low. I have been on antibiotics and antimicrobials for 10 months to combat my SIBO. So far, no luck. My hydrogen level remains elevated. My question is this. Is this particular protocol good to disrupt established and tough biofilms? Or is this protocol better for someone who would be using this protocol as a first round against SIBO? Has it ever been used with success on SIBO patients who had tough biofilms to break down? Finally, is there a reason why EDTA is not included in the biofilm buster formula?   Ales: Hello Dr. Cabral, I have a question regarding earth probiotic strains like B.coagulus, B.clausii, B.subtilis. Lately, I have seen many products of these particular strains being used, especially in combination with botanicals and biofilm removers to help with SIBO. Is there any real evidence regarding soil based probiotics or you aren't convinced of their efficacy? With SIBO or in general?   Ales: Hello Dr. Cabral, in my last question I forgot to add that I work in a functional medicine clinic, where we analyse gut microbiom. We see very often low counts of akkermansia muciniphila, which is critical for healthy gut barrier. Soil based probiotics are suppose to indirectly increase akkermansia. Do you see any valuable evidence of that?   Thank you for tuning into this weekend's Cabral HouseCalls and be sure to check back tomorrow for our Mindset & Motivation Monday show to get your week started off right!   - - - Show Notes and Resources: StephenCabral.com/2487 - - - Get a FREE Copy of Dr. Cabral's Book: The Rain Barrel Effect - - - Join the Community & Get Your Questions Answered: CabralSupportGroup.com - - - Dr. Cabral's Most Popular At-Home Lab Tests: > Complete Minerals & Metals Test (Test for mineral imbalances & heavy metal toxicity) - - - > Complete Candida, Metabolic & Vitamins Test (Test for 75 biomarkers including yeast & bacterial gut overgrowth, as well as vitamin levels) - - - > Complete Stress, Mood & Metabolism Test (Discover your complete thyroid, adrenal, hormone, vitamin D & insulin levels) - - - > Complete Food Sensitivity Test (Find out your hidden food sensitivities) - - - > Complete Omega-3 & Inflammation Test (Discover your levels of inflammation related to your omega-6 to omega-3 levels) - - - Get Your Question Answered On An Upcoming HouseCall: StephenCabral.com/askcabral - - - Would You Take 30 Seconds To Rate & Review The Cabral Concept? The best way to help me spread our mission of true natural health is to pass on the good word, and I read and appreciate every review!

AMA Research Challenge finalist, Kanita Chaudry shares her research on the efficacy of a treatment for neuroblastoma cancer tumors in children. Kanita Chaudhry is an MD/PhD candidate at University at Buffalo Jacobs School of Medicine and Biomedical Sciences. The AMA Research Challenge is the largest national, multi-specialty research event for medical students, residents and fellows, and international medical graduates to showcase and present research. Learn more by visiting: https://www.ama-assn.org/about/events/ama-research-challenge

Yves Tumor - "God Is A Circle," a 2022 single on Warp. Shortly after the end of spooky season, Yves Tumor dropped the chilling single “God Is A Circle” to the delight of the many fans who have been gripped by the Turin-based artist's enigmatic take on glam rock. The single follows last year's EP The Asymptotical World and 2020's full-length Heaven To a Tortured Mind. Produced by Noah Goldstein (Frank Ocean, Arcade Fire), and mixed by Alan Moulder (My Bloody Valentine, Nine Inch Nails), the song is built upon a beat of labored breaths for a moody post-punk-indebted rocker that features squelching guitars, fuzzed-out bass, and desperate shrieks. Swedish electronic artist Ecco2K and Lebanon-born artist Thoom bestow backing vocals as Yves Tumor sings about detachment and strained relationships, “There's places in my mind that I cannot go / There's people in my life I still don't know.” The song is paired perfectly with a campy horror-movie-style video by Jordan Hemmingway which adds to the ominous feel of the song. Watch the video and read the full post at KEXP.org.Support the show: https://www.kexp.org/donateSee omnystudio.com/listener for privacy information.

Picolé De Limão é um quadro do canal Não Inviabilize. Aqui você ouve as suas histórias misturadas às minhas! Use a hashtag #Tumor e comente a história no nosso grupo do telegram: https://t.me/naoinviabilize PUBLICIDADE ITAÚ Golpe do Cartão https://www.youtube.com/watch?v=sUeBXQpDWC4 /  Golpe da Falsa Central https://www.youtube.com/watch?v=A6Gsg_VHgnY / Golpe no WhatsApp https://www.youtube.com/watch?v=vs27aeCECXc   Envie a sua história bem detalhada para naoinviabilize@gmail.com, seu anonimato será mantido, todos os nomes, profissões e locais são trocados para preservar a sua identidade. Site: naoinviabilize.com.br Transcrição dos episódios: naoinviabilize.com/episodios Assine e fortaleça o meu trabalho: apoia.se/naoinviabilize Histórias em Libras no Youtube: youtube.com/naoinviabilize Instagram: instagram.com/naoinviabilize TikTok: tiktok.com/@naoinviabilize Twitter: twitter.com/naoinviabilize Facebook: facebook.com/naoinviabilize

In 2014, David and Chalece Neilsen were eagerly awaiting the arrival of their baby when it was discovered that their little girl suffered from a rare form of cancer. She was born prematurely at 25 weeks and given the name Allison Faith. After a fortnight in a NICU incubator under excellent doctor care, the Neilsens' held their baby for the first and last time as she passed away. The couple each mourned in their own way, leaning heavily on the support of friends and family. And as they continued to struggle with infertility issues, they discovered that Resiliency is not what we think. They join this episode of Relentlessy Resilient to share how it is worth fighting for resilience and peace in the hardest of trials. Even though we live in challenging times we can become Relentlessly Resilient as we lean on and learn from one another's experiences. Hosts Jennie Taylor and Michelle Scharf are no strangers to overcoming adversity; Michelle lost her husband to cancer, while Jennie's husband Major Brent Taylor was killed in the service of our country. Their stories bond them together and now listeners can join them weekly as they visit with others enduring challenges and who teach us how they are exercising resiliency, finding value in their grief, and purpose in moving forward.  Listen to the Relentlessly Resilient Podcast regularly on your favorite platform, at kslpodcasts.com, kslnewsradio.com, or on the KSL App. Join the Resilience conversation on Facebook at @RelentlesslyResilient and Instagram @RelentlesslyResilientPodcast. Produced by KellieAnn Halvorsen.See omnystudio.com/listener for privacy information.

To have your question featured in a future video, please email: questions@drmdc.health

The compound has received attention for over a decade for chemoprotective and chemotherapeutic properties, including against breast cancer and colon cancer, showing it could reduce cancer cell glucose uptake.

Welcome to The Times of Israel's Daily Briefing, your 15-minute audio update on what's happening in Israel, the Middle East and the Jewish world, from Sunday through Thursday. Knesset correspondent Carrie Keller-Lynn and health and science reporter Nathan Jeffay join host Jessica Steinberg for today's podcast. Keller-Lynn talks about Tuesday's swearing-in of the 25th Knesset, with newcomers elated by their wins and the opposition heralding the end of democracy, with concerns over a lack of unity in the government. Jeffay speaks about a Hebrew University study that examines plummeting sperm counts worldwide, which could point to a wider decline in aspects of men's health. Keller-Lynn also discusses the lack of outside activists at the ongoing United Nations Climate Conference COP27 in Egypt's Sharm el Sheikh, part of the Egyptian efforts to quash the usual protests. Jeffay looks at a new technology under trial, which offers a fuller report on the DNA of tumors. Discussed articles include: Far-right vows upped security under new gov't; Liberman warns of ‘ayatollah regime' Sperm counts worldwide have plunged 62% in under 50 years, Israeli-led study finds Egyptians keep tight leash on climate confab, muffling traditional din of protests Israeli hospital: New tech gave instant DNA info on tumors, jump-starts treatment Subscribe to The Times of Israel Daily Briefing on iTunes, Spotify, PlayerFM, Google Play, or wherever you get your podcasts. IMAGE: Likud leader MK Benjamin Netanyahu, Prime Minister Yair Lapid, and Party leaders at a swearing-in ceremony of the 25th Knesset, at the Israeli parliament in Jerusalem, November 15, 2022. (Photo by Olivier Fitoussi/Flash90)See omnystudio.com/listener for privacy information.

Listen to a blog summary of a research paper published in Volume 13, entitled, "Predictive molecular biomarkers for determining neoadjuvant chemosensitivity in muscle invasive bladder cancer." _______________________________________________ Neoadjuvant chemotherapy (NAC) is a type of cancer treatment involving the administration of chemotherapy drugs before surgery. The goal of NAC is to shrink the tumor(s) in order to make it/them easier to remove during surgery and to decrease the chance of cancer recurrence after treatment. NAC is typically well tolerated by patients and has been shown to improve outcomes in patients with bladder cancer. Predictive biomarkers are being increasingly used in oncology to identify patients who are likely to respond to chemotherapy. In the past, the decision to administer chemotherapy was based on tumor type and stage. However, it is now understood that there is considerable heterogeneity within these groups, and that not all patients will respond to the same treatment. Predictive biomarkers can help to overcome this challenge by identifying those patients who are most likely to benefit from chemotherapy. There are a number of different types of predictive biomarkers, which can be divided into two broad categories: tumor biomarkers and host biomarkers. Tumor biomarkers are usually specific to the tumor type and can include markers of cell proliferation and DNA repair. Host biomarkers are usually found in the blood or other bodily fluids and can include markers of inflammation, immune function and metabolism. The use of predictive biomarkers has the potential to improve the efficacy of chemotherapy and reduce toxicity by avoiding its use in patients who are unlikely to benefit. In a new study, researchers Neal Murphy, Andrew J. Shih, Paras Shah, Oksana Yaskiv, Houman Khalili, Anthony Liew, Annette T. Lee, and Xin-Hua Zhu from Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Northwell Health Cancer Institute, Feinstein Institutes for Medical Research, and Mayo Clinic aimed to develop and validate a predictive biomarker panel for response to NAC in patients with muscle-invasive bladder cancer (MIBC). Their research paper was published on November 2, 2022, in Oncotarget's Volume 13, entitled, “Predictive molecular biomarkers for determining neoadjuvant chemosensitivity in muscle invasive bladder cancer.” Full blog - https://www.oncotarget.org/2022/11/15/biomarkers-may-predict-neoadjuvant-chemosensitivity-in-bladder-cancer/ DOI - https://doi.org/10.18632/oncotarget.28302 Correspondence to - Neal Murphy - nmurphy2@northwell.edu, Annette T. Lee - alee@northwell.edu, and Xin-Hua Zhu - xzhu1@northwell.edu Press release - https://www.oncotarget.com/index.php?journal=oncotarget&page=news&op=press&item=oncotarget-predictive-molecular-biomarkers-for-determining-neoadjuvant-chemosensitivity-in-muscle-invasive-bladder-cancer Keywords - muscle invasive bladder cancer, neoadjuvant chemotherapy, gene expression, molecular subtyping, canonical correlation analysis About Oncotarget Oncotarget is a primarily oncology-focused, peer-reviewed, open access journal. Papers are published continuously within yearly volumes in their final and complete form, and then quickly released to Pubmed. On September 15, 2022, Oncotarget was accepted again for indexing by MEDLINE. Oncotarget is now indexed by Medline/PubMed and PMC/PubMed. To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: SoundCloud - https://soundcloud.com/oncotarget Facebook - https://www.facebook.com/Oncotarget/ Twitter - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/OncotargetYouTube LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/

In a small study, researchers modified patients' immune cells to target their particular cancer—but it only worked for a third of volunteers.

