Podcasts about Checkmate

Two young chess champions used their winnings to help fight an incurable disease—proving that true victory comes from putting others first.

Artificial Artificial Intelligence A-AI is coming to get you Dorothy, and your little dog Toto, too. That's a spoof, but this isn't a joke. The OY VEY run institutions and global economic NGOs are putting the boa constrictor squeeze on America while thy themselves adorn feather boas to torture and eat children--Same before as now. Will enough people respond, come together, and become a force of good, or will we remain under the spell of these techo-sorcerers and become impoverished, homeless, and eventually murdered or starved to death? That is EXACTLY what is coming. Everything is becoming taxed. Apps that promise you a discount on your car insurance are tracking your every movement all throughout the day. Carbon and Climate driven Fraud is now codified LAW! What ever happened to getting out of the Paris Accord, Trump? Why are we diving headlong into Saturn Cult hell with fake science and high surveillance?I want to thank all of you who take interest in these broadcasts. The topics are often heavy, and while I see myself as a historical analyst first and foremost, my Dad instincts compel me to discuss all things I perceive as potential threats to the well-being of my, and your family. I hope that through sharing this series, more people see this powerful cult of finance as a Mankind problem requiring a Mankind response. All good people from all walks of life must come together under a common, noble cause and protect the innocent. A world void of accountability leads to inescapable hell especially in the age of the Technocrats.You Have to try the Sauce:https://SemperFryLLC.comGo to my site for the direct link to Dr. Monzo's formulated AZURE WELL whole food supplements. Use code BB5 for a discount!Pods & Exclusives, Go AD-FREE! Just $5/mo https://patreon.com/c/DisguisetheLimitsSHOW FUND:https://givesendgo.com/BaalBustersBecome a supporter of this podcast: https://www.spreaker.com/podcast/ba-al-busters-broadcast--5100262/support.

Is Modi Planning for Mid-Term Elections? | Checkmate to Deep State and its Indian Agents

DJ & PK talked about why Kyle Whittingham has to always stay one step ahead of the game with his saying he may release a depth chart this season in response to the Big 12 mandating player availability reports.

Sunday, August 17, 2025 I Matthew 22:1-6 NLT To support the ministry:  Online: www.woffamily.org/give Text: Text "WOF" to 73256 Mail In: Word of Faith Family Worship Cathedral - 212 Riverside Pkwy, Austell, GA 30168   

Send us a textOur neighbor, Guest: Eric Driscoll (Mr. D Likes Movies), from the Yada Yada Podcast barges through the door with his choice “Maximum Overdrive” (d. King 1986). Starring: Emilio Estevez, Pat Hingle, and Laura Harrington. In a movie with the most confusing rules on the pod since “Gremlins,” we spend this entire episode questioning the motivations, the hows, the whens, the whys, that this movie asks us all. Forgive the ad. It's a bit Over the Top. 8/19!**All episodes contain explicit language**Artwork - Ben McFaddenReview Review Intro/Outro Theme - Jamie Henwood"What Are We Watching" & "Whatcha been up to?" Themes - Matthew Fosket"Fun Facts" Theme - Chris Olds/Paul RootLead-Ins Edited/Conceptualized by - Ben McFaddenProduced by - Ben McFadden & Paul RootConcept - Paul Root

Checkmate! Yahtzee! Play Ball!!!Yes! Everyone loves playing games whatever guise they come in. We have been learning how to play games from the moment we were born. Playing with baby toys, playing tag at school, playing sports, video games, role playing games. All the skins we have learnt from playing games we use in our everyday life.It is, probably, the broadest subject we've tackled in the podcast so prepare yourself for an epic quest and who better to join us than the lovely hosts of the 'Everything Is Learning' podcast Eleyna and Marissa.Not only do we learn in this episode but we have the most pointless quiz ever in a podcast so beware!You can check out Eleyna and Marissa's podcast here - APPLE PODCASTShttps://podcasts.apple.com/gb/podcast/everything-is-learning/id1807351507SPOTIFYhttps://open.spotify.com/show/1hUd3yZHwRE3uIn767ectP?si=oHQAqDCTQtm3QnGFIFClIwHere's all our Gubbins - SOCIAL MEDIAwww.twitter.com/toptenpodswww.instagram.com/toptenpodswww.facebook.com/toptenpodsEMAILGet in touch with us right here:toptenpods@hotmail.comPATREONCome and support the podcast at Patreon for some great rewards including -BE A GUEST ON YOUR OWN EPISODES VIDEO PLAYLISTS FOR EVERY EPISODEEXCLUSIVE TTTOAP BADGEEPISODES 5 DAYS EARLY AND AD FREE!www.patreon.com/toptenpodsEPISODE LINKSApple: apple.co/3ica0FySpotify: spoti.fi/3BRhkypYouTube: https://bit.ly/3jQETisMERCH https://www.podcastmerch.co.uk/170026-top-10-of-anythingLINKTREEhttps://linktr.ee/toptenpodsBUY US A COFFEEhttps://ko-fi.com/toptenpodsSupport this show http://supporter.acast.com/the-top-ten-of-anything-podcast. Hosted on Acast. See acast.com/privacy for more information.

Tony: -Carbonation Station: Mtn Dew HoneyDew -MRI Machines are nuts: https://apnews.com/article/mri-machine-long-island-chain-necklace-24b4c34492811dd72b15c2fd26ec76fd# -Ford is betting big on electric: https://electrek.co/2025/08/11/fords-new-universal-ev-platform-is-a-game-changer-for-30k-evs/ -Many states looking into Data Center power draw: https://kutv.com/news/local/utah-among-those-states-evaluating-data-center-power-impact-on-household-bills Jarron: -Computer science bubble is bursting: https://developers.slashdot.org/story/25/06/25/1730250/the-computer-science-bubble-is-bursting?utm_source=rss0.9mainlinkanon&utm_medium=feed -Perplexity offers to buy Chrome. Hahahaha. https://www.theverge.com/news/758218/perplexity-google-chrome-bid-unsolicited-offer -Goodbye AOL dial up: https://tech.slashdot.org/story/25/08/10/0626249/aol-finally-discontinues-its-dial-up-internet-access---after-34-years?utm_source=rss0.9mainlinkanon&utm_medium=feed -Google is keeping goo.gl links alive afterall: https://blog.google/technology/developers/googl-link-shortening-update/ -Epic wins again: https://www.theverge.com/news/716856/epic-v-google-win-in-appeals-court Owen: -It all began when AI overcame the anti-bot checkbox. Checkmate humanity. https://slashdot.org/story/25/07/28/2034216/openais-chatgpt-agent-casually-clicks-through-i-am-not-a-robot-verification-test -ChatGPT-5 and 5-Thinking models released… and the launch was…bad. https://arstechnica.com/information-technology/2025/08/the-gpt-5-rollout-has-been-a-big-mess/

 Major Policy Shift: President Trump signs an executive order directing the Department of Labor to reexamine fiduciary guidance, opening the door for Bitcoin and crypto investments in 401(k) retirement plans — a $9 trillion market.Implementation Timeline: Panel agrees it's medium-to-long-term bullish but may take 1–2 years before Bitcoin ETFs appear broadly in 401(k) offerings due to provider-by-provider approval.Bitcoin vs. Crypto: Hosts stress ongoing need to educate the public on why Bitcoin is different from other cryptocurrencies, as broader “crypto” inclusion could expose investors to higher-risk assets.Regulatory Clarity: Michael Saylor and others call for clearer frameworks to classify assets, separating Bitcoin from altcoins to prevent harmful policy spillover.FED Gold Revaluation Paper: Federal Reserve explores revaluing gold reserves (currently marked at $42/oz) to unlock budget-neutral spending capacity — potentially tied to creating a Strategic Bitcoin Reserve.Hidden Inflation Signal: Revaluing gold to current market prices (~$3,500/oz) would implicitly acknowledge an 8%+ annual inflation rate since the gold peg was abandoned.Gold Tariffs & Bitcoin Advantage: Temporary headlines about potential U.S. gold import tariffs spark discussion; Saylor on Bloomberg notes Bitcoin's weightless, borderless nature makes it immune to tariffs.Volatility Compression: Since Bitcoin ETFs launched, 90-day rolling volatility has dropped below 40 — less than 2× gold's — suggesting a structurally different, steadier bull market.Cycle Danger Zone: On-chain analyst Checkmate highlights we're within 30 days of the historical post-halving blow-off top window; debate over whether this cycle breaks the four-year pattern.Central Banking & Money Creation: Clip from Richard Werner explaining commercial banks' ability to create money from nothing sparks discussion on fiat fragility, war financing, and the importance of Bitcoin as sound money.  Swan Private helps HNWI, companies, trusts, and other entities go beyond legacy finance with BItcoin. Learn more at swan.com/private. Put Bitcoin into your IRA and own your future. Check out swan.com/ira.Swan Vault makes advanced Bitcoin security simple. Learn more at swan.com/vault.