Dr. Ray Lee is the CEO of Teclison, focused on overcoming the limitations of existing immunotherapy for treating liver cancer in part caused by the fact that the liver is a highly immunotolerant organ. The key is to make the tumor a low-oxygen environment and delivering a drug that only works on the tumor. Ray elaborates, "First, let me explain what the TATE represents. It stands for the Trans-arterial TEC-001 Embolization. TEC-001 is the pipeline compound we've been trying to develop. This compound is a so-called prodrug. In other words, by itself, it has a low activity. But once in the low-oxygen environment, the drug is going to be activated. What we're trying to develop is to create a very innovative way to convert the tumor into an environment with low oxygen. And this low-oxygen environment is exclusive within the tumor but not in the normal liver nor in the systemic organs." "So once they have this catheter in place, they will inject our drugs, the TEC-001, directly through the catheter into the tumor and then follow by the embolization. And what I mean by embolization is injecting a special kind of material, like a block in the tumor vessel, and cutting off the blood flow. So that means the tumor is no longer able to receive any blood, so they are not getting enough nutrients or oxygen, which makes the tumor be in a very low-oxygen environment. And that is how our drug is going to be almost immediately activated within the tumor after the embolization procedure, and that's how it works." #Teclison #LiverCancer #Cancer #SolidTumors #Immunotherapy #CancerImmunotherapy #LiverMetastasis #LungCancer #ColorectalCancer Teclison.com Download the transcript here

Dr. Ray Lee is the CEO of Teclison, focused on overcoming the limitations of existing immunotherapy for treating liver cancer in part caused by the fact that the liver is a highly immunotolerant organ. The key is to make the tumor a low-oxygen environment and delivering a drug that only works on the tumor. Ray elaborates, "First, let me explain what the TATE represents. It stands for the Trans-arterial TEC-001 Embolization. TEC-001 is the pipeline compound we've been trying to develop. This compound is a so-called prodrug. In other words, by itself, it has a low activity. But once in the low-oxygen environment, the drug is going to be activated. What we're trying to develop is to create a very innovative way to convert the tumor into an environment with low oxygen. And this low-oxygen environment is exclusive within the tumor but not in the normal liver nor in the systemic organs." "So once they have this catheter in place, they will inject our drugs, the TEC-001, directly through the catheter into the tumor and then follow by the embolization. And what I mean by embolization is injecting a special kind of material, like a block in the tumor vessel, and cutting off the blood flow. So that means the tumor is no longer able to receive any blood, so they are not getting enough nutrients or oxygen, which makes the tumor be in a very low-oxygen environment. And that is how our drug is going to be almost immediately activated within the tumor after the embolization procedure, and that's how it works." #Teclison #LiverCancer #Cancer #SolidTumors #Immunotherapy #CancerImmunotherapy #LiverMetastasis #LungCancer #ColorectalCancer Teclison.com Listen to the podcast here

Rey and Roland finally release their Malignant review recorded over a year ago. After some heavy audio editing we thinks its time for the masses to HEAR US! Buy merch: https://www.mokuestmerch.com/ Donate: https://www.patreon.com/mokueststudios Subscribe to our Youtube channel: https://www.youtube.com/channel/UCDKvcE9r66b5nyrI9Q381dA --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app --- Send in a voice message: https://anchor.fm/cinekuest-video/message Support this podcast: https://anchor.fm/cinekuest-video/support

Un grupo de científicos españoles ha identificado las células responsables de la recaída en el cáncer de colon, el segundo que más mata en España, y han podido observar cómo viajan por el torrente sanguíneo. Eduard Batlle, jefe del laboratorio de cáncer colorrectal en el IRB Barcelona, ha estado al frente de este equipo. En el informativo 24 horas de RNE, ha explicado que son estudios preliminares con ratones que se tienen que verificar en pacientes: "Hay un estudio en marcha en Holanda, independiente de nuestra investigación, y estamos expectantes". Asimismo, Batlle cuenta que estas células mantienen cierta similitud con las del cáncer de páncreas, por lo que también están investigando "hasta qué punto este mecanismo puede estar presente en otros tipos de tumor". Aunque afirma que aún estamos lejos de erradicar la mortalidad del cáncer de colon, se muestra optimista y cree que este tipo de investigaciones "se van a traducir en avances substanciales".Escuchar audio

In this episode, our team provides a comprehensive review of the differential diagnosis for mediastinal masses, their workup, and biopsy considerations. Listen as we dive deeper into the perioperative planning and operative approach for resection of these masses with special considerations for patients with thymoma.  Learning Objectives: -Discuss the differential diagnosis of a mediastinal mass -Review the workup of a mediastinal mass -Outline indications for biopsy and describe the various approaches -Describe the operative techniques for thymectomy, pearls & potential pitfalls   Hosts:  Megan Lenihan MD, Kelly Daus MD, Peter White MD, and Brian Louie MD Referenced Material https://pubmed.ncbi.nlm.nih.gov/21847052/ Detterbeck FC, Nicholson AG, Kondo K, Van Schil P, Moran C. The Masaoka-Koga stage classification for thymic malignancies: clarification and definition of terms. J Thorac Oncol. 2011 Jul;6(7 Suppl 3):S1710-6. doi: 10.1097/JTO.0b013e31821e8cff. PMID: 21847052. https://pubmed.ncbi.nlm.nih.gov/33468329/ Ahmad U. The eighth edition TNM stage classification for thymic tumors: What do I need to know? J Thorac Cardiovasc Surg. 2021 Apr;161(4):1524-1529. doi: 10.1016/j.jtcvs.2020.10.131. Epub 2020 Nov 13. PMID: 33468329. https://pubmed.ncbi.nlm.nih.gov/34695605/ Marx A, et al. The 2021 WHO Classification of Tumors of the Thymus and Mediastinum: What Is New in Thymic Epithelial, Germ Cell, and Mesenchymal Tumors? J Thorac Oncol. 2022 Feb;17(2):200-213. doi: 10.1016/j.jtho.2021.10.010. Epub 2021 Oct 22. PMID: 34695605. https://pubmed.ncbi.nlm.nih.gov/22882218/ Meriggioli MN, Sanders DB. Muscle autoantibodies in myasthenia gravis: beyond diagnosis? Expert Rev Clin Immunol. 2012 Jul;8(5):427-38. doi: 10.1586/eci.12.34. PMID: 22882218; PMCID: PMC3505488. https://pubmed.ncbi.nlm.nih.gov/34339670/ Raja SM, Guptill JT, McConnell A, Al-Khalidi HR, Hartwig MG, Klapper JA. Perioperative Outcomes of Thymectomy in Myasthenia Gravis: A Thoracic Surgery Database Analysis. Ann Thorac Surg. 2022 Mar;113(3):904-910. doi: 10.1016/j.athoracsur.2021.06.071. Epub 2021 Jul 30. PMID: 34339670. Ad referenced in episode: A team at the Brooke Army Medical Center is working to better define proficiency-based metrics for competency in commonly performed general surgery procedures. If you are a PGY4/5 general surgery resident or practicing surgeon who performs robotic assisted cholecystectomies or inguinal hernia repairs, reach out to the PI, Robert Laverty, MD, at rblaverty@gmail.com, for more information on how you could be compensated up to $400 for recording and submitting those videos. Please visit https://behindtheknife.org to access other high-yield surgical education podcasts, videos and more.   If you liked this episode, check out other clinical challenge episodes here: https://behindtheknife.org/podcast-series/clinical-challenges/

Both benign and malignant oral tumors are common occurrences in dogs. The key to successful therapy is early detection and intervention. In this podcast, Dr. Alexandra Gareau discusses practical clinical approaches to canine oral tumors in general practice. She'll cover excisional vs incisional biopsies, the importance of clinical staging prior to definitive treatment and the prognosis of different tumor types.

Eduard Batlle, jefe del equipo de investigadores que han identificado las células causantes de la metástasis, explica en 'Más de uno' la importancia de este hallazgo y cómo podría evitar que muchos pacientes recaigan en la enfermedad.