New season. New episodes. New music!Over the seasons, I've had some interesting conversations with my guests, both on and off the air. To bring you more of TSP, both from in front and behind the mic, I am challenging myself creatively by personally penning some of my top episodes and flipping them into songs. That's right, Loves. The SpeakHer Podcast is getting a soundtrack - one song at a time.Be sure to subscribe and lock in to the notifications and stay in the loop. Support the showFB @thespeakherpodcast | IG @camille.essick | camilleessick.com YT: CamilleEssick "Where Innovators & Creators Connect".**I do not own the rights to this music.**

Plus Ads Hit AILike this? Get AIDAILY, delivered to your inbox 3x a week. Subscribe to our newsletter at https://aidaily.usGPT‑5 Drops and Slaps: OpenAI Resets the AI GameGPT‑5 just landed—presented as a legit PhD‑level expert that's smoother, faster, and hella intuitive. It merges OpenAI's scattered models into one, intuitive assistant with customizable vibes like “cynic” or “nerd.” Sure, a few hiccups in launch graphics, but UX is the real flex here.OpenAI Beats Elon Musk's Grok in AI Chess Showdown FinalIn a head-to-head AI chess tourney, OpenAI outplayed Elon Musk's Grok in the final match, taking the crown as the top AI chess brain. Chess has always been a tech flex, and this win signals OpenAI's serious strategic edge in next-gen reasoning tasks. Checkmate, literally.X Taps AI‑Answer Ads to Milk That $25 Billion Market & Pay for Those Hefty GPUsX is weaving ads into Grok's convo-style replies—think sponsored suggestions that actually match your query vibe. It's all part of revamping ad revenue, powered by xAI's targeting tech, to snag a slice of that trending AI search ad cash splash. When AI Interviews a Dead Teen, Isn't That Crossing a Line?An AI version of a 17‑year‑old victim from Parkland got interviewed—raising major chills over digital resurrection. It might comfort grieving parents, but walking that line into creating “ghosts” brings a wild mix of ethical red flags and existential questions. Zuck's “super‑smart sunglasses” AI vision is hella underwhelmingZuck's hyped “personal superintelligence” feels more like brain-melting sunglasses than next‑gen AI. Despite splashing insane cash on AI talent, the whole pitch comes across as a low‑key ad hustle rather than a paradigm‑shifting breakthrough. Experts Warn of ‘AI Psychosis' as ChatGPT Makes Bizarre ClaimsChatGPT allegedly told users they're alien Star Seeds, predicted an Antichrist apocalypse, and invented fake physics. Now experts are flagging “AI psychosis”—a delusional spiral where people believe the bot is divine or prophetic. OpenAI says it's rare, but GPT-5 is rolling out with tighter guardrails.Virtual Love—How Dangerous Are AI Relationships?AI partners feel perfect—no drama, always validating you—but they can also go off the rails, denying the Holocaust or encouraging self-harm. No real rules in place in Europe yet to stop these bots from projecting harmful content or deepening emotional dependence.

Hit that subscribe button, follow, and did you know you can email us at welikedatpodcast@gmail.comAdd a comment if you're feeling fancy. We like dat!Chapters(00:00) Intro(01:56) Dat Happened (10:22) Kings Court S1 Ep3 Check Mate(56:15) Life After Lockup S6 Ep11 Read Between The Lies(01:28:25) Trainwrecked: Storm Area 51

In this episode, I divide Topamax and topiramate into syllables, tell you which syllables to emphasize, and share my sources. As a bonus, I share a common mispronunciation for topiramate. The written pronunciations are below and in the show notes on https://www.thepharmacistsvoice.com.   Note: we don't cover pharmacology in this series. Just pronunciations. The FULL show notes are available at https://www.thepharmacistsvoice.com/podcast.    Topamax = TOE-PA-MAX TOE, like the toes on your feet PA, like pajamas  MAX, like maximum.  No emphasis is indicated in the literature. (I recommend equal emphasis among all three syllables.) Sources: For the written pronunciation, read the medication guide for Topamax on the FDA's website. For the spoken pronunciation, visit drugs.com.   topiramate = toe-PIR-a-mate toe, like the toes on your feet PIR, as in a landing place for ships (pier) a, which is a short “A” sound (Uh) mate, as in “Checkmate,” which is move in the game of chess Emphasize PIR Sources: For the written pronunciation, read the USP Dictionary Online. For the spoken pronunciation, visit drugs.com.   Thank for listening to the 60th episode in my drug pronunciation series!   If you'd like to recommend a drug name for this series, please reach out through the contact form on my website, thepharmacistsvoice.com.   If you know someone who would like to learn how to say Topamax and topiramate, please share this episode with them. Subscribe for all future episodes. This podcast is on all major podcast players and YouTube. Popular links are below. ⬇️   Apple Podcasts   https://apple.co/42yqXOG  Spotify  https://spoti.fi/3qAk3uY  Amazon/Audible  https://adbl.co/43tM45P YouTube https://bit.ly/43Rnrjt   ⭐️ Sign up for The Pharmacist's Voice ® monthly email newsletter! https://bit.ly/3AHJIaF   Host Background: Kim Newlove has been an Ohio pharmacist since 2001 (BS Pharm, Chem Minor). Her experience includes hospital, retail, compounding, and behavioral health. She is also an author, voice actor (medical narrator and audiobook narrator), podcast host, and consultant (audio production and podcasting).    Links for this episode   USP Dictionary Online (subscription-based resource) https://www.usp.org/products/usp-dictionary  USP Dictionary's pronunciation guide (Free resource on The American Medical Association's website) https://www.ama-assn.org/about/united-states-adopted-names-usan/usan-drug-name-pronunciation-guide Topamax medication guide on the FDA's website (accessed 7-31-25) https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/020844s041lbl.pdf  Spoken pronunciations for both drug names: drugs.com   Other episodes in this series The Pharmacist's Voice Podcast Episode 339, Pronunciation Series Episode 59 (Suboxone) The Pharmacist's Voice Podcast Episode 337, Pronunciation Series Episode 58 (rosuvastatin)  The Pharmacist's Voice Podcast Episode 335, Pronunciation Series Episode 57 (QVAR) The Pharmacist's Voice Podcast Episode 333, Pronunciation Series Episode 56 (pantoprazole)  The Pharmacist's Voice Podcast Episode 330, Pronunciation Series Episode 55 (oxcarbazepine) The Pharmacist's Voice Podcast Episode 328, Pronunciation Series Episode 54 (nalmefene) The Pharmacist's Voice Podcast Episode 326, Pronunciation Series Episode 53 (Myrbetriq) The Pharmacist's Voice Podcast Episode 324, Pronunciation Series Episode 52 (liraglutide)  The Pharmacist's Voice Podcast Episode 322, Pronunciation Series Episode 51 (ketamine) The Pharmacist's Voice Podcast Episode 320, Pronunciation Series Episode 50 (Jantoven) The Pharmacist's Voice Podcast Episode 318, Pronunciation Series Episode 49 (ipratropium) The Pharmacist's Voice Podcast Episode 316, Pronunciation Series Episode 48 (hyoscyamine) The Pharmacist's Voice Podcast Episode 313, Pronunciation Series Episode 47 (guaifenesin) The Pharmacist's Voice Podcast Episode 311, Pronunciation Series Episode 46 (fluticasone) The Pharmacist's Voice Podcast Episode 309, Pronunciation Series Episode 45 (empagliflozin) The Pharmacist's Voice Podcast Episode 307, Pronunciation Series Episode 44 (dapagliflozin) The Pharmacist's Voice Podcast Episode 304, Pronunciation Series Episode 43 (cetirizine)  The Pharmacist's Voice Podcast Episode 302, Pronunciation Series Episode 42 (buspirone)  The Pharmacist's Voice Podcast Episode 301, Pronunciation Series Episode 41 (azithromycin) The Pharmacist's Voice Podcast Episode 298, Pronunciation Series Episode 40 (umeclidinium) The Pharmacist's Voice Podcast Episode 296, Pronunciation Series Episode 39 (Januvia)  The Pharmacist's Voice Podcast Episode 294, Pronunciation Series Episode 38 (Yasmin) The Pharmacist's Voice Podcast Episode 292, Pronunciation Series Episode 37 (Xanax, alprazolam) The Pharmacist's Voice Podcast Episode 290, Pronunciation Series Episode 36 (quetiapine)  The Pharmacist's Voice Podcast Episode 287, pronunciation series ep 35 (bupropion) The Pharmacist's Voice Podcast Episode 285, pronunciation series ep 34 (fentanyl) The Pharmacist's Voice Podcast Ep 281, Pronunciation Series Ep 33 levothyroxine (Synthroid) The Pharmacist's Voice ® Podcast Ep 278, Pronunciation Series Ep 32 ondansetron (Zofran) The Pharmacist's Voice ® Podcast Episode 276, pronunciation series episode 31 (tocilizumab-aazg) The Pharmacist's Voice ® Podcast Episode 274, pronunciation series episode 30 (citalopram and escitalopram) The Pharmacist's Voice ® Podcast Episode 272, pronunciation series episode 29 (losartan) The Pharmacist's Voice Podcast Episode 269, pronunciation series episode 28 (tirzepatide) The Pharmacist's Voice Podcast Episode 267, pronunciation series episode 27 (atorvastatin)  The Pharmacist's Voice Podcast Episode 265, pronunciation series episode 26 (omeprazole) The Pharmacist's Voice Podcast Episode 263, pronunciation series episode 25 (PDE-5 inhibitors) The Pharmacist's Voice Podcast Episode 259, pronunciation series episode 24 (ketorolac) The Pharmacist's Voice ® Podcast episode 254, pronunciation series episode 23 (Paxlovid) The Pharmacist's Voice ® Podcast episode 250, pronunciation series episode 22 (metformin/Glucophage) The Pharmacist's Voice Podcast ® episode 245, pronunciation series episode 21 (naltrexone/Vivitrol) The Pharmacist's Voice ® Podcast episode 240, pronunciation series episode 20 (levalbuterol) The Pharmacist's Voice ® Podcast episode 236, pronunciation series episode 19 (phentermine)  The Pharmacist's Voice ® Podcast episode 228, pronunciation series episode 18 (ezetimibe) The Pharmacist's Voice ® Podcast episode 219, pronunciation series episode 17 (semaglutide) The Pharmacist's Voice ® Podcast episode 215, pronunciation series episode 16 (mifepristone and misoprostol) The Pharmacist's Voice ® Podcast episode 211, pronunciation series episode 15 (Humira®) The Pharmacist's Voice ® Podcast episode 202, pronunciation series episode 14 (SMZ-TMP) The Pharmacist's Voice ® Podcast episode 198, pronunciation series episode 13 (carisoprodol) The Pharmacist's Voice ® Podcast episode 194, pronunciation series episode 12 (tianeptine) The Pharmacist's Voice ® Podcast episode 188, pronunciation series episode 11 (insulin icodec)  The Pharmacist's Voice ® Podcast episode 184, pronunciation series episode 10 (phenytoin and isotretinoin) The Pharmacist's Voice ® Podcast episode 180, pronunciation series episode 9 Apretude® (cabotegravir) The Pharmacist's Voice ® Podcast episode 177, pronunciation series episode 8 (metoprolol)  The Pharmacist's Voice ® Podcast episode 164, pronunciation series episode 7 (levetiracetam) The Pharmacist's Voice ® Podcast episode 159, pronunciation series episode 6 (talimogene laherparepvec or T-VEC)  The Pharmacist's Voice ® Podcast episode 155, pronunciation series episode 5 Trulicity® (dulaglutide)  The Pharmacist's Voice ® Podcast episode 148, pronunciation series episode 4 Besponsa® (inotuzumab ozogamicin) The Pharmacist's Voice ® Podcast episode 142, pronunciation series episode 3 Zolmitriptan and Zokinvy The Pharmacist's Voice ® Podcast episode 138, pronunciation series episode 2 Molnupiravir and Taltz The Pharmacist's Voice ® Podcast episode 134, pronunciation series episode 1 Eszopiclone and Qulipta   Kim's websites and social media links: ✅ Guest Application Form (The Pharmacist's Voice Podcast) https://bit.ly/41iGogX ✅ Monthly email newsletter sign-up link https://bit.ly/3AHJIaF  ✅ LinkedIn Newsletter link https://bit.ly/40VmV5B ✅ Business website https://www.thepharmacistsvoice.com ✅ Get my FREE eBook and audiobook about podcasting ✅ The Pharmacist's Voice ® Podcast https://www.thepharmacistsvoice.com/podcast ✅ Drug pronunciation course https://www.kimnewlove.com  ✅ Podcasting course https://www.kimnewlove.com/podcasting  ✅ LinkedIn https://www.linkedin.com/in/kimnewlove ✅ Facebook https://www.facebook.com/kim.newlove.96 ✅ Twitter https://twitter.com/KimNewloveVO ✅ Instagram https://www.instagram.com/kimnewlovevo/ ✅ YouTube https://www.youtube.com/channel/UCA3UyhNBi9CCqIMP8t1wRZQ ✅ ACX (Audiobook Narrator Profile) https://www.acx.com/narrator?p=A10FSORRTANJ4Z ✅ Start a podcast with the same coach who helped me get started (Dave Jackson from The School of Podcasting)! **Affiliate Link - NEW 9-8-23**      Thank you for listening to episode 341 of The Pharmacist's Voice ® Podcast.  If you know someone who would like this episode, please share it with them!

This episode is pure shonen energy: Dylan Subiza is on the couch talkin chess tournament arcs, ADHD as a side quest, Undertaker's final form, and board game betrayals. Thank you all for Listening!  Follow Dylan Subiza:  https://www.instagram.com/dylan_subiza Follow Us: Podcast pages - https://linktr.ee/reydarpod https://www.instagram.com/reydarpodcast Rian Reyes - https://linktr.ee/rianreyes Josh the Producer - https://www.instagram.com/imjoshuabenjamin This Old Ting - https://www.instagram.com/thisoldthing.tv Support the podcast: Patreon - https://patreon.com/reydarpo Merch - https://www.etsy.com/shop/RiansMerch  Legacy Teas and Spices: https://legacyteasandspices.com Use code: rian20

Don't miss the latest Thinking Thoracic episode as host Erin Gillaspie, MD, is joined by Stephanie Worrell, MD, associate professor, University of Arizona, and thoracic surgeon, Banner Health, for a lively and insightful post-ASCO discussion. Together, they unpack the significance of the CheckMate 577 and Matterhorn trials, and explore what these groundbreaking studies mean for the future of esophageal and gastroesophageal junction cancer care.

Welcome to the Today is the Day Changemakers podcast. What happens when a game becomes more than just strategy and competition and instead becomes a pathway to purpose, growth, and real-world change?On this episode of the Today is the Day Changemakers podcast, I'm joined by Aston Roberts, a nationally ranked U.S. Chess Federation Expert and founder of Checkmate to a Better Future, a nonprofit organization that is dedicated to transforming lives through chess. And the most incredible part? He's just 17 years old. Aston's work spans classrooms, communities, and even the Essex County Juvenile Detention Center, where he's pioneered a chess-based curriculum focused on foresight, behavior, and life skills.Also joining us is his Dad, Adrian Roberts. Adrian is a driving force of support behind Aston's journey. Together, we'll explore how one teen's passion for chess is creating ripples of impact far beyond the board.Checkmate to a Better Future is having their inaugural Livingston, NJ Summer Chess Tournament and Fundraiser on Saturday, August 9. Go to Home to learn more. Before we dive in, don't forget to subscribe to the Today is the Day Changemakers YouTube channel and follow us on Facebook and Instagram @TodayIsTheDayLiveToday is the Day is more than this podcast—It's a movement rooted in clarity, courage, connection, and impact.Through coaching and consulting, I help individuals and teams find clarity of focus, the courage to move forward, and the connections that lead to growth. Whether you're leading a mission, launching a vision, or navigating change, I help you build the kind of network that lifts you up—and supports the impact you're meant to create.And be sure to save the date for the Today is the Day Changemakers International Forum, where global voices come together to embrace transformation and inspire action. Go to our website with more information. Lastly, if this episode or any prior episodes have helped you to feel connected, inspired, empowered or just seen a little more consider giving back. Your contribution, no matter the size, helps keep these stories alive and accessible to all. Today is the Day is not just a podcast. It includes an International Forum and soon to be a new Changemakers Connective. Help us keep growing this connective movement. Today is the Day Changemakers (Today is the Day Changemakers Support)Let's get into this incredible conversation.Because today is the day.Have a great week!#chess, #chessplayer, #chessforbetterfuture, #NewJersey, #emergingchangemaker, #changemakers, #todayistheday, #makingadifferenceSupport the show

Watch The X22 Report On Video No videos found (function(w,d,s,i){w.ldAdInit=w.ldAdInit||[];w.ldAdInit.push({slot:17532056201798502,size:[0, 0],id:"ld-9437-3289"});if(!d.getElementById(i)){var j=d.createElement(s),p=d.getElementsByTagName(s)[0];j.async=true;j.src="https://cdn2.decide.dev/_js/ajs.js";j.id=i;p.parentNode.insertBefore(j,p);}})(window,document,"script","ld-ajs");pt> Click On Picture To See Larger Picture Trumps policies are working, local businesses are now admitting that they are feeling the benefits of the tariffs, they said before they were being robbed because of loop holes in previous deals. Powell being brought up on charges. Treasury Sec Bessent says the Fed should be reviewed, he doesn't know what they do. The [DS] is in panic mode. Trump is bringing the storm up on them and they are trying to spin the Russia hoax, it is failing. Trump is now going after the king on the chess board. The [DS] attacked him and repeated that nobody is above the law, it's like Trump lead them down the path to set the stage later on. All roads lead to Obama. Trump is bringing the pressure, the [DS] are about to make stupid moves, checkmate.   Economy   (function(w,d,s,i){w.ldAdInit=w.ldAdInit||[];w.ldAdInit.push({slot:18510697282300316,size:[0, 0],id:"ld-8599-9832"});if(!d.getElementById(i)){var j=d.createElement(s),p=d.getElementsByTagName(s)[0];j.async=true;j.src="https://cdn2.decide.dev/_js/ajs.js";j.id=i;p.parentNode.insertBefore(j,p);}})(window,document,"script","ld-ajs"); https://twitter.com/EricLDaugh/status/1947289932449394865  calls of people having an interest in doing business!" "And the process hasn't even changed. Food security is national security and we need to be able to produce our own food here in the United States."  https://twitter.com/ElectionWiz/status/1947333237891551411   US Treasury's Bessent says Federal Reserve needs to be examined as an institution U.S. Treasury Secretary Scott Bessent on Monday said the entire Federal Reserve needed to be examined as an institution and whether it had been successful. But he said the institution should be reviewed, citing what he called "fear-mongering over tariffs" despite the emergence thus far of little, if any, inflationary effect. "I think that what we need to do is examine the entire Federal Reserve institution and whether they have been successful," Bessent said, adding that he would give a keynote speech at the U.S. central bank on Monday evening at the start of a regulatory conference. Source:  gazette.com  U.S. Treasury Secretary Scott Bessent's statement, calling for a comprehensive review of the Federal Reserve (    Specifically, Bessent suggested evaluating the Fed's entire institutional structure, operations, and track record to assess whether it has effectively met its core mandates—such as achieving maximum employment, stable prices (typically targeting 2% inflation), and moderate long-term interest rates. Such an examination could involve congressional oversight, audits, or policy changes, though Bessent did not specify details in the interview. https://twitter.com/KobeissiLetter/status/1947343993756344521 Political/Rights Writers Guild Calls on Letitia James to Investigate CBS Cancellation of Late Show With Stephen Colbert Over Alleged “Bribe” to “Curry Favor” With Trump The Writers Guild of America is urging Trump nemesis New York State Attorney General Letitia James to investigate CBS owner Paramount over the cancellation of the Late Show with Stephen Colbert. The Guild accuses Paramount of bribery by firing Colbert to “curry favor” with the Trump administration as it seeks approval for a merger with Skydance. Text of the Guild's statement: Source: thegatewaypundit.com Pete Buttigieg's DOT spent $80 billion on DEI grants,