Amir Jafri is the CEO and Founder of Immunicom, targeting the molecules and proteins produced by cancer. Using a subtractive approach, Immunicom has developed technology intended to remove the elements that are suppressing the immune system and allowing the tumor to shield itself from the immune system. After treatment, patients in clinical trials are seeing immune cells infiltrate their solid tumor cancers. Amir explains, "What we will do is then design our own molecules that will neutralize what the molecule of cancer is producing. But instead of making our molecule into a drug, which is normally what would happen, we actually put it into this proprietary liquid cartridge that we have. It's got a liquid chemical matrix, and there's like a little cartridge, and our molecule goes in there. That cartridge attaches to what's called a plasmapheresis machine." "Now, that machine is very similar to a dialysis machine. These machines exist all over the world and they've been around for 30 years. The patient sits down, and their blood and plasma attach to the machine. They just sit in a comfortable chair, and their plasma is then taken by the machine and sent through our cartridge. And then we will pull out, in a very, very exquisite way, the molecule that the cancer is producing that is suppressing the immune system." @Immunicom #ImmuneSystem #Immunotherapy #MedicalDevice #HealthTech #MedTech #Oncology #Cancer #Tumors Immunicom.com Download the transcript here

Amir Jafri is the CEO and Founder of Immunicom, targeting the molecules and proteins produced by cancer. Using a subtractive approach, Immunicom has developed technology intended to remove the elements that are suppressing the immune system and allowing the tumor to shield itself from the immune system. After treatment, patients in clinical trials are seeing immune cells infiltrate their solid tumor cancers. Amir explains, "What we will do is then design our own molecules that will neutralize what the molecule of cancer is producing. But instead of making our molecule into a drug, which is normally what would happen, we actually put it into this proprietary liquid cartridge that we have. It's got a liquid chemical matrix, and there's like a little cartridge, and our molecule goes in there. That cartridge attaches to what's called a plasmapheresis machine." "Now, that machine is very similar to a dialysis machine. These machines exist all over the world and they've been around for 30 years. The patient sits down, and their blood and plasma attach to the machine. They just sit in a comfortable chair, and their plasma is then taken by the machine and sent through our cartridge. And then we will pull out, in a very, very exquisite way, the molecule that the cancer is producing that is suppressing the immune system." @Immunicom #ImmuneSystem #Immunotherapy #MedicalDevice #HealthTech #MedTech #Oncology #Cancer #Tumors Immunicom.com Listen to the podcast here

Episode SummaryChimeric antigen receptors, or CARs, repurpose the build-in targeting and homing signals of our immune system to direct T cells to find and eliminate cancers. Although CAR-T cells have transformed the care of liquid tumors in the circulating blood, like B cell leukemia and lymphoma, CAR-T therapy has shown limited efficacy against solid tumors. To unlock the full potential of CAR-T therapies, better receptor designs are needed. Unfortunately, the space of potential designs is too large to check one by one. To design better CARs, Dan and his co-author Camillia Azimi developed CAR Pooling, an approach to multiplex CAR designs by testing many at once with different immune costimulatory domains. They select the CARs that exhibit the best anti-tumor response and develop novel CARs that endow the T cells with better anti-tumor properties. Their methods and designs may help us develop therapies for refractory, treatment-resistant cancers, and may enable CAR-T cells to cure infectious diseases, autoimmunity, and beyond.About the AuthorDuring his PhD in George Church's lab at Harvard Medical School, Dan studied interactions between bacterial transcription and translation, built and measured libraries of tunable synthetic biosensors, and constructed a new version of the E. coli genome capable of incorporating new synthetic amino acids into its proteins. He also built a high-throughput microbial genome design and analysis software platform called Millstone.As a Jane Coffin Childs Postdoctoral Fellow at UCSF, Dan is currently applying these high-throughput synthetic approaches to engineer T cells for the treatment of cancer and autoimmune disease. He is also working in the Bluestone, Roybal, and Marson labs.Key TakeawaysBy genetically engineering the chimeric antigen receptor (CAR), T cells can be programmed to target new proteins that are markers of cancer, infectious diseases, and other important disorders.However, to realize this vision, more powerful CARs with better designs are needed - current CAR-T therapies have their restraints, including limited performance against solid tumors and lack of persistence and long-term efficacy in patients.An important part of the CAR response is “costimulation,” which is mediated by the 4-1BB or CD28 intracellular domains in all CARs currently in the clinic. Better designs of costimulatory domains could unlock the next-generation of CAR-T therapies.Since there are so many possibilities for costimulatory domain designs, it's difficult to test them all in the lab.Based on his experience in the Church Lab, Dan has developed tools to “multiplex” biological experiments; that is, to test multiple biological hypotheses in the same experiment and increase the screening power.Dan and his co-author Camillia Azimi developed “CAR Pooling”, a multiplexed approach to test many CAR designs at once.Using CAR Pooling, Dan tested 40 CARs with different costimulatory domains in pooled assays and identified several novel cosignaling domains from the TNF receptor family that enhance persistence or cytotoxicity over FDA-approved CARs.To characterize the different CARs, Dan also used RNA-sequencing.ImpactThe CAR Pooling approach may enable new, potent CAR-T therapies that can change the game for solid tumors and other cancers that are currently tough to treat.Highly multiplexed approaches like CAR Pooling will allow us to build highly complex, programmable systems and design the future of cell engineering beyond CAR-T.In addition to new therapeutics, high-throughput studies will allow us to understand the “design rules” of synthetic receptors and improve our understanding of basic immunology.Paper: Pooled screening of CAR T cells identifies diverse immune signaling domains for next-generation immunotherapies 

After noticing a weakness on the left side of her face, Tiffany McConathy and her husband Jeremy took their 9 month old daughter Nora to her Pediatrician in September of 2021. Nora's 1st diagnosis was Bell's Palsy. Six weeks later as Nora was feeling worse, Nora went back to the doctor and this time they were going to put tubes in her ears.Tiffany then insisted on an MRI and finally the 3rd of 4th doctor that Tiffany had spoken with agreed to it.What followed was a diagnosis of a very rare Brain and Spinal Cord tumor called ETMR. 5 months later Nora passed away as the doctors decided not to complete the treatment that she needed to at least give her a fighting chance, because Nora had Covid, with her main symptom being sneezing. After Nora passed away Tiffany was denied the opportunity to get a Research Autopsy again because of Covid, even though the CDC did not have a policy that  an autopsy like this could not be performed.Nora will also talk about the Nora's Princess Warrior's Foundation that she and Jeremy started to honor the memory of Nora, which is just in its infancy.

(2:55) - Researchers 3D Bioprint Breast Cancer TumorsThis episode was brought to you by Mouser, our favorite place to get electronic components for any project. Click HERE to learn more about how machine learning is being leveraged to more accurately detect cancer via imaging techniques.

Today's Song of the Day is "God Is A Circle" the new single from Yves Tumor, out now.

En nuestro episodio semanal del cuerpo habla lo que la boca calla vamos a dar esta información sobre la formación de los tumores y crecimiento glial dentro del cerebro. Déjanos tus comentarios y siguenos en Instagram quantum_gdl y Telegram en nuestro canal Centro Quantum.

To help prepare you for your PM&R Board Exams, we're bringing you a podcast series dedicated to current practices and core knowledge. Main Learning Objectives: • o Review common types of secondary bone tumors o Discuss pertinent imaging and additional work up for secondary bone tumors o Review physiatric management for patients with secondary bone tumors Credits: Episode was written and hosted by: Subha Hanif, MD and Jessica Cheng, MD This episode was reviewed for accuracy by: Jessica Cheng, MD and Ying Guo, MD This podcast series is directed by: Benjamin Gill, DO, MBA; Rosie Conic, MD, PhD; Sre Gorukanti, MD Please send feedback to aapdigitaloutreach@gmail.com so we can best suit your learning needs! Content for this series is based off of current PM&R learning materials and is created by residents for residents. It is not an official board review study guide.

Reacciones al discurso del Presidente Biden sobre el riesgo de la democracia en elecciones y aprovechó para lanzar pullas al partido Republicano y al  expresidente Trump.Powerball creció a $1.500 millones de dólares.Daniela Castro regresa a la tienda donde fue acusada de robo hace 4 años.Erika Buenfil, revela que tiene un fantasma en la casa.