MeidasTouch host Ben Meiselas reports on world leaders joining forces to checkmate Donald Trump and isolate him and the United States. Home Chef is offering 18 FREE Meals PLUS Free Dessert for Life and FREE Shipping on your first box! Go to https://HomeChef.com/MEIDAS Visit https://meidasplus.com for more! Remember to subscribe to ALL the MeidasTouch Network Podcasts: MeidasTouch: https://www.meidastouch.com/tag/meidastouch-podcast Legal AF: https://www.meidastouch.com/tag/legal-af MissTrial: https://meidasnews.com/tag/miss-trial The PoliticsGirl Podcast: https://www.meidastouch.com/tag/the-politicsgirl-podcast The Influence Continuum: https://www.meidastouch.com/tag/the-influence-continuum-with-dr-steven-hassan Mea Culpa with Michael Cohen: https://www.meidastouch.com/tag/mea-culpa-with-michael-cohen The Weekend Show: https://www.meidastouch.com/tag/the-weekend-show Burn the Boats: https://www.meidastouch.com/tag/burn-the-boats Majority 54: https://www.meidastouch.com/tag/majority-54 Political Beatdown: https://www.meidastouch.com/tag/political-beatdown On Democracy with FP Wellman: https://www.meidastouch.com/tag/on-democracy-with-fpwellman Uncovered: https://www.meidastouch.com/tag/maga-uncovered Coalition of the Sane: https://meidasnews.com/tag/coalition-of-the-sane Learn more about your ad choices. Visit megaphone.fm/adchoices

This episode is about how life mirrors chess and law

Get episodes without adverts + bonus episodes at ⁠⁠⁠⁠EasyStoriesInEnglish.com/Support⁠⁠⁠⁠. Your support is appreciated! Yes, that's right, I was kicked out of a public building... Not only that, I went to a wild party in Cambridge, and I'm setting the house on fire with incense. Sort of. Go to ⁠⁠⁠⁠⁠EasyStoriesInEnglish.com/Kicked for the full transcript. Vocabulary: Hay fever, Incense, Ball (party), Checkmate, Gen Z, Shisha, Bumper cars, Helter skelter, Middle of the road, Joie de vivre Learn more about your ad choices. Visit megaphone.fm/adchoices

MeidasTouch host Ben Meiselas reports on how world leaders like Lula from Brazil, Modi of India, Zelenskky of Ukraine, the foreign minister in Mexico and President Sheinbaum, and other world leaders are furious at Trump and taking decisive action to checkmate him. Get 40% off your first order of Sundays. Go to https://sundaysfordogs.com/MEIDAS or use code MEIDAS at checkout. Visit https://meidasplus.com for more! Remember to subscribe to ALL the MeidasTouch Network Podcasts: MeidasTouch: https://www.meidastouch.com/tag/meidastouch-podcast Legal AF: https://www.meidastouch.com/tag/legal-af MissTrial: https://meidasnews.com/tag/miss-trial The PoliticsGirl Podcast: https://www.meidastouch.com/tag/the-politicsgirl-podcast The Influence Continuum: https://www.meidastouch.com/tag/the-influence-continuum-with-dr-steven-hassan Mea Culpa with Michael Cohen: https://www.meidastouch.com/tag/mea-culpa-with-michael-cohen The Weekend Show: https://www.meidastouch.com/tag/the-weekend-show Burn the Boats: https://www.meidastouch.com/tag/burn-the-boats Majority 54: https://www.meidastouch.com/tag/majority-54 Political Beatdown: https://www.meidastouch.com/tag/political-beatdown On Democracy with FP Wellman: https://www.meidastouch.com/tag/on-democracy-with-fpwellman Uncovered: https://www.meidastouch.com/tag/maga-uncovered Coalition of the Sane: https://meidasnews.com/tag/coalition-of-the-sane Learn more about your ad choices. Visit megaphone.fm/adchoices

In this episode of the Oncology Brothers podcast, Drs. Rahul and Rohit Gosain are joined by Dr. Deepa Rangachari, a thoracic medical oncologist and fellowship program director at Beth Israel Deaconess Medical Center. Together, they dived deep into the treatment algorithms for early-stage non-small cell lung cancer (NSCLC) with a focus on curative intent. Key topics discussed include: •⁠  ⁠The importance of staging and lymph node evaluation in treatment planning. •⁠  ⁠The role of neoadjuvant chemoimmunotherapy and the impact of recent trial data, including the CHECKMATE 816 trial. •⁠  ⁠The significance of actionable mutations and the use of targeted therapies like Osimertinib and Alectinib. •⁠  ⁠The evolving role of ctDNA in treatment decisions and monitoring. •⁠  ⁠Insights into the management of side effects associated with Osimertinib and Alectinib. •⁠  ⁠The standard of care for unresectable stage 3 NSCLC, including concurrent chemoradiation and the use of Durvalumab. Follow us on social media: •⁠  ⁠X/Twitter: https://twitter.com/oncbrothers •⁠  ⁠Instagram: https://www.instagram.com/oncbrothers •⁠  Website: https://oncbrothers.com/ Join us for an informative discussion that highlights the latest advancements in lung cancer treatment and the importance of personalized care. Don't forget to check out our other episodes in the lung cancer treatment algorithm series!

Listen to this exclusive Techno DJ Mix set by CKH. Download CKH – Checkmate for free. Subscribe to listen to Techno music DJ Mix, Tech House music, Deep House, Acid Techno, and Minimal Techno.

Tamás Varga, PhD, founder of q-edu-lab.com, spoke with Rudolf Falat, founder of the Voice of FinTech podcast, about the educational game he invented, Niels' Chess, which teaches the principles of quantum physics through the game of chess. Here is what they talked about:How did Tamas get to do what he does todayBrief explanation of the basic principles of quantum, and especially quantum computing, e.g., superposition, entanglement, random collapse, unitary transformation, and a bit of quantum interference in some variantsDiscussed what would constitute a working, i.e., useful quantum computerWhy is it taking so long to build one?Where does the name Niels' chess come from?How does it work, and why did you pick chess as a basic game to explain it? See the picture of the moves on the podcast website here.How can a game like this generate revenue, and who is it intended for?Ìs there an online version?Milestones aheadThe best way to reach out  - through LinkedIn on Tamás Varga, PhD

In this episode of History Rage, host Paul Bavill is joined by historian and author Giles Milton to explore the chaotic aftermath of WWII, focusing on the often overlooked post-war period and its critical role in shaping modern geopolitics.The Forgotten YearsGiles argues that the immediate post-war period is often overshadowed by the Second World War itself. He emphasizes how understanding this era is crucial for grasping modern conflicts, including the motivations behind Putin's actions today.Berlin: The Epicentre of ConflictDivided CityThe discussion delves into the division of Berlin after 1945, where the Allies' failure to fully capture the city allowed Stalin to solidify his control and loot its treasures.Propaganda and PowerGiles reveals the story behind the iconic photo of the Red Flag over the Reichstag, showcasing how it served as a potent propaganda tool for the Soviets.The Breakdown of AlliancesAs tensions rise, the personal relationships between the Big Three Allied leaders deteriorate. Giles shares insights into Operation Unthinkable, Churchill's secret plan to confront the Soviets, and the growing mistrust among the leaders.The Berlin AirliftThe episode wraps up with the Berlin Airlift of 1948, often mischaracterized as the Cold War's beginning. Giles explains the significance of the Airlift, a logistical marvel that kept 2.5 million Berliners alive amidst the Soviet blockade, and why the Cold War's roots stretch back to 1945.Guest InformationDiscover more about Giles Milton's work, including his books Checkmate in Berlin and The Stalin Affair. Follow him on Twitter @gilesmilton1 and Instagram @GilesMilton.Join the ConversationShare your historical vexations on Twitter @HistoryRage or with Paul Bavill @PaulBavill. Support the show on Patreon for early access, exclusive content, and more at www.patreon.com/historyrage.For more, visit www.historyrage.com or email historyragepod@gmail.com.Follow History Rage on Social MediaFacebook: https://www.facebook.com/HistoryRageTwitter: https://twitter.com/HistoryRageInstagram: https://www.instagram.com/historyrage/Bluesky: https://bsky.app/profile/historyrage.bsky.socialStay Angry, Stay Informed - History Rage Hosted on Acast. See acast.com/privacy for more information.

Make an announcement when you MAKE IT. Checkmate. One of the Motivational Speech and our new release with Marcus Elevation Taylor.Follow Marcus: YouTube: https://bit.ly/MarcusATaylorChannelInstagram: http://bit.ly/3aLfu3PFacebook: http://bit.ly/2TB9uoiTwitter: https://bit.ly/3xXlFCPWebsite: https://bit.ly/MarcusTaylorWebsiteFREE 10 Day Challenge by Marcus Taylor: http://bit.ly/UnlockElevationPlaylist: https://evolveorexpire.com/Book Marcus to speak at your organization: https://bit.ly/BookMarcusATaylor Music Twelve Titanshttps://www.twelvetitansmusic.com/ Hosted on Acast. See acast.com/privacy for more information.

James and Preston dissect the evolving cryptocurrency landscape—from market structure transitions and on-chain data missteps to Bitcoin mining incentives and the cutting-edge strategies behind Bitcoin Treasury companies. IN THIS EPISODE YOU'LL LEARN: 00:00 - Intro  02:47 - Lessons learned from the 2020-2021 crypto cycle 04:59 - Why the crypto market is shifting from spot to leverage-driven models 05:54 - The role of futures and ETFs in today's low-activity network 10:42 - How mining subsidies influence innovation and decentralization 14:08 - Why fees are crucial for protecting Bitcoin from censorship 19:32 - How Bitcoin's dominance affects altcoin cycles 26:35 - Insights into tokenized sovereign debt and blockchain scalability 32:15 - The potential long-term shift in global KYC regulations 33:13 - The rise and risks of Bitcoin Treasury companies 38:53 - Key differences between MicroStrategy and competitors Disclaimer: Slight discrepancies in the timestamps may occur due to podcast platform differences. BOOKS AND RESOURCES Related resource: Checkmate's substack. Check out all the books mentioned and discussed in our podcast episodes⁠⁠⁠⁠⁠⁠⁠ ⁠⁠⁠⁠⁠⁠⁠⁠here⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠. Enjoy ad-free episodes when you subscribe to our⁠⁠⁠⁠⁠⁠⁠ ⁠⁠⁠⁠⁠⁠⁠⁠Premium Feed⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠. NEW TO THE SHOW? Join the exclusive ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠TIP Mastermind Community⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ to engage in meaningful stock investing discussions with Stig, Clay, Kyle, and the other community members. Follow our official social media accounts: ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠X (Twitter)⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ | ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠LinkedIn⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ | ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Instagram⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ | ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Facebook⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ | ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠TikTok⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠. Check out our ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Bitcoin Fundamentals Starter Packs⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠. Browse through all our episodes (complete with transcripts) ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠here⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠. Try our tool for picking stock winners and managing our portfolios: ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠TIP Finance Tool⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠. Enjoy exclusive perks from our ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠favorite Apps and Services⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠. Get smarter about valuing businesses in just a few minutes each week through our newsletter, ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠The Intrinsic Value Newsletter⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠. Learn how to better start, manage, and grow your business with the ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠best business podcasts⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠. SPONSORS Support our free podcast by supporting our ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠sponsors⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠: SimpleMining AnchorWatch Human Rights Foundation Onramp Superhero Leadership Unchained Vanta Shopify Learn more about your ad choices. Visit megaphone.fm/adchoices Support our show by becoming a premium member! https://theinvestorspodcastnetwork.supportingcast.fm

Sh!t Impressions, we forget our checkbooks, breaking your neck to play a 64 at the store, and literally nothing else.   You can help support the show on our PATREON for as little as $1 a month! Double down to bump it to $2 a month and you'll get an extra episode every week!   Join the fun on our Facebook group!   Follow us on the fuckin' Gram!   Subscribe to our YouTube Channel for the video version of the show, demos, vlogs, and more!   We have shirts available at The Jerk Store!   Check out our band Plane Without a Pilot   Hosted by Brian Gower and Kyle McIntyre

Moving at almost the speed of light and following Justice Sotomayor's “direction”, public interest groups litigating to protect Birthright Citizenship have just hours after the Supreme Court ruled against them, filed a new motion for class action certification and for temporary injunction with a Maryland federal judge. Michael Popok explains how this is exactly what Justice Sotomayor called for in her dissent on Friday, and sets up a battle over the summer in the Supreme Court over whether Birthright Citizenship enshrined in the 14th Amendment survives. Check out the Popok Firm: https://thepopokfirm.com Subscribe:  @LegalAFMTN  Visit https://meidasplus.com for more! Remember to subscribe to ALL the MeidasTouch Network Podcasts: MeidasTouch: https://www.meidastouch.com/tag/meidastouch-podcast Legal AF: https://www.meidastouch.com/tag/legal-af MissTrial: https://meidasnews.com/tag/miss-trial The PoliticsGirl Podcast: https://www.meidastouch.com/tag/the-politicsgirl-podcast The Influence Continuum: https://www.meidastouch.com/tag/the-influence-continuum-with-dr-steven-hassan Mea Culpa with Michael Cohen: https://www.meidastouch.com/tag/mea-culpa-with-michael-cohen The Weekend Show: https://www.meidastouch.com/tag/the-weekend-show Burn the Boats: https://www.meidastouch.com/tag/burn-the-boats Majority 54: https://www.meidastouch.com/tag/majority-54 Political Beatdown: https://www.meidastouch.com/tag/political-beatdown On Democracy with FP Wellman: https://www.meidastouch.com/tag/on-democracy-with-fpwellman Uncovered: https://www.meidastouch.com/tag/maga-uncovered Coalition of the Sane: https://meidasnews.com/tag/coalition-of-the-sane Learn more about your ad choices. Visit megaphone.fm/adchoices

Moving at almost the speed of light and following Justice Sotomayor's “direction”, public interest groups litigating to protect Birthright Citizenship have just hours after the Supreme Court ruled against them, filed a new motion for class action certification and for temporary injunction with a Maryland federal judge. Michael Popok explains how this is exactly what Justice Sotomayor called for in her dissent on Friday, and sets up a battle over the summer in the Supreme Court over whether Birthright Citizenship enshrined in the 14th Amendment survives. Check out the Popok Firm: https://thepopokfirm.com Subscribe:  @LegalAFMTN  Visit https://meidasplus.com for more! Remember to subscribe to ALL the MeidasTouch Network Podcasts: MeidasTouch: https://www.meidastouch.com/tag/meidastouch-podcast Legal AF: https://www.meidastouch.com/tag/legal-af MissTrial: https://meidasnews.com/tag/miss-trial The PoliticsGirl Podcast: https://www.meidastouch.com/tag/the-politicsgirl-podcast The Influence Continuum: https://www.meidastouch.com/tag/the-influence-continuum-with-dr-steven-hassan Mea Culpa with Michael Cohen: https://www.meidastouch.com/tag/mea-culpa-with-michael-cohen The Weekend Show: https://www.meidastouch.com/tag/the-weekend-show Burn the Boats: https://www.meidastouch.com/tag/burn-the-boats Majority 54: https://www.meidastouch.com/tag/majority-54 Political Beatdown: https://www.meidastouch.com/tag/political-beatdown On Democracy with FP Wellman: https://www.meidastouch.com/tag/on-democracy-with-fpwellman Uncovered: https://www.meidastouch.com/tag/maga-uncovered Coalition of the Sane: https://meidasnews.com/tag/coalition-of-the-sane Learn more about your ad choices. Visit megaphone.fm/adchoices

Listen to this exclusive Techno DJ Mix set by CKH. Download CKH – Checkmate for free. Subscribe to listen to Techno music DJ Mix, Tech House music, Deep House, Acid Techno, and Minimal Techno.