Dr. Vamsi Velcheti and Dr. Benjamin Neel, of the NYU Langone Perlmutter Cancer Center, and Dr. John Heymach, of MD Anderson Cancer Center, discuss new therapeutic approaches for KRAS-mutant lung cancers and therapy options for RAS-altered tumors.   TRANSCRIPT Dr. Vamsidhar Velcheti: Hello, I'm Dr. Vamsidhar Velcheti, your guest host for the ASCO Daily News podcast today. I'm the medical director of the Thoracic Oncology Program at Perlmutter Cancer Center at NYU Langone Health. I'm delighted to welcome two internationally renowned physician-scientists, Dr. John Heymach, the chair of Thoracic-Head & Neck Medical Oncology at the MD Anderson Cancer Center, and my colleague, Dr. Benjamin Neel, the director of the Perlmutter Cancer Center at NYU Langone Health, and professor of Medicine at NYU Grossman School of Medicine. So, we'll be discussing new therapeutic approaches today for KRAS-mutant lung cancers, and we will talk about emerging new targeted therapy options for RAS-altered tumors. Our full disclosures are available in the show notes, and the disclosures of all the guests of the podcast can be found on our transcript at: asco.org/podcast. Dr. Heymach and Dr. Neel, it's such a great pleasure to have you here for the podcast today. Dr. John Heymach: My pleasure to be here. Dr. Benjamin Neel: Same here. Dr. Vamsidhar Velcheti: Dr. Neel, let's start off with you. As you know, RAS oncogenes were first discovered nearly four decades ago. Why is RAS such a challenging therapeutic target? Why has it taken so long to develop therapeutic options for these patients? Dr. Benjamin Neel: Well, I think a good analogy is the difference between kinase inhibitors and RAS inhibitors. So, kinase inhibitors basically took advantage of an ATP-binding pocket that's present in all kinases, but is different from kinase to kinase, and can be accessed by small molecule inhibitors. So, the standard approach that one would've thought of taking, would be to go after the GTP-binding pocket. The only problem is that the affinity for binding GTP by KRAS is three to four orders of magnitude higher. So, actually getting inhibitors that are GTP-binding inhibitors is pretty much very difficult. And then, until recently, it was felt that RAS was a very flat molecule and there weren't any surfaces that you could stick a small molecule inhibitor in. So, from a variety of biochemical and medicinal-pharmacological reasons, RAS was thought to be impervious to small molecule development. But as is often the case, a singular and seminal insight from a scientist, Kevan Shokat, really broke the field open, and now there's a whole host of new approaches to trying to drug RAS. Dr. Vamsidhar Velcheti: So, Dr. Neel, can you describe those recent advances in drug design that have enabled these noble new treatments for KRAS-targeted therapies? Dr. Benjamin Neel: So, it starts actually with the recognition that for many years, people were going after the wrong RAS. And by the wrong RAS, the overwhelming majority of the earlier studies on the structure, and for that matter, the function of RAS centered on HRAS or Harvey RAS. We just mutated in some cancers, most prominently, bladder cancer, and head & neck cancer, but not on KRAS, which is the really major player in terms of oncogenes in human cancer. So, first of all, we were studying the wrong RAS. The second thing is that we were sort of thinking that all RAS mutants were the same. And even from the earliest days, back in the late eighties, it was pretty clear that there were different biochemical properties in all different RAS mutants. But this sort of got lost in the cause and in the intervening time, and as a result, people thought all RASes were the same and they were just studying mainly G12V and G12D, which are more difficult to drug. And then, the third and most fundamental insight was the idea of trying to take advantage of a particular mutation in KRAS, which is present in a large fraction of lung cancer patients, which is, KRAS G12C. So, that's a mutation of glycine 12 to cysteine and Kevan's really seminal study was to use a library of covalently adducting drugs, and try to find ways to tether a small molecule in close enough so that it could hit the cysteine. And what was really surprising was when they actually found the earliest hits with this strategy, which was actually based on some early work by Jim Wells at Sunesis in the early part of this century, they found that it was actually occupying the G12C state or the inactive state of RAS. And this actually hearkens back to what I said earlier about all RASes being the same. And in fact, what's been recently re-appreciated is that some RAS mutants, most notably, G12C, although they're impervious to the gap which converts the active form into the inactive form, they still have a certain amount of intrinsic ability to convert from the inactive form. And so, they always cycle into the inactive form at some slow rate, and that allows them to be accessed by these small molecules in the so-called Switch-II Pocket, and that enables them to position a warhead close enough to the cysteine residue to make a covalent adduct and inactivate the protein irreversibly. Scientists at a large number of pharmaceutical companies and also academic labs began to understand how to access various other pockets in RAS, and also even new strategies, taking advantage of presenting molecules to RAS on a chaperone protein. So, there's now a whole host of strategies; you have a sort of an embarrassment of riches from an impoverished environment that we started with prior to 2012. Dr. Vamsidhar Velcheti: Thank you, Dr. Neel. So, Dr. Heymach, lung cancer has been a poster child for personalized therapy, and we've had like a lot of FDA-approved agents for several molecularly-defined subsets of lung cancer. How clinically impactful is a recent approval of Sotoracib for patients with metastatic lung cancer? Dr. John Heymach: Yeah. Well, I don't think it's an exaggeration to say this is the biggest advance for targeted therapies for lung cancer since the initial discovery of EGFR inhibitors. And let me talk about that in a little more detail. You know, the way that lung cancer therapy, like a lot of other cancer therapies, has advanced is by targeting specific driver oncogenes. And as Dr. Neel mentioned before, tyrosine kinases are a large percentage of those oncogenes and we've gotten very good at targeting tyrosine kinases developing inhibitors. They all sort of fit into the same ATP pocket, or at least the vast majority of them now. There are some variations on that idea now like allosteric inhibitors. And so, the field has just got better and better. And so, for lung cancer, the field evolved from EGFR to ALK, to ROS1 RET fusions, MEK, and so forth. What they all have in common is, they're all tyrosine kinases. But the biggest oncogene, and it's about twice as big as EGFR mutation, are KRAS mutations. And as you mentioned, this isn't a tyrosine kinase. We never had an inhibitor. And the first one to show that it's targetable, to have the first drug that does this, is really such an important breakthrough. Because once the big breakthrough and the concept is there, the pharmaceutical companies in the field can be really good at improving and modulating that. And that's exactly what we see. So, from that original insight that led to the design of the first G12C inhibitors, now there's dozens, literally dozens of G12C inhibitors and all these other inhibitors based on similar concepts. So, the first one now to go into the clinic and be FDA-approved is Sotoracib. So, this again, as you've heard, is inhibitor G12C, and it's what we call an irreversible inhibitor. So, it fits into this pocket, and it covalently links with G12C. So, when it's linked, it's linked, it's not coming off. Now, the study that led to its FDA approval was called the CodeBreak 100 study. And this was led in part, by my colleague Ferdinandos Skoulidis, and was published in The New England Journal in the past year. And, you know, there they studied 126 patients, and I'll keep just a brief summary, these were all refractory lung cancer patients. They either had first-line therapy, most had both chemo and immunotherapy. The primary endpoint was objective response rate. And for the study, the objective response rate was 37%, the progression-free survival was 6.8 months, the overall survival was 12.5 months. Now you might say, well, 37%, that's not as good as an EGFR inhibitor or the others. Well, this is a much harder thing to inhibit. And you have to remember in this setting, the standard of care was docetaxel chemotherapy. And docetaxel usually has a response rate of about 10 to 13%, progression-free survival of about 3 months. So, to more than double that with a targeted drug and have a longer PFS really is a major advance. But it's clear, we've got to improve on this and I think combinations are going to be incredibly important now. There's a huge number of combination regimens now in testing. Dr. Vamsidhar Velcheti: Thank you, Dr. Heymach. So, Dr. Neel, just following up on that, unlike other targeted therapies in lung cancer, like EGFR, ALK, ROS, and RET, the G12C inhibitors appear to have somewhat modest, I mean, though, certainly better than docetaxel that Dr. Heymach was just talking about; why is it so hard to have more effective inhibitor of KRAS here? Is it due to the complex nature of RAS-mutant tumors? Or is it our approach for targeting RAS? Is it a drug-related problem, or is it the disease? Dr. Benjamin Neel: Well, the short answer is I think that's a theoretical discussion at this point and there isn't really good data to tell you, but I suspect it's a combination of those things. We'll see with the new RAS(ON) inhibitors, which seem to have deeper responses, even in animal models, if those actually work better in the clinic, then we'll know at least part of it was that we weren't hitting RAS hard enough, at least with the single agents. But I also think that it's highly likely that since KRAS-mutant tumors are enriched in smokers, and smokers have lots of mutations, that they are much more complex tumours, and therefore there's many more ways for them to escape. Dr. Vamsidhar Velcheti: Dr. Heymach, you want to weigh in on that? Dr. John Heymach: Yeah, I think that's right. I guess a couple of different ways to view it is the problem that the current inhibitors are not inhibiting the target well enough, you know, in which case we say we get better and better inhibitors will inhibit it more effectively, or maybe we're inhibiting it, but we're not shutting down all the downstream pathways or the feedback pathways that get turned on in response, in which case the path forward is going to be better combinations. Right now, I think the jury is still out, but I think the data supports that we can do better with better inhibitors, there's room to grow. But it is also going to be really important hitting these compensatory pathways that get turned on. I think it's going to be both, and it seems like KRAS may turn on more compensatory pathways earlier than things like EGFR or ALK2, you know, and I think it's going to be a great scientific question to figure out why that is. Dr. Vamsidhar Velcheti: Right. And just following up on that, Dr. Heymach, so, what do we know so far about primary and acquired resistance to KRAS G12C inhibitors? Dr. John Heymach: Yeah. Well, it's a great question, and we're still very early in understanding this. And here, if we decide to call it primary resistance - meaning you never respond in the first place, and acquired - meaning you respond and then become resistant, we're not sure why some tumors do respond and don't respond initially. Now, it's been known for a long time, tumors differ in what we call their KRAS-dependence. And in cell lines and in mouse models, when you study this in the lab, there are some models where if you block KRAS, those cells will die immediately. They are fully dependent. And there's other ones that become sort of independent and they don't really seem to care if you turn down KRAS, they've sort of moved on to other things they're dependent on. One way this can happen is with undergoing EMT where the cell sort of changes its dependencies. And EMT is probably a reason some of these tumors are resistant, to start with. It may also matter what else is mutated along with KRAS, what we call the co-mutations, the additional mutations that occur along with it. For example, it seems like if this gene KEAP1 is mutated, tumors don't respond as well, to begin with. Now, acquired resistance is something we are gaining some experience with. I can say in the beginning, we all knew there'd be resistance, we were all waiting to see it, and what we were really hoping for was the case like with first-generation inhibitors with EGFR, where there was one dominant mechanism. In the first-generation EGFR, we had one mutation; T790M, that was more than half the resistance. And then we could develop drugs for that. But unfortunately, that's not the case. It looks like the resistance mechanisms are very diverse, and lots of different pathways can get turned on. So, for acquired resistance, you can have additional KRAS mutations, like you can have a KRAS G12D or V, or some other allele, or G13, I didn't even realize were commonly mutated, like H95 or Y96 can get mutated as well. So, we might be able to inhibit with better inhibitors. But the more pressing problem is what we call bypass; when these other pathways get turned on. And for bypass, we know that the tumor can turn on MET with MET amplification, NRAS, BRAF, MAP kinase, and we just see a wide variety. So, it's clear to us there isn't going to be a single easy to target solution like there was for EGFR. This is going to be a long-term problem, and we're going to have to work on a lot of different solutions and get smarter about what we're doing. Dr. Vamsidhar Velcheti: Yeah. Thank you very much, Dr. Heymach. And Dr. Neel, just following up on that, so, what do you think our strategies should be or should look like while targeting KRAS-mutant tumors? Like, do we focus on better ways to inhibit RAS, or do we focus on personalized combination approaches based on various alterations or other biomarkers? Dr. Benjamin Neel: Yeah. Well, I'd like to step back a second and be provocative, and say that we've been doing targeted therapies, so to speak, for a long time, and it's absolutely clear that targeted therapies never cure. And so, I think we should ask the bigger question, "Why is it that targeted therapies never cure?" And I would start to conceive of an answer to that question by asking which therapies do cure. And the therapies that we know do cure are immune therapies, or it's therapies that generate durable immune response against the tumor. And the other therapies that we know that are therapies in some cases against some tumors, and radiation therapy in some cases against some tumors. Probably the only way that those actually converge on the