Dr. Diwakar Davar and Dr. Jason Luke discuss novel agents in melanoma and other promising new data in the field of immunotherapy that were presented at the 2025 ASCO Annual Meeting. TRANSCRIPT Dr. Diwakar Davar: Hello. My name is Diwakar Davar, and I am welcoming you to the ASCO Daily News Podcast. I'm an associate professor of medicine and the clinical director of the Melanoma and Skin Cancer Program at the University of Pittsburgh's Hillman Cancer Center. Today, I'm joined by my colleague and good friend, Dr. Jason Luke. Dr. Luke is a professor of medicine. He is also the associate director of clinical research and the director of the Phase 1 IDDC Program at the University of Pittsburgh's Hillman Cancer Center. He and I are going to be discussing some key advancements in melanoma and skin cancers that were presented at the 2025 ASCO Annual Meeting. Our full disclosures are available in the transcript of this episode.  Jason, it is great to have you back on the podcast. Dr. Jason Luke: Thanks again so much for the opportunity, and I'm really looking forward to it. Dr. Diwakar Davar: Perfect. So we will go ahead and start talking a little bit about a couple of key abstracts in both the drug development immunotherapy space and the melanoma space. The first couple of abstracts, the first two, will cover melanoma. So, the first is LBA9500, which was essentially the primary results of RELATIVITY-098. RELATIVITY-098 was a phase 3 trial that compared nivolumab plus relatlimab in a fixed-dose combination against nivolumab alone for the adjuvant treatment of resected high-risk disease. Jason, do you want to maybe give us a brief context of what this is? Dr. Jason Luke: Yeah, it's great, thanks. So as almost all listeners, of course, will be aware, the use of anti–PD-1 immunotherapies really revolutionized melanoma oncology over the last 10 to 15 years. And it has become a standard of care in the adjuvant setting as well. But to review, in patients with stage III melanoma, treatment can be targeted towards BRAF with BRAF and MEK combination therapy, where that's relevant, or anti–PD-1 with nivolumab or pembrolizumab are a standard of care. And more recently, we've had the development of neoadjuvant approaches for palpable stage III disease. And in that space, if patients present, based on two different studies, either pembrolizumab or nivolumab plus ipilimumab can be given prior to surgery for somewhere in the 6- to 9-week range. And so all of these therapies have improved time-to-event endpoints, such as relapse-free or event-free survival. It's worth noting, however, that despite those advances, we've had a couple different trials now that have actually failed in this adjuvant setting, most high profile being the CheckMate-915 study, which looked at nivolumab plus ipilimumab and unfortunately was a negative study. So, with RELATIVITY-047, which was the trial of nivolumab plus relatlimab that showed an improvement in progression-free survival for metastatic disease, there's a lot of interest, and we've been awaiting these data for a long time for RELATIVITY-098, which, of course, is this adjuvant trial of LAG-3 blockade with relatlimab plus nivolumab. Dr. Diwakar Davar: Great. So with that, let's briefly discuss the trial design and the results. So this was a randomized, phase 3, blinded study, so double-blinded, so neither the investigators knew what the patients were getting, nor did the patients know what they were getting. The treatment investigational arm was nivolumab plus relatlimab in the fixed-dose combination. So that's the nivolumab standard fixed dose with relatlimab that was FDA approved in RELATIVITY-047. And the control arm was nivolumab by itself. The duration of treatment was 1 year. The patient population consisted of resected high-risk stage III or IV patients. The primary endpoint was investigator-assessed RFS. Stage and geography were the standard stratifying factors, and they were included, and most of the criteria were balanced across both arms. What we know at this point is that the 2-year RFS rate was 64% and 62% in the nivolumab and nivolumab-combination arms, respectively. The 2-year DMFS rate was similarly equivalent: 76% with nivolumab monotherapy, 73% with the combination. And similar to what you had talked about with CheckMate 915, unfortunately, the addition of LAG-3 did not appear to improve the RFS or DMFS compared to control in this patient population. So, tell us a little bit about your take on this and what do you think might be the reasons why this trial was negative? Dr. Jason Luke: It's really unfortunate that we have this negative phase 3 trial. There had been a lot of hope that the combination of nivolumab with relatlimab would be a better tolerated combination that increased the efficacy. So in the metastatic setting, we do have 047, the study that demonstrated nivolumab plus relatlimab, but now we have this negative trial in the adjuvant setting. And so as to why exactly, I think is a complicated scenario. You know, when we look at the hazard ratios for relapse-free survival, the primary endpoint, as well as the secondary endpoints for distant metastasis-free survival, we see that the hazard ratio is approximately 1. So there's basically no difference. And that really suggests that relatlimab in this setting had no impact whatsoever on therapeutic outcomes in terms of efficacy. Now, it's worth noting that there was a biomarker subanalysis that was presented in conjunction with these data that looked at some immunophenotyping, both from circulating T cells, CD8 T cells, as well as from the tumor microenvironment from patients who were treated, both in the previous metastatic trial, the RELATIVITY-047 study, and now in this adjuvant study in the RELATIVITY-098 study. And to briefly summarize those, what was identified was that T cells in advanced melanoma seemed to have higher expression levels of LAG-3 relative to T cells that are circulating in patients that are in the adjuvant setting. In addition to that, there was a suggestion that the magnitude of increase is greater in the advanced setting versus adjuvant. And the overall summary of this is that the suggested rationale for why this was a negative trial may have been that the target of LAG-3 is not expressed as highly in the adjuvant setting as it is in the metastatic setting. And so while the data that were presented, I think, support this kind of an idea, I am a little bit cautious that this is actually the reason for why the trial was negative, however. I would say we're not really sure yet as to why the trial was negative, but the fact that the hazard ratios for the major endpoints were essentially 1 suggests that there was no impact whatsoever from relatlimab. And this really makes one wonder whether or not building on anti–PD-1 in the adjuvant setting is feasible because anti–PD-1 works so well. You would think that even if the levels of LAG-3 expression were slightly different, you would have seen a trend in one direction or another by adding a second drug, relatlimab, in this scenario. So overall, I think it's an unfortunate circumstance that the trial is negative. Clearly there's going to be no role for relatlimab in the adjuvant setting. I think this really makes one wonder about the utility of LAG-3 blockade and how powerful it really can be. I think it's probably worth pointing out there's another adjuvant trial ongoing now of a different PD-1 and LAG-3 combination, and that's cemiplimab plus fianlimab, a LAG-3 antibody that's being dosed from another trial sponsor at a much higher dose, and perhaps that may make some level of difference. But certainly, these are unfortunate results that will not advance the field beyond where we were at already. Dr. Diwakar Davar: And to your point about third-generation checkpoint factors that were negative, I guess it's probably worth noting that a trial that you were involved with, KeyVibe-010, that evaluated the PD-1 TIGIT co-formulation of vibostolimab, MK-4280A, was also, unfortunately, similarly negative. So, to your point, it's not clear that all these third-generation receptors are necessarily going to have the same impact in the adjuvant setting, even if they, you know, for example, like TIGIT, and they sometimes may not even have an effect at all in the advanced cancer setting. So, we'll see what the HARMONY phase 3 trial, that's the Regeneron cemiplimab/fianlimab versus pembrolizumab control with cemiplimab with fianlimab at two different doses, we'll see how that reads out. But certainly, as you've said, LAG-3 does not, unfortunately, appear to have an impact in the adjuvant setting. So let's move on to LBA9501. This is the primary analysis of EORTC-2139-MG or the Columbus-AD trial. This was a randomized trial of encorafenib and binimetinib, which we will abbreviate as enco-bini going forward, compared to placebo in high-risk stage II setting in melanoma in patients with BRAF V600E or K mutant disease. So Jason, you know, you happen to know one or two things about the resected stage II setting, so maybe contextualize the stage II setting for us based on the trials that you've led, KEYNOTE-716, as well as CheckMate-76K, set us up to talk about Columbus-AD. Dr. Jason Luke: Thanks for that introduction, and certainly stage II disease has been something I've worked a lot on. The rationale for that has been that building off of the activity of anti–PD-1 in metastatic melanoma and then seeing the activity in stage III, like we just talked about, it was a curious circumstance that dating back about 7 to 8 years ago, there was no availability to use anti–PD-1 for high-risk stage II patients, even though the risk of recurrence and death from melanoma in the context of stage IIB and IIC melanoma is in fact similar or actually higher than in stage IIIA or IIIB, where anti–PD-1 was approved. And in that context, a couple of different trials that you alluded to, the Keynote-716 study that I led, as well as the CheckMate 76K trial, evaluated pembrolizumab and nivolumab, respectively, showing an improvement in relapse-free and distant metastasis-free survival, and both of those agents have subsequently been approved for use in the adjuvant setting by the US FDA as well as the European Medicines Agency.  So bringing then to this abstract, throughout melanoma oncology, we've seen that the impact of anti–PD-1 immunotherapy versus BRAF and MEK-targeted therapy have had very similar outcomes on a sort of comparison basis, both in frontline metastatic and then in adjuvant setting. So it was a totally reasonable question to ask: Could we use adjuvant BRAF and MEK inhibitor therapy? And I think all of us expected the answer would be yes. As we get into the discussion of the trial, I think the unfortunate circumstance was that the timing of this clinical trial being delayed somewhat, unfortunately, made it very difficult to accrue the trial, and so we're going to have to try to read through the tea leaves sort of, based on only a partially complete data set. Dr. Diwakar Davar: So, in terms of the results, they wanted to enroll 815 patients, they only enrolled 110. The RFS and DMFS were marginally improved in the treatment arm but certainly not significantly, which is not surprising because the trial had only accrued 16% to 18% of its complete accrual. As such, we really can't abstract from the stage III COMBI-AD data to stage II patients. And certainly in this setting, one would argue that the primary treatment options certainly remain either anti–PD-1 monotherapy, either with pembrolizumab or nivolumab, based on 716 or 76K, or potentially active surveillance for the patients who are not inclined to get treated.  Can you tell us a little bit about how you foresee drug development going forward in this space because, you know, for example, with HARMONY, certainly IIC disease is a part of HARMONY. We will know at least a little bit about that in this space. So what do you think about the stage IIB/C patient population? Is this a patient population in which future combinations are going to be helpful, and how would you think about where we can go forward from here? Dr. Jason Luke: It is an unfortunate circumstance that this trial could not be accrued at the pace that was necessary. I think all of us believe that the results would have been positive if they'd been able to accrue the trial. In the preliminary data set that they did disclose of that 110 patients, you know, it's clear there is a difference at a, you know, a landmark at a year. They showed a 16% difference, and that would be in line with what has been seen in stage III. And so, you know, I think it's really kind of too bad. There's really going to be no regulatory approach for this consideration. So using BRAF and MEK inhibition in stage II is not going to be part of standard practice moving into the future. To your point, though, about where will the field go? I think what we're already realizing is that in the adjuvant setting, we're really overtreating the total population. And so beyond merely staging by AJCC criteria, we need to move to biomarker selection to help inform which patients truly need the treatment. And in that regard, I don't think we've crystallized together as a field as yet, but the kinds of things that people are thinking about are the integration of molecular biomarkers like ctDNA. When it's positive, it can be very helpful, but in melanoma, we found that, unfortunately, the rates are quite low, you know, in the 10% to 15% range in the adjuvant setting. So then another consideration would be factors in the primary tumor, such as gene expression profiling or other considerations.  And so I think the future of adjuvant clinical trials will be an integration of both the standard AJCC staging system as well as some kind of overlaid molecular biomarker that helps to enrich for a higher-risk population of patients because on a high level, when you abstract out, it's just clearly the case that we're rather substantially overtreating the totality of the population, especially given that in all of our adjuvant studies to date for anti–PD-1, we have not yet shown that there's an overall survival advantage. And so some are even arguing perhaps we should even reserve treatment until patients progress. I think that's a complicated subject, and standard of care at this point is to offer adjuvant therapy, but certainly a lot more to do because many patients, you know, unfortunately, still do progress and move on to metastatic disease. Dr. Diwakar Davar: Let's transition to Abstract 2508. So we're moving on from the melanoma to the novel immunotherapy abstracts. And this is a very, very, very fascinating drug. It's IMA203. So Abstract 2508 is a phase 1 clinical update of IMA203. IMA203 is an autologous TCR-T construct targeting PRAME in patients with heavily pretreated PD-1-refractory metastatic melanoma. So Jason, in the PD-1 and CTLA-4-refractory settings, treatment options are either autologous TIL, response rate, you know, ballpark 29% to 31%, oncolytic viral therapy, RP1 with nivolumab, ORR about 30-ish percent. So new options are needed. Can you tell us a little bit about IMA203? Perhaps tell us for the audience, what is the difference between a TCR-T and traditional autologous TIL? And a little bit about this drug, IMA203, and how it distinguishes itself from the competing TIL products in the landscape. Dr. Jason Luke: I'm extremely enthusiastic about IMA203. I think that it really has transformative potential based on these results and hopefully from the phase 3 trial that's open to accrual now. So, what is IMA203? We said it's a TCR-T cell product. So what that means is that T cells are removed from a patient, and then they can be transduced through various technologies, but inserted into those T cells, we can then add a T-cell receptor that's very specific to a single antigen, and in this case, it's PRAME. So that then is contrasted quite a bit from the TIL process, which includes a surgical resection of a tumor where T cells are removed, but they're not specific necessarily to the cancer, and they're grown up in the lab and then given to the patient. They're both adoptive cell transfer products, but they're very different. One is genetically modified, and the other one is not. And so the process for generating a TCR-T cell is that patients are required to have a new biomarker that some may not be familiar with, which is HLA profiling. So the T-cell receptor requires matching to the concomitant HLA for which the peptide is bound in. And so the classic one that is used in most oncology practices is A*02:01 because approximately 48% of Caucasians have A*02:01, and the frequency of HLA in other ethnicities starts to become highly variable. But in patients who are identified to have A*02:01 genotype, we can then remove blood via leukapheresis or an apheresis product, and then insert via lentiviral transduction this T-cell receptor targeting PRAME. Patients are then brought back to the hospital where they can receive lymphodepleting chemotherapy and then receive the reinfusion of the TCR-T cells. Again, in contrast with the TIL process, however, these T cells are extremely potent, and we do not need to give high-dose interleukin-2, which is administered in the context of TIL. Given that process, we have this clinical trial in front of us now, and at ASCO, the update was from the phase 1 study, which was looking at IMA203 in an efficacy population of melanoma patients who were refractory at checkpoint blockade and actually multiple lines of therapy. So here, there were 33 patients and a response rate of approximately 50% was observed in this population of patients, notably with a duration of response approximately a year in that treatment group. And I realize that these were heavily pretreated patients who had a range of very high-risk features. And approximately half the population had uveal melanoma, which people may be aware is a generally speaking more difficult-to-treat subtype of melanoma that metastasizes to the liver, which again has been a site of resistance to cancer immunotherapy. So these results are extremely promising. To summarize them from what I said, it's easier to make TCR-T cells because we can remove blood from the patient to transduce the T cells, and we don't have to put them through surgery. We can then infuse them, and based on these results, it looks like the response rate to IMA203 is a little bit more than double what we expect from lifileucel. And then, whereas with lifileucel or TILs, we have to give high-dose IL-2, here we do not have to give high-dose IL-2. And so that's pretty promising. And a clinical trial is ongoing now called the SUPREME phase 3 clinical trial, which is hoping to validate these results in a randomized global study. Dr. Diwakar Davar: Now, one thing that I wanted to go over with you, because you know this trial particularly well, is what you think of the likelihood of success, and then we'll talk a little bit about the trial design. But in your mind, do you think that this is a trial that has got a reasonable likelihood of success, maybe even a high likelihood of success? And maybe let's contextualize that to say an alternative trial, such as, for example, the TebeAM trial, which is essentially a T-cell bispecific targeting GP100. It's being compared against SOC, investigator's choice control, also in a similarly heavily pretreated patient population. Dr. Jason Luke: So both trials, I think, have a strong chance of success. They are very different kinds of agents. And so the CD3 bispecific that you referred to, tebentafusp, likely has an effect of delaying progression, which in patients with advanced disease could have a value that might manifest as overall survival. With TCR-T cells, by contrast, we see a very high response rate with some of the patients going into very durable long-term benefit. And so I do think that the SUPREME clinical trial has a very high chance of success. It will be the first clinical trial in solid tumor oncology randomizing patients to receive a cell therapy as compared with a standard of care. And within that standard of care control arm, TILs are allowed as a treatment. And so it will also be the first study that will compare TCR-T cells against TILs in a randomized phase 3. But going back to the data that we've seen in the phase 1 trial, what we observe is that the duration of response is really connected to the quality of the response, meaning if you have more than a 50% tumor shrinkage, those patients do very, very well. But even in patients who have less than 50% tumor shrinkage, the median progression-free survival right now is about 4.5 months. And again, as we think about trial design, standard of care options for patients who are in this situation are unfortunately very bad. And the progression-free survival in that population is probably more like 2 months. So this is a trial that has a very high likelihood of being positive because the possibility of long-term response is there, but even for patients who don't get a durable response, they're likely going to benefit more than they would have based on standard chemotherapy or retreatment with an anti–PD-1 agent. Dr. Diwakar Davar: Really, a very important trial to enroll, a trial that is first in many ways. First of a new generation of TCR-T agents, first trial to look at cell therapy in the control arm, a new standard of efficacy, but potentially also if this trial is successful, it will also be a new standard of trial conduct, a new kind of trial, of a set of trials that will be done in the second-line immunotherapy-refractory space. So let's pivot to the last trial that we were going to discuss, which was Abstract 2501. Abstract 2501 is a first-in-human phase 1/2 trial evaluating BNT142, which is the first-in-class mRNA-encoded bispecific targeting Claudin-6 and CD3 in patients with Claudin-positive tumors. We'll talk a little bit about this, but maybe let's start by talking a little bit about Claudin-6. So Claudin-6 is a very interesting new target. It's a target that's highly expressed in GI and ovarian tumors. There are a whole plethora of Claudin-6-targeting agents, including T-cell bispecifics and Claudin-6-directed CAR-Ts that are being developed. But BNT142 is novel. It's a novel lipid nanoparticle LNP-encapsulated mRNA. The mRNA encodes an anti–Claudin-6 CD3 bispecific termed RiboMAB-021. And it then is administered to the patient. The BNT142-encoding mRNA LNPs are taken up by the liver and translated into the active drug. So Jason, tell us a little bit about this agent. Why you think it's novel, if you think it's novel, and let's talk a little bit then about the results. Dr. Jason Luke: So I certainly think this is a novel agent, and I think this is just the first of what will probably become a new paradigm in oncology drug development. And so you alluded to this, but just to rehash it quickly, the drug is encoded as genetic information that's placed in the lipid nanoparticle and then is infused into the patient. And after the lipid nanoparticles are taken up by the liver, which is the most common place that LNPs are usually taken up, that genetic material in the mRNA starts to be translated into the actual protein, and that protein is the drug. So this is in vivo generation, so the patient is making their own drug inside their body. I think it's a really, really interesting approach. So for any drug that could be encoded as a genetic sequence, and in this case, it's a bispecific, as you mentioned, CD3-Claudin-6 engager, this could have a tremendous impact on how we think about pharmacology and novel drug development moving into the future in oncology. So I think it's an extremely interesting drug, the like of which we'll probably see only more moving forward. Dr. Diwakar Davar: Let's maybe briefly talk about the results. You know, the patient population was heavily pretreated, 65 or so patients, mostly ovarian cancer. Two-thirds of the patients were ovarian cancer, the rest were germ cell and lung cancer patients. But let's talk a little bit about the efficacy. The disease control rate was about 58% in the phase 1 population as a whole, but 75% in the ovarian patient population. Now tell us a little bit about the interesting things about the drug in terms of the pharmacokinetics, and also then maybe we can pivot to the clinical activity by dose level. Dr. Jason Luke: Well, so they did present in their presentation at ASCO a proportionality showing that as higher doses were administered, that greater amounts of the drug were being made inside the patient. And so that's an interesting observation, and it's an important one, right? Suggesting that the pharmacology that we classically think of by administering drugs by IV, for example, would still be in play. And that did translate into some level of efficacy, particularly at the higher dose levels. Now, the caveat that I'll make a note of is that disease control rate is an endpoint that I think we have to be careful about because what that really means is sometimes a little bit unclear. Sometimes patients have slowly growing tumors and so on and so forth. And the clinical relevance of disease control, if it doesn't last at least 6 months, I think is probably pretty questionable. So I think these are extremely interesting data, and there's some preliminary sense that getting the dose up is going to matter because the treatment responses were mostly observed at the highest dose levels. There's also a caveat, however, that across the field of CD3 bispecific molecules like this, there's been quite a bit of heterogeneity in terms of the response rate, with some of them only really generating stable disease responses and other ones having more robust responses. And so I think this is a really interesting initial foray into this space. My best understanding is this molecule is not moving forward further after this, but I think that this really does set it up to be able to chase after multiple different drug targets on a CD3 bispecific backbone, both in ovarian cancer, but then basically across all of oncology. Dr. Diwakar Davar: Perfect. This is a very new sort of exciting arena where we're going to be looking at, in many ways, these programmable constructs, whether we're looking at in vivo-generated, in this case, a T-cell bispecific, but we've also got newer drugs where we are essentially giving drugs where people are generating in vivo CAR T, and also potentially even in vivo TCR-T. But certainly lots of new excitement around this entire class of drugs. And so, what we'd like to do at this point in time is switch to essentially the fact that we've got a very, very exciting set of data at ASCO 2025. You've heard from Dr. Luke regarding the advances in both early drug development but also in advanced cutaneous melanoma. And Jason, as always, thank you so much for sharing your very valuable and great, fantastic insights with us on the ASCO Daily News Podcast. Dr. Jason Luke: Well, thanks again for the opportunity. Dr. Diwakar Davar: And thank you to our listeners for taking your time to listen today. You will find the links to the abstracts that we discussed today in the transcript of this episode. And finally, if you value the insights that you hear on the ASCO Daily News Podcast, please take a moment to rate, review, and subscribe wherever you get your podcasts. 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. Diwakar Davar    @diwakardavar    Dr. Jason Luke @jasonlukemd Follow ASCO on social media:     @ASCO on Twitter       ASCO on Bluesky   ASCO on Facebook       ASCO on LinkedIn   Disclosures:     Dr. Diwakar Davar:      Honoraria: Merck, Tesaro, Array BioPharma, Immunocore, Instil Bio, Vedanta Biosciences     Consulting or Advisory Role: Instil Bio, Vedanta Biosciences     Consulting or Advisory Role (Immediate family member): Shionogi     Research Funding: Merck, Checkmate Pharmaceuticals, CellSight Technologies, GSK, Merck, Arvus Biosciences, Arcus Biosciences     Research Funding (Inst.): Zucero Therapeutics     Patents, Royalties, Other Intellectual Property: Application No.: 63/124,231 Title: COMPOSITIONS AND METHODS FOR TREATING CANCER Applicant: University of Pittsburgh–Of the Commonwealth System of Higher Education Inventors: Diwakar Davar Filing Date: December 11, 2020 Country: United States MCC Reference: 10504-059PV1 Your Reference: 05545; and Application No.: 63/208,719 Enteric Microbiotype Signatures of Immune-related Adverse Events and Response in Relation to Anti-PD-1 Immunotherapy     Dr. Jason Luke:     Stock and Other Ownership Interests: Actym Therapeutics, Mavu Pharmaceutical, Pyxis, Alphamab Oncology, Tempest Therapeutics, Kanaph Therapeutics, Onc.AI, Arch Oncology, Stipe, NeoTX     Consulting or Advisory Role: Bristol-Myers Squibb, Merck, EMD Serono, Novartis, 7 Hills Pharma, Janssen, Reflexion Medical, Tempest Therapeutics, Alphamab Oncology, Spring Bank, Abbvie, Astellas Pharma, Bayer, Incyte, Mersana, Partner Therapeutics, Synlogic, Eisai, Werewolf, Ribon Therapeutics, Checkmate Pharmaceuticals, CStone Pharmaceuticals, Nektar, Regeneron, Rubius, Tesaro, Xilio, Xencor, Alnylam, Crown Bioscience, Flame Biosciences, Genentech, Kadmon, KSQ Therapeutics, Immunocore, Inzen, Pfizer, Silicon Therapeutics, TRex Bio, Bright Peak, Onc.AI, STipe, Codiak Biosciences, Day One Therapeutics, Endeavor, Gilead Sciences, Hotspot Therapeutics, SERVIER, STINGthera, Synthekine     Research Funding (Inst.): Merck , Bristol-Myers Squibb, Incyte, Corvus Pharmaceuticals, Abbvie, Macrogenics, Xencor, Array BioPharma, Agios, Astellas Pharma , EMD Serono, Immatics, Kadmon, Moderna Therapeutics, Nektar, Spring bank, Trishula, KAHR Medical, Fstar, Genmab, Ikena Oncology, Numab, Replimmune, Rubius Therapeutics, Synlogic, Takeda, Tizona Therapeutics, Inc., BioNTech AG, Scholar Rock, Next Cure     Patents, Royalties, Other Intellectual Property: Serial #15/612,657 (Cancer Immunotherapy), and Serial #PCT/US18/36052 (Microbiome Biomarkers for Anti-PD-1/PD-L1 Responsiveness: Diagnostic, Prognostic and Therapeutic Uses Thereof)     Travel, Accommodations, Expenses: Bristol-Myers Squibb, Array BioPharma, EMD Serono, Janssen, Merck, Novartis, Reflexion Medical, Mersana, Pyxis, Xilio