first mechanism I said that cures tumors, which is generating a durable immune response. And so, the only way, in my view, it is to durably cure an evolving disease, like a cancer, is to have an army that can fight an evolving disease. And the only army I know of is the immune system. So, I think ultimately, what we need to do is understand in detail, how all of these different mutations that lead to cancer affect immune response and create targetable lesions in the immune response, and then how the drugs we'd give affect that. So, in the big picture, the 50,000-foot picture, that what we really need to spend more attention on, is understanding how the drugs we give and the mutations that are there in the first place affect immune response against the tumor, and ultimately try to develop strategies that somehow pick up an immune response against the tumor. Now in the short run, I think there's also lots of combination strategies that we can think of, John, you know, alluded to some of them earlier. I mean one way for the G12C inhibitors, getting better occupancy of the drug, and also blocking this so-called phenomenon of adaptive resistance, where you derepress the expression of receptor tyrosine kinases, and their ligands, and therefore bypass through normal RAS or upregulate G12C into the GTP state more, that can be attacked by combining, for example, with the SHIP2 inhibitor or a SOS inhibitor. Again, the issue there will be therapeutic index. Can we achieve that with a reasonable therapeutic index? Also in some cases, like not so much in lung cancer, but in colon cancer, it appears as if a single dominant receptor tyrosine kinase pathway, the EGF receptor pathway, is often the mechanism of adaptive resistance to RAS inhibitors, and so, combining a RAS inhibitor with an EGF receptor inhibitor is a reasonable strategy. And then of course, some of the strategies they're already getting at, what I just mentioned before, which is to try to combine RAS inhibitors with checkpoint inhibitors. I think that's an expected and understandable approach, but I think we need to get a lot more sophisticated about the tumor microenvironment, and how that's affecting the immune response. And it's not just going to be, you know, in most cases combining with a checkpoint inhibitor. I think we ought to stop using the term immunotherapy to refer to checkpoint inhibitors. Checkpoint inhibitors are one type of immunotherapy. We don't refer to antibiotics when we mean penicillin. Dr. Vamsidhar Velcheti: Dr. Heymach, as you know, like, there's a lot of discussion about the role of KRAS G12C inhibitors in the frontline setting. Do you envision these drugs are going to be positioning themselves in the frontline setting as a combination, or like as a single agent? Are there like a subset of patients perhaps where you would consider like a single agent up front? Dr. John Heymach: So, I think there's no question G12C inhibitors are moving to the first-line question. And the question is just how you get there. Now, the simplest and most straightforward approach is to say, “Well, we'll take our standard and one standard might be immunotherapy alone, a PD-1 inhibitor alone, or chemo with the PD-1 inhibitor, and just take the G12C inhibitor and put it right on top.” And that's a classic strategy that's followed. That may not be that simple. It's not obvious that these drugs will always work well together or will be tolerated together. So, I think that's still being worked out. Now, an alternative strategy is you could say, “Well, let's get a foot in a door in the first-line setting by finding where chemotherapy and immunotherapy don't work well, and pick that little subgroup.” There are some studies there using STK11-mutant tumors, and they don't respond well to immunotherapy and chemotherapy and say, “Well, let's pick that first.” And that's another strategy, but that's not to get it for everybody in the first-line setting. That's just to pick a little subgroup. Or we may develop KRAS G12C inhibitor combinations by themselves that are so effective they can beat the standard. So, what I think is going to happen is a couple things; I think they'll first be some little niches where it gets in there first. I think eventually, we'll figure out how to combine them with chemotherapy and immunotherapy so it goes on top. And then I think over time, we'll eventually develop just more effective, targeted combos where we can phase out the chemo, where the chemo goes to the back of the line, and this goes to the front of the line. Dr. Vamsidhar Velcheti: And Dr. Heymach, any thoughts on the perioperative setting and the adjuvant/neoadjuvant setting, do you think there's any role for these inhibitors in the future? Dr. John Heymach: Yeah, this is a really exciting space right now. And so that makes this a really challenging question because of how quickly things are moving. I'll just briefly recap for everybody. Until recently, adjuvant therapy was just chemotherapy after you resected a lung cancer. That was it. And it provided about a 5% benefit in terms of five-year disease-free survival. Well, then we had adjuvant immunotherapy, like atezolizumab, approved, then we had neoadjuvant chemo plus immunotherapy approved; that's a CheckMate 816. And just recently, the AEGEAN study, which I'm involved with, was announced to be a positive study. That's neoadjuvant plus adjuvant chemo plus immunotherapy. So now, if you say, well, how are you going to bring a G12C inhibitor in there? Well, you can envision a few different ways; if you can combine with chemo and immunotherapy, you could bring it up front and bring it afterwards, or you could just tack it in on the back, either with immunotherapy or by itself, if you gave neoadjuvant chemo plus immunotherapy first, what we call the CheckMate 816 regimen. So, it could fit in a variety of ways. I'll just say neoadjuvant is more appealing because you can measure the response and see how well it's working, and we in fact have a neoadjuvant study going. But the long-term benefit may really come from keeping the drug going afterwards to suppress microscopic metastatic disease. And that's what I believe is going to happen. I think you're going to need to stay on these drugs for a long while to keep that microscopic disease down. Dr. Vamsidhar Velcheti: Dr. Neel, any thoughts on novel agents in development beyond KRAS G12C inhibitors? Are there any agents or combinations that you'd be excited about? Dr. Benjamin Neel: Well, I think that the YAP/TAZ pathway inhibitors, the TEAD inhibitors in particular, are potentially promising. I mean, it seems as if the MAP kinase pathway and the GAPT pathway act in parallel. There's been multiple phases which suggest that YAP/TAZ reactivation can be a mechanism of sort of state-switching resistance. And so, I think those inhibitors are different than the standard PI3 kinase pathway inhibitor, PI3 kinase mTOR inhibitor, rapamycin. I also think as we've alluded to a couple of times, the jury's still out in the clinic, of course, but it'll be very exciting to see how this new set of RAS inhibitors works. The sort of Pan-RAS inhibitors, especially the ones that hit the GTP ON state. So, the G12C inhibitors and the initial preclinical G12D inhibitors that have been recorded, they all work by targeting the inactive state of RAS, the RAS-GDP state. And so, they can only work on mutants that cycle, at least somewhat, and they also don't seem to be as potent as targeting the GTP or active state of RAS. And so, at least the Rev meds compounds, which basically use cyclophilin, they basically adapt the mechanism that cyclosporine uses to inhibit calcineurin. They basically use the same kind of a strategy and build new drugs then that bind cyclophilin and present the drug in a way that can inhibit multiple forms of RAS. So, it'll be interesting to see if they are much more efficacious in a clinic as they appear to be in the lab, whether they can be tolerated. So, I think those are things to look out for. Dr. Vamsidhar Velcheti: Dr. Heymach? Dr. John Heymach: Yeah, I agree with that. I'm excited to see that set of compounds coming along. One of the interesting observations is that when you inhibit one KRAS allele like G12C, you get these other KRAS alleles commonly popping up. And it's a little -- I just want to pause for a second to comment on this, because this is a little different than EGFR. If you inhibit a classic mutation, you don't get multiple other separate EGFR alleles popping up. You may get a secondary mutation in cyst on the same protein, but you don't get other alleles. So, this is a little different biology, but I think the frequency that we're seeing all these other KRAS alleles pop up tells us, I think we're going to need some pan-KRAS type strategy as a partner for targeting the primary driver. So for example, a G12C inhibitor plus a pan-KRAS strategy to head off these other alleles that can be popping up. So, I think that's going to be probably a minimum building block that you start putting other things around. And by partnering an allele-specific inhibitor where you might be able to inhibit it a little more potently and irreversibly with a pan-KRAS, you may solve some of these problems at the therapeutic window. You can imagine KRAS is so important for so many different cells in your body that if you potently inhibit all KRAS in your body, bad things are likely to happen somewhere. But if you can potently inhibit the mutant allele and then dampen the other KRAS signaling that's popping up, it's more hopeful. Dr. Benjamin Neel: There is a mouse model study from Mariano Barbacid's lab, which suggests that postnatal, KRAS at least, complete inhibition is doable. So, you could take out KRAS postnatally and the mice are okay. Whether that translates to human of course, is not at all clear. And you still have the other RAS alleles, the HRAS, the NRAS that you'd still have to contend with. Dr. John Heymach: Yeah, it's an interesting lesson. We've shied away from a lot of targets we thought weren't feasible. I did a lot of my training with Judah Folkman who pioneered targeting angiogenesis. And I remember hearing this idea of blocking new blood vessels. I said, "Well, everyone is just going to have a heart attack and die." And it turns out you can do it. You have to do it carefully, and in the right way but you can separate malignant or oncogenic signaling from normal signaling in an adult, pretty reasonably in a lot of cases where you don't think you could. Dr. Vamsidhar Velcheti: All right. So, Dr. Neel, and Dr. Heymach, any final closing comments on the field of RAS-targeted therapies, you know, what can we hope for? What can patients hope for, let's say five years from now, what are we looking at? Dr. John Heymach: Well, I'll give my thoughts I guess first, from a clinical perspective, I think we're already seeing the outlines of an absolute explosion in targeting KRAS over the next five years. And I think there's a really good likelihood that this is going to be the major place where we see progress, at least in lung cancer, over these next five years. It's an example of a problem that just seemed insolvable for so long, and here I really want to acknowledge the sustained support for clinical research and laboratory research focused around RAS. You know, the NCI had specific RAS initiatives and we've had big team grants for KRAS, and it shows you it's worth these large-scale efforts because you never know when that breakthrough is going to happen. But sometimes it just takes, you know, opening that door a little bit and everybody can start rushing through. Well, I think for KRAS, the door has been opened and everybody is rushing through at a frantic rate right now. So, it's really exciting, and stay tuned. I think the landscape of RAS-targeting is going to look completely different five years from now. Dr. Benjamin Neel: So, I agree that the landscape will definitely look different five years from now, because it's reflective of stuff that's been in process for the last five years. And it takes about that long to come through. I want to make two comments; one of which is to slightly disagree with my friend, John, about these big initiatives. And I would point out that this RAS breakthrough did not come from a big initiative, it came from one scientist thinking about a problem uniquely in a different way. We need a basic science breakthrough, it almost always comes from a single lab person, thinking about a problem, often in isolation, in his own group. What big initiatives can help with is engineering problems. Once you've opened the door, and you want to know what the best way is to get around the house, then maybe big initiatives help. But I do think that there's been too much focus on the big team initiative and not enough on the individual scientists who often promote the breakthrough. And then in terms of where I see the field going, what I'd really like to see, and I think in some pharmaceutical companies and biotechs, you're seeing this now, and also in academia, but maybe not enough, is that sort of breaking down of the silos between immunotherapy and targeting therapy. Because I agree with what John said, is that targeted therapy, is just sophisticated debulking. If we want to really make progress-- and on the other hand, immunotherapy people don't seem to, you know, often recognize that these oncogenic mutations in the tumor actually affect the immune system. So, I think what we need is a unification of these two semi-disparate areas of therapeutics in a more fulsome haul and that will advance things much quicker. Dr. Vamsidhar Velcheti: Thank you both, Dr. Neel and Dr. Heymach, for sharing all your valuable insights with us today on the ASCO Daily News podcast. We really appreciate it. Thank you so much. Dr. John Heymach: Thanks for asking us. Dr. Benjamin Neel: It's been great having us. Dr. Vamsidhar Velcheti: And thank you all to our listeners, and thanks for joining us today. If you value our insights that you hear on the ASCO Daily News podcast, please take a moment to rate, review and subscribe. Disclaimer: The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy, should not be construed as an ASCO endorsement. Follow today's speakers: Dr. Vamsi Velcheti @VamsiVelcheti Dr. Benjamin Neel @DrBenNeel Dr. John Heymach Want more related content? Listen to our podcast on novel therapies in lung cancer.    Advances in Lung Cancer at ASCO 2022 Follow ASCO on social media: @ASCO on Twitter ASCO on Facebook ASCO on LinkedIn Disclosures: Dr. Vamsi Velcheti: Honoraria: Honoraria Consulting or Advisory Role: Bristol-Myers Squibb, Merck, Foundation Medicine, AstraZeneca/MedImmune, Novartis, Lilly, EMD Serono, GSK, Amgen Research Funding (Inst.): Genentech, Trovagene, Eisai, OncoPlex Diagnostics, Alkermes, NantOmics, Genoptix, Altor BioScience, Merck, Bristol-Myers Squibb, Atreca, Heat Biologics, Leap Therapeutics, RSIP Vision, GlaxoSmithKline Dr. Benjamin Neel: None disclosed Dr. John Heymach: None disclosed    