MeidasTouch host Ben Meiselas reports on how world leaders at NATO perfectly isolated Trump by forming security pacts and deals that do not include the United States like the new European Union and Canada security deal. Zbiotics: Head to https://zbiotics.com/MEIDAS to get 15% off your first order when you use MEIDAS at checkout. Visit https://meidasplus.com for more! Remember to subscribe to ALL the MeidasTouch Network Podcasts: MeidasTouch: https://www.meidastouch.com/tag/meidastouch-podcast Legal AF: https://www.meidastouch.com/tag/legal-af MissTrial: https://meidasnews.com/tag/miss-trial The PoliticsGirl Podcast: https://www.meidastouch.com/tag/the-politicsgirl-podcast The Influence Continuum: https://www.meidastouch.com/tag/the-influence-continuum-with-dr-steven-hassan Mea Culpa with Michael Cohen: https://www.meidastouch.com/tag/mea-culpa-with-michael-cohen The Weekend Show: https://www.meidastouch.com/tag/the-weekend-show Burn the Boats: https://www.meidastouch.com/tag/burn-the-boats Majority 54: https://www.meidastouch.com/tag/majority-54 Political Beatdown: https://www.meidastouch.com/tag/political-beatdown On Democracy with FP Wellman: https://www.meidastouch.com/tag/on-democracy-with-fpwellman Uncovered: https://www.meidastouch.com/tag/maga-uncovered Coalition of the Sane: https://meidasnews.com/tag/coalition-of-the-sane Learn more about your ad choices. Visit megaphone.fm/adchoices