In a new James clinical trial, the influenza vaccine is injected directly into the melanoma of a patient. In this episode, Contreras, a James surgical oncologist, explains how he expanded upon a basic concept that has been around for decades to create this clinical trial. The idea is that while the influenza vaccine will not have a direct effect on the melanoma, “it puts the entire immune system on high alert and it is better able to recognize any foreign cells in the body, which in this case are the melanoma cells,” he said. The clinical trial started a few months ago and enrolls patients with both early-stage and later-stage melanomas. For the patients with early-stage melanomas, the vaccine is administered before surgery, with the hope that it will shrink the tumor. For patients with the later stages of this disease, the vaccine is combined with immunotherapy “to augment and further enhance what we're already doing,” Contreras said. Because the clinical trial is in the early stages, regulations prohibit Contreras from discussing the specific results. However, he said he remains hopeful the influenza vaccine will be an effective form of treatment for patients with melanomas, could see application around the world, especially in poorer countries, and could potentially be used to treat other forms of cancer.

(00:32) Could you provide a little bit of background about yourself?(01:43) Could you give a brief overview of the new melanoma assay?(04:53) Is the assay able to provide diagnostic, prognostic and classification information, and potential therapeutic implications?(05:12) Could you talk a little more about the MSI assessment in this panel? (05:59) Which patients should have this testing?(07:01) How are these results used in patient care?(08:39) Is there anything else you'd like to add?

Dr Pamela Kunz from the Yale Cancer Center in Palo Alto, California, discusses recent therapeutic advances in neuroendocrine tumors. CME information and select publications here (http://www.researchtopractice.com/OncologyTodayNeuroendocrine22).

In this episode, host Alyssa Watson, DVM, welcomes back Sarah Boston, DVM, DVSc, DACVS, to talk about her recent Clinician's Brief article, “Incisional Biopsy of Oral Tumors.” Dr. Boston explains why tissue biopsy is definitively better than aspiration of oral tumors and shares some good tips for how to get the most out of your samples. She also discusses how to set the specialist up for success when you're planning on referring and reminds us about what else we could be doing at the time of biopsy.Resource:https://www.cliniciansbrief.com/article/incisional-biopsy-oral-tumorsContact us:Podcast@briefmedia.comWhere to find us:Cliniciansbrief.com/podcastsFacebook.com/clinciansbriefTwitter: @cliniciansbriefInstagram: @clinicians.briefThe Team:Alyssa Watson, DVM - HostAlexis Ussery - Producer & Digital Content CoordinatorRandall Stupka - Podcast Production & Sound Editing

What is a soft tissue sarcoma? Soft tissue sarcomas are a broad category of tumors including those that arise from the connective, muscle, or nervous tissues in dogs and cats. These tumors are the result of abnormal production of these cell types in an uncontrolled manner. Connective, muscle, and nervous tissues are present throughout the entire body; therefore, these tumors can develop over the chest, back, side, legs, and facial tissues of your pet. Soft tissue sarcomas make up about 15% of cancers of the skin affecting dogs and about 7% of those affecting cats. Fibrosarcomas are common in dogs and are a type of soft tissue sarcoma (see handout "Fibrosarcoma in Dogs" for more information). "Soft tissue sarcomas make up about 15% of cancers of the skin affecting dogs and about 7% of those affecting cats." Even though soft tissue tumors arise from many different types of cells, they all behave in a similar manner and their treatment is typically the same. What causes soft tissue sarcomas? The reason why a particular pet may develop this, or any tumor or cancer, is not straightforward. Very few tumors and cancers have a single known cause. Most seem to be caused by a complex mix of risk factors, some environmental and some genetic or hereditary. For most cases of soft tissue sarcomas, no direct cause has been determined for their development. Sarcomas at injection sites occur in cats but are rare in dogs (see handout “Post-Vaccination Sarcoma in Cats” for further information on this type of sarcoma). In cats exposed to a form of the feline leukemia virus (called feline sarcoma virus), the development of sarcomas on the head and neck sometimes occurs. What are the clinical signs of soft tissue sarcomas? The clinical signs depend on where the tumor is located and the tissues that are affected. Often, pets have a noticeable mass that is growing in size. Signs associated with soft tissue sarcomas include the following: Pets that have tumors arising from muscle tissue may show signs of pain in the affected region and may have a distinct firm and growing mass (tumor). Tumors that are located on the limbs may cause changes in your pet's ability to walk and the limbs may have obvious swelling. Pets that have tumors arising from nervous tissue may be unable to use the affected limb or may show other neurological signs. Pets with intestinal tumors may have signs of an intestinal blockage, such as vomiting, diarrhea, lack of appetite, weight loss, and abdominal pain. Pets with soft tissue sarcomas in the mouth often have halitosis (bad breath), difficulty eating, loss of appetite, bleeding in the mouth, or obvious tumors in the mouth. Signs of a soft tissue sarcoma affecting the reproductive system depend on the location of the tumor. For example, if the prostate is affected, difficulty with urinating or defecating may be observed. How are soft tissue sarcomas diagnosed? In some cases, a fine needle aspiration (FNA) may be performed. FNA involves taking a small needle with a syringe to suction a sample of cells directly from the tumor and placing them on a microscope slide. A veterinary pathologist then examines the slide under a microscope. If a diagnosis is not confirmed by this method, a biopsy may be needed. A biopsy is a surgical excision of a piece of the tumor. Pieces of the tumor are then examined under the microscope. This is called histopathology. A biopsy is beneficial because it gives an indication as to how aggressive the tumor is and how its treatment should be approached. Staging (searching for potential spread to other locations in the body) may be recommended. This may include blood work, urinalysis, radiographs (X-rays) of the lungs, and possibly an abdominal ultrasound. If any lymph nodes are enlarged or feel abnormal, further sampling may be pursued to determine if any spread is present. "If any lymph nodes are enlarged or feel abnormal, further sampling may be pursued to determine if any spread is present." How do these tumors typically progress? This is entirely dependent on the location and grade of the tumor. Typically, the higher the grade (these tumors are graded from I to III) the more likely that spread is possible. However, one of the biggest concerns with soft tissue sarcomas is their ability to invade the local surrounding tissues. They can almost be described as an 'octopus', where the bulk of the tumor is the head and the microscopic cells that invade the surrounding tissue are like small tentacles. These ‘tentacles' become challenging to treat when managing your pet's tumor, either by surgery or radiation therapy. "...one of the biggest concerns with soft tissue sarcomas is their ability to invade the local surrounding tissues." What are the treatments for these types of tumors? The most commonly pursued treatment for all soft tissue sarcomas is surgery. Because these tumors typically produce ‘tentacles' of abnormal cells, wide margins (the amount of tissue that needs to be removed) must be obtained for the best control of the tumor. If microscopic cells are left behind after surgery, recurrence of the tumor is much more likely. If cells are left behind (determined through histopathology), either a second surgery or a combination of surgery and radiation therapy may be pursued. Chemotherapy is not usually pursued as a primary treatment unless surgery or radiation are not options for your pet based on the tumor size or location. Chemotherapy may be an option after surgery. Metronomic chemotherapy (daily administration of lower doses of chemotherapy rather than traditional schedules) may be recommended. These therapies will be discussed with you if they are relevant to your pet's particular type of sarcoma.

En el Mes internacional del Cáncer de Hígado, hablamos con la jefa de Servicio de Oncología Médica del Complejo Hospitalario de Navarra, la doctora Ruth Vera, y con el director de la Unidad de Hepatología de la Clínica Universidad de Navarra, el doctor Bruno Sangro. 

Show Notes Radioactive implant wipes tumors in unprecedented pre-clinical success | New Atlas (00:52) Pancreatic cancer is notoriously difficult to diagnose and treat, with tumor cells of this type highly evasive and loaded with mutations that make them resistant to many drugs.  3.2 percent of all cancers, yet is the third leading cause of cancer-related death Engineers at Duke University have developed a novel delivery system for cancer treatment and demonstrated its potential against one of the disease's most troublesome forms A radioactive implant completely eliminated tumors in the majority of the rodents The team wanted to figure out a way to implant into the tumor without causing damage to the surrounding tissue. Created one from more biocompatible materials (instead of titanium)  that wouldn't post the same risks to the human body. Synthetic chains of amino acids known as elastin-like polypeptides (ELPs), which form a stable gel-like material in the warmer environment of the body. This substance was injected into tumors in various mouse models of pancreatic cancer along with a radioactive element called iodine-131. ELP entombs the iodine-131 and prevents it from leaking into the body. Allows it to emit beta radiation that penetrates into the surrounding tumor. Once the radiation is spent, the ELP biogel safely degrades into harmless amino acids. The treatment was tested in combination with a common chemotherapy drug called paclitaxel. Across all the models tested, the scientists report a 100% response rate to the treatment.  In three quarters of the models, the dual treatment completely eliminated the tumors 80% of the time. The scientists deployed the novel treatment against pancreatic cancer because they wanted to explore its potential against one of the trickiest forms of the disease, but believe these results bode well for its wider application. Study author Jeff Schaal, explains the significance of their finding: “We did a deep dive through over 1,100 treatments across preclinical models and never found results where the tumors shrank away and disappeared like ours did … When the rest of the literature is saying that what we're seeing doesn't happen, that's when we knew we had something extremely interesting." In a first, scientists grow fully mature hair follicles in cultures | Interesting Engineering (07:12) According to a press release, researchers from Japan generated hair follicles in cultures while working on the processes of hair follicle growth and hair pigmentation.  Could contribute to the development of different applications such as hair loss treatment, animal testing and drug screenings. Scientists have been trying to understand the essential mechanisms of hair follicle development through animal models for a long while. Hair follicle morphogenesis wasn't something that could be reproduced in a culture dish until now. Morphogenesis is the process when the outer layer of skin and the connective tissue interacts while the embryo develops. Researchers built hair follicle organoids by controlling the structure generated from the two types of embryonic cells tapping into a low concentration of extracellular matrices. Extracellular matrix is a network that supplies structure for cells and tissue in the body. These matrices change the spacing between the two types of embryonic cells from a dumbbell-shape to core-shell configuration.  Fully mature hair follicles with approximately 3 millimeter (mm)-long hair shafts were produced by the hair follicle organoids on the 23rd day of being cultured. Researchers included a melanocyte-stimulating drug that helps produce hair color pigmentation in the culture medium.  The findings could help understand how physiological and pathological processes develop in relation to other organ systems as well.  Junji Fukuda, a professor with the faculty of engineering at Yokohama National University, speaks on next steps: “Our next step is to use cells from human origin, and apply for drug development and regenerative medicine.” Team uses live plant cells in 3D printing | Futurity (11:35) Researchers have developed a reproducible way of studying cellular communication among varied types of plant cells by “bioprinting” those cells with a 3D printer. Communication is key to understanding more about plant cell functions. Could ultimately lead to creating better crop varieties and optimal growing environments. They bioprinted cells from the model plant Arabidopsis thaliana and from soybeans to study not just whether plant cells would live after being bioprinted but also how they acquire and change their identity and function.  Lisa Van den Broeck, first author of a paper, describes the work: “A plant root has a lot of different cell types with specialized functions … There are also different sets of genes being expressed; some are cell-specific. We wanted to know what happens after you bioprint live cells and place them into an environment that you design. Are they alive and doing what they should be doing?” Live plant cells without cell walls, or protoplasts, were bioprinted along with nutrients, growth hormones, and a thickening agent called agarose. Agarose helps provide cells strength and scaffolding “When you print the bioink, you need it to be liquid, but when it comes out, it needs to be solid. Mimicking the natural environment helps keep cellular signals and cues occurring as they would in soil,” explained  Professor Ross Sozzani, co-corresponding author of the paper. The research showed that more than half of the 3D bioprinted cells were viable and divided over time to form microcalli, or small colonies of cells. Also bioprinted individual cells to test whether they could regenerate, or divide and multiply, which showed that Arabidopsis root and shoot cells needed different combinations of nutrients and scaffolding for optimal viability. More than 40% of individual soybean embryonic cells remained viable two weeks after bioprinting and also divided over time to form microcalli. End off with Professor Sozzani: “All told, this study shows the powerful potential of using 3D bioprinting to identify the optimal compounds needed to support plant cell viability and communication in a controlled environment,”  IKEA Is Using Driverless Trucks to Move Its Furniture in Texas | SIngularity Hub (18:49) Thanks to its mild climate, expansive highway network, and lax regulations, Texas has become the country's proving ground for driverless trucks. traveling the state's highways partially driver-free for a couple of years already autonomous mode on highways, but safety drivers take over to navigate city streets This week Kodiak Robotics announced a partnership to transport IKEA products using a heavy-duty self-driving truck. The route runs from an IKEA distribution center in Baytown, east of Houstin, to a store in Frisco, 290 miles away just north of Dallas. Kodiak has been around since 2018, and is focused on building a technology stack specifically for long-haul trucks.  Use a modular hardware approach that includes easy-to-install “mirror pods” with lidar and cameras. Seems like this company is on the rise with self driving trucks partnerships in place with CEVA Logistics and U.S. Express In August announced an agreement with Pilot Companies to develop services for self-driving trucks at Pilot and Flying J travel centers.  Kodiak's founder and CEO Don Burnette hopes the IKEA pilot will lead to a long-term relationship between the two companies, and an expansion of delivery routes for the furniture store.  Burnette told Forbes: “Up until now we've primarily been working with other carriers who work on behalf of shippers as their customers, and this is the first time we're working with a shipper directly … It was a really good opportunity to build that relationship and understand their operational needs.” New VR app lets you step inside your smartphone videos | Freethink (24:40) Startup Wist Labs is developing a VR app that converts your smartphone clips into 3D videos — giving you a chance to walk inside your memories using a VR headset. To create a memory with Wist, a user opens the app and records a video.  The app collects the information it needs to make the 2D clip look three-dimensional. Co-founder Andrew McHugh explained to Freethink: “During capture, we save color, depth, device pose, audio, and scene information … Depth is captured using the LiDAR sensors on the Pro model iPhones and iPads.” Once the app processes the video, the user can play it back using mobile AR or a VR headset. Video example of how it works  The next steps for Wist Labs are to close pre-seed funding, launch a beta, and then roll out features to fill in those gaps and improve the app.  McHugh plans to continue using it to capture and share memories of his first child McHugh explaining how the experience has been using it: “I loaded [an ultrasound video] into our VR app, shared it with my mom who lives halfway across the country, and we were able to both walk around that moment together … It's better than a video because it feels like you're actually there.”

Comedian, Kimbles Hume, discusses experiencing 3 miscarriages, IVF, finding a tumor in her spine, a son with epilepsy and taking up 28 painkillers per day. Sponsor:Is there something interfering with your happiness or is preventing you from achieving your goals? https://betterhelp.com/leo and enjoy 10% off your first month and start talking to mental health professional today!! 1-on-1 Coaching: If you want go from feeling hopeless to hopeful, lonely to connected and like a burden to a blessing, then go to 1-on-1 coaching, go to www.thrivewithleo.com. Let's get to tomorrow, together. National Suicide Prevention Lifeline800-273-TALK [800-273-8255]1-800-SUICIDE [800-784-2433]Teen Line (Los Angeles)800-852-8336The Trevor Project (LGBTQ Youth Hotline)866-488-7386National Domestic Violence Hotline800-799-SAFE [800-799-7233]Crisis Text LineText "Connect" to 741741 in the USALifeline Chathttps://suicidepreventionlifeline.org/chat/International Suicide Hotlines: http://www.suicide.org/international-suicide-hotlines.htmlhttps://www.nowmattersnow.org/skillshttps://sobermeditations.libsyn.com/ www.suicidesafetyplan.com https://scaa.club/

In this episode, Dr. Daniel Correa speaks with author and podcast host, Nora McInerny. Nora discusses her husband's terminal brain tumor (glioblastoma multiforme) diagnosis, how they confronted his illness together, and her journey moving forward with grief upon his passing. Next, Dr. Correa talks with Dr. Maisha Robinson, neurologist and assistant professor in the department of neurology at Mayo Clinic Jacksonville where she established the clinic's first neuropalliative care program. Dr. Robinson explains what palliative care is and how families can support their loved ones in preparing for end-of-life care. Additional Resources:   https://noraborealis.com/ https://ttfa.org/ https://www.brainandlife.org/disorders-a-z/disorders/brain-and-spinal-tumors https://www.brainandlife.org/articles/the-411-on-palliative-and-hospice-care https://www.brainandlife.org/articles/sadness-at-the-death-of-a-family-member-has-both https://988lifeline.org/current-events/the-lifeline-and-988/ Social Media:   Guest: @noraborealis (Twitter and Instagram) Hosts: Dr. Daniel Correa @neurodrcorrea; Dr. Audrey Nath @AudreyNathMDPhD 

To help prepare you for your PM&R Board Exams, we're bringing you a podcast series dedicated to current practices and core knowledge. Main Learning Objectives: • Discuss various types of primary bone tumors found in the pediatric population • Describe the presentation for different primary bone tumors • Review Physiatric management for a patient following a primary bone tumor diagnosis Credits: Episode was written and hosted by: Subha Hanif, MD and Jessica Cheng, MD This episode was reviewed for accuracy by: Jessica Cheng, MD and Ying Guo, MD This podcast series is directed by: Benjamin Gill, DO, MBA; Rosie Conic, MD, PhD; Sre Gorukanti, MD Please send feedback to aapdigitaloutreach@gmail.com so we can best suit your learning needs! Content for this series is based off of current PM&R learning materials and is created by residents for residents. It is not an official board review study guide.

In this episode, we invite Dr. Amir Ali, PharmD, BCOP to discuss with us the pathophysiology, risk factors, prevention, and treatment clinical pearls of tumor lysis syndrome TLS). Key Concepts TLS is caused by rapid cell death of cancerous cells that results in intracellular contents “spilling” into the blood – this leads to high serum uric acid, high serum potassium, high serum phosphate, and LOW calcium. These laboratory abnormalities cause acute kidney injury (via crystal formation in the kidney), arrhythmias (from hyperkalemia), and seizures (from high phosphate and low calcium). Patients at highest risk for TLS are those with hematologic malignancies (lymphomas and leukemias), especially if WBC or LDH labs are very high. Prevention is the Key! The primary prevention approach for TLS is hydration, allopurinol, and sometimes a low dose of rasburicase. The treatment of TLS involves more aggressive hydration and rasburicase. References Coiffier B, Altman A, Pui CH, Younes A, Cairo MS. Guidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based review [published correction appears in J Clin Oncol. 2010 Feb 1;28(4):708]. J Clin Oncol. 2008;26(16):2767-2778. doi:10.1200/JCO.2007.15.0177 Cairo MS, Coiffier B, Reiter A, Younes A; TLS Expert Panel. Recommendations for the evaluation of risk and prophylaxis of tumour lysis syndrome (TLS) in adults and children with malignant diseases: an expert TLS panel consensus. Br J Haematol. 2010;149(4):578-586. doi:10.1111/j.1365-2141.2010.08143.x Jones GL, Will A, Jackson GH, Webb NJ, Rule S; British Committee for Standards in Haematology. Guidelines for the management of tumour lysis syndrome in adults and children with haematological malignancies on behalf of the British Committee for Standards in Haematology. Br J Haematol. 2015;169(5):661-671. doi:10.1111/bjh.13403

Charcie Smiley overcame a deadly tumor on her pancreas that was causing seizures and low blood sugar that doctors originally did not know the cause. Growing up in the rural town of Moundridge, Kansas in the mennonite culture, Charcie, the youngest of 2 girls, was the tomboy with big dreams. Now in Houston, a mom of three, has taken her passion for health and fitness into a thriving career as a sponsored athlete with ProSupps and her own female-centric online coaching business helping fellow moms get their lives back on track. Having a bright horizon ahead of her, Charcie Smiley is no stranger to adversity, but where others may have counted her down and out, she has a different journey to live. Michael-David shares his raw and intense mindset that has pulled him from a habitually self-destructive mindset paired with survival behaviors and turned his life around by taking full ownership and responsibility of his life and the 35,000 decisions we make as adults on a daily basis. Becoming a student of life and uncovering and moving through the layers we all pack on as we attempt to survive through hard times, his empathy, compassion and perspectives have impacted millions around the world as he empowers others with the reminder that you are just one decision away from creating a better life. Follow 35KaDay on all social media channels as well as subscribe to the YouTube channel at the link below or simply enter @35KaDay on social, video or audio platform today! Links: linktr.ee/35KaDay

About Inventor Robert Sabin:I am 75 yrs. old with a number of patents. I have a couple of yrs. of college with no degree. 3 publications. I previously for many years worked in the precious metal field, melting and refining gold, silver, platinum and palladium. Inventing to me is a cure for anxiety and insomnia.My patented cold weather mask is a lightweight silicone mask covering the mouth and nose, and looks a bit like a N95 mask. There is a huge unmet need for inhalation of warm air in cooler climates and winter. The harmful affects of breathing cold air is well known in theArt. 25 million asthmatics can use this mask along with 100 million Americans who walk, taken together with the military, Athletics, outdoor workers, outdoor sports enthusiasts and more. It is powered by a lithium ion battery attached to the mask or on an armband. With an internal heating pad. Lightweight. 3 heat settings for different cold conditions.Working with company in China to manufacture. Patented. Prototype made.Second invention is a patented therapeutic heat mask powered by a heat gun, which is an upscale hair dryer, which is computer controlled for airflow and temperature. The proposed temperature mimics the Finnish sauna which has been used for 7000+yrs at temperatures of about 156F to 214F. To millions of people without toxicity.There is abundant published reports that these non-toxic temperatures kill the bacilli causing pulmonary TB at 176F for 20 minutes invitro or the virus causing COVID-19 at 136F for 15minutes. Tumor cells are proven to be especially sensitive to heat, and it is written in stone that heat denatures protein, and the second law of thermodynamics Proven, discloses that heat traffics from hot to cold.The upshot is that mycobacterium TBCausing TB,MDR-TB, XDR-TB, and The virus causing COVID-19, and all variants, and cancer cells will be killed extremely fast, TB text discloses that you can assess if a new therapeutic for TB works, can be see in a couple of days, similar assessment for the virus causing COVID-19, and cancer cells of certain types of cancer in the respiratory system/ Lung.A safe, non- toxic, non-invasive, 100%Natural, severely cost effective, portable, treatment is proposed.A one hour treatment period is proposed. Administered 180F to 190F heated air for one hour through the invention to myself numerous times without any toxicity. Robert was recently awarded patent on the treatment of Alzheimer's disease with a plant derived compound.Robert SabinTailwings@aol.com E mail516-669-1184 CellBrian FriedInvention Licensing Representation:Brian Friedbrian@inventorsmart.comwww.brianfried.com--------------------------------------------About Got Invention Show:Welcome to the Got Invention Show!Listen to inventors interviews sharing their invention story to the world!Are you patent pending?Do you have a prototype to show and demonstrate?Are you looking to earn royalties from your invention?Are you looking for a manufacturer?Do you want to raise money or find an investor?Do you want to sell your invention?Learn from other inventors or let's see and hear about your big invention idea! Show & tell us about your invention, have your very own video interview to be proud of!Your video can be used to:Post to your social mediaAdd on your websiteSend to bloggers & editorsPitch to licensees or investorsListen to inventor interviews or sign up: www.gotinventionshow.comYour Host of Got Invention Show, Brian Fried. Brian is the host of Got Invention Radio, with interviews of high profile guests including the U.S. Patent & Trademark Office, Lori Greiner from ABC's Shark Tank, & over 150 individual interviews. www.gotinvention.comBrian connects and guides inventors to earn royalties from their inventions to licensees and brand properties looking for new ideas and intellectual property to expand existing or add to new product lines. Inventor Smart: www.inventorsmart.com Host Inventor Expert and Mentor Brian Fried: www.brianfried.com

Doc of Detox:Visit our website: http://bit.ly/docofdetoxA-Z Masterclass: https://www.internationaltraininginstituteofhealth.com/...Visit our store: http://bit.ly/docofdetoxstoreDaily Cleansing Tea: http://bit.ly/docofdetoxteaHumic/Fulvic: http://bit.ly/humicfulvicIonic Calcium: http://bit.ly/ioniccalciumLight Therapy: http://bit.ly/bioptronlightEssential Oils: http://bit.ly/docofdetoxoilsStructured Water: http://bit.ly/docofdetoxwaterHealthy to 100 Book: http://bit.ly/healthyto100Doc of Detox Library: http://bit.ly/docofdetoxlibrary

In this episode, Dr. Audrey Nath talks with figure skater, Olympic gold medalist, and cancer research advocate, Scott Hamilton. Scott speaks about his brain tumor diagnosis and shares information about the CARES foundation where they fund innovative cancer research. Then, Dr. Nath talks with Dr. Chirag Patel, neuro-oncologist at Anderson Cancer Center. Dr. Patel explains more about different types of brain tumors and cancers, how they are diagnosed, and the various therapies that are available for treatment.   Additional Resources:    https://www.brainandlife.org/disorders-a-z/disorders/pituitary-tumors  https://www.brainandlife.org/disorders-a-z/disorders/brain-and-spinal-tumors  https://www.scottcares.org/   https://www.scottcares.org/scotthamiltonandfriends    Social Media:    Guest: Scott Hamilton @ScottHamilton84 (Instagram) @ScottHamilton84 (Twitter)  Hosts: Dr. Daniel Correa @neurodrcorrea; Dr. Audrey Nath @AudreyNathMDPhD

Five red heifers delivered to Israel have left many wondering if this could all be a part of a biblical prophecy signaling a start to the End Times.ANDWhile Scott Baio continues to act and direct, his most important role these days is as a real-life family man and husband to wife, Renee Sloan.To see videos and photos referenced in this episode, visit GodUpdates!https://www.godupdates.com/red-heifers-in-israel/https://www.godupdates.com/star-of-happy-days-actor-scott-baio-s-wife/

Richard Wu, MD, PhD, and the James are at the forefront of a new type of cancer treatment in which lymphocytes from a patient's immune system are removed from a tumor, enhanced in the lab and then returned to the body to better detect and kill cancer cells. It's called: tumor-infiltrating lymphocyte (TIL) therapy and it is currently being used in clinical trials at the James and other leading cancer centers. Wu explains that the lymphatic system includes T cells and B cells that fight cancer. “In the patients I treat, the cancer has been infiltrated by T cells, but for some reason their tumor doesn't shrink,” he said. “The cancer cells have found a way to shut off the immune system.” The T cells are removed from within what Wu describes as the “suppressive environment” of the tumor, and these millions of cells are “exposed to a potent stimulus to regrow and regain function.” Millions of T cells become billions and, because they are from the patient's body, the immune system “can recognize them and maximize their cancer-killing potential.” Still in the early stages, the James TIL clinical trials have focused on melanoma and lung cancer. “We are at the tip of the iceberg,” Wu said. “I see TIL as a platform therapy and we're only at the beginning and there are multiple ways it is being explored so we can make it work even better … This is what drives me in my daily work, seeing patients who haven't responded to standard treatment options and coming up with a new approach, never being satisfied with the status quo.”

Libertarians are making a comeback, and it is starting right here with Mindy Robinson. Mindy is fighting back against the corruption of the government, and most importantly, fighting for YOU and YOUR RIGHTS. Support Mindy Robinson at her website: https://electmindyrobinson.com/ Melinda Avila joins to expose how her vaccine injured husband is being denied life-saving care for not receiving his second vaccine after being injured! Now he has massive, cancerous tumors! If you are - or know of - a physician able to help Melinda's husband, email Lauren Witzke at: lauren@stewpeters.com! Nick Ochs joins to expose the crimes of the government, as he preps to be shuttled into jail, and sent away from his family for standing strong at J6! Go to:  https://www.givesendgo.com/OchsFamilyFund to support Ochs family while he is away. Arizona has banned abortion! Arizona, after the disassembling of Roe v. Wade has reverted back to a law signed in 1901. This is a HUGE victory for the right of a newborn's life. Don't Let Antifa Win! Vote For Lauren for Miss Stars & Stripes! https://msstripes.org/2022/lauren-witzke Libertarians are making a comeback, and it is starting right here with Mindy Robinson. Mindy is fighting back against the corruption of the government, and most importantly, fighting for YOU and YOUR RIGHTS. Support Mindy Robinson at her website: https://electmindyrobinson.com/ Watch this new segment NOW at https://StewPeters.com! Visit our friends at Goldco! Call 855-706-GOLD or visit https://goldco.com/stew Prepare your family for famine and shortages by purchasing food through: https://heavensharvest.com/ If your dog as been feeling tired or not having the energy it used to, this 1 ingredient could be the reason: https://dogfoodexposed.com/STEW Righteously stand against vaccine tyranny by supporting Christopher Key. Reset your testosterone by trying IGF1+: https://www.vaccine-police.com/ Check out https://nootopia.com/StewPeters for help increasing your mental & physical strength to battle the deep-state's KRYPTONITE plot against Americans! Destress today, Stew crew sleep sound! Use promo code STEWPETERS10 at checkout for 10% off your order. http://www.magbreakthrough.com/stewpeters Check out: https://kuribl.com/ STEW20 for 20% off your order or premium CBD! CACOA is a super food, and may be the missing link to strength and happiness. Buy it now: https://shop.earthechofoods.com/stew Check out: https://patriotsbreakfastclub.com/, for premium coffee, mugs, and more! Use promo code STEW10 at checkout for 10% off! Go Ad-Free, Get Exclusive Content, Become a Premium user: https://www.stewpeters.com/subscribe/ Follow Stew on Gab: https://gab.com/RealStewPeters See all of Stew's content at https://StewPeters.com Watch full episodes here: https://redvoicemedia.net/stew-full-shows