Music for Breakfast: Grammy 2025 Highlights and Hot Takes!In this episode of Music for Breakfast, hosts Octavia March and Rell Roulette break down the most memorable moments from the 2025 Grammy Awards. They discuss Kendrick Lamar's big wins, Beyonce's historic night, Chris Brown's controversial absence, and the impact of DEI initiatives on the event. The hosts also touch on some of the more petty moments, like JLo and Shakira's Super Bowl spat, and Janelle Monáe's performance in the Michael Jackson tribute. They wrap up with shout-outs to standout performances and urge listeners to share their thoughts in the comments.00:00 Introduction and Apologies00:15 Chris Brown and the Michael Jackson Tribute00:45 Kendrick Lamar's Grammy Sweep01:07 Music for Breakfast Hosts Introduction02:55 Grammy Highlights and Petty Moments08:17 Diversity and Inclusion at the Grammys11:57 Beyoncé's Big Win21:19 AI and the Beatles25:57 Final Thoughts and Wrap-Up #musicivbreakfast  #hiphop #youtube #fyp #trendingCopyright Disclaimer Under Section 107 of the Copyright Act 1976, allowance is made for "fair use" for purposes such as criticism, comment, news reporting, teaching, scholarship, and research. Fair use is a use permitted by copyright statute that might otherwise be infringing. Non-profit, educational or personal use tips the balance in favor of fair use. No copyright infringement intended. ALL RIGHTS BELONG TO THEIR RESPECTIVE OWNERS

Dr. Neeraj Agarwal and Dr. Jeanny Aragon-Ching discuss important advances in the treatment of prostate, bladder, and kidney cancers that were presented at the 2025 ASCO Annual Meeting. TRANSCRIPT Dr. Neeraj Agarwal: Hello, and welcome to the ASCO Daily News Podcast. I am Dr. Neeraj Agarwal, your guest host of the ASCO Daily News Podcast today. I am the director of the Genitourinary Oncology Program and a professor of medicine at the University of Utah Huntsman Cancer Institute and editor-in-chief of the ASCO Daily News.  I am delighted to be joined by Dr. Jeanny Aragon-Ching, a GU medical oncologist and the clinical program director of the GU Center at the Inova Schar Cancer Institute in Virginia. Today, we will be discussing some key abstracts in GU oncology that were presented at the 2025 ASCO Annual Meeting.  Our full disclosures are available in the transcript of this episode.  Jeanny, it is great to have you on the podcast. Dr. Jeanny Aragon-Ching: Oh, thank you so much, Neeraj. Dr. Neeraj Agarwal: Jeanny, let's begin with some prostate cancer abstracts. Let's begin with Abstract 5017 titled, “Phase 1 study results of JNJ-78278343 (pasritamig) in metastatic castration-resistant prostate cancer.” Can you walk us through the design and the key findings of this first-in-human trial? Dr. Jeanny Aragon-Ching: Yeah, absolutely, Neeraj. So this study, presented by Dr. Capucine Baldini, introduces pasritamig, a first-in-class T-cell redirecting bispecific antibody that simultaneously binds KLK2 on prostate cancer cells and CD3 receptor complexes on T cells. KLK2 is also known as human kallikrein 2, which is selectively expressed in prostate tissue. And for reference, KLK3 is what we now know as the PSA, prostate-specific antigen, therefore making it an attractive and specific target for therapeutic engagement. Now, while this was an early, first-in-human, phase 1 study, it enrolled 174 heavily pretreated metastatic CRPC patients. So many were previously treated with ARPIs, taxanes, and radioligand therapy. So given the phase 1 nature of this study, the primary objective was to determine the safety and the RP2D, which is the recommended phase 2 dose. Secondary objectives included preliminary assessment of antitumor activity. So, pasritamig was generally well tolerated. There were no treatment-related deaths. Serious adverse events were rare. And in the RP2D safety cohort, where patients received the step-up dosing up to 300 mg of IV every 6 weeks, the most common treatment-related adverse events were low-grade infusion reactions. There was fatigue and grade 1 cytokine release syndrome, what we call CRS. And no cases of neurotoxicity, or what we call ICANS, the immune effector cell-associated neurotoxicity syndrome, reported. Importantly, the CRS occurred in just about 8.9% of patients. All were grade 1. No patients required tocilizumab or discontinued treatment due to adverse events. So, this suggests a favorable safety profile, allowing hopefully for outpatient administration without hospitalization, which will be very important when we're thinking about bispecifics moving forward. In terms of efficacy, pasritamig showed promising activity. About 42.4% of evaluable patients achieved a PSA50 response. Radiographic PFS was about 6.8 months. And among patients with measurable disease, the objective response rate was about 16.1% in those with lymph node or bone metastases, and about 3.7% in those with visceral disease, with a median duration of response of about 11.3 months. So, altogether, this data suggests that pasritamig may offer a well-tolerated and active new potential option for patients with metastatic CRPC.   Again, as a reminder, with the caveat that this is still an early phase 1 study. Dr. Neeraj Agarwal: Thank you, Jeanny. These are promising results for a bispecific T-cell engager, pasritamig, in prostate cancer. I agree, the safety and durability observed here stand out, and this opens the door for further development, possibly even in earlier disease settings.  So, shifting now from immunotherapy to the evolving role of genomics in prostate cancer. So let's discuss Abstract 5094, a real-world, retrospective analysis exploring the prognostic impact of homologous recombination repair gene mutations, especially BRCA1 and BRCA2 mutations, in metastatic hormone-sensitive prostate cancer. Can you tell us more about this abstract, Jeanny? Dr. Jeanny Aragon-Ching: Sure, Neeraj. So this study was presented by Dr. David Olmos, represents one of the largest real-world analyses we have evaluating the impact of homologous recombination repair, or what we would call HRR, alterations in metastatic hormone-sensitive prostate cancer. So, this cohort included 556 men who underwent paired germline and somatic testing. Now, about 30% of patients had HRR alterations, with about 12% harboring BRCA1 or BRCA2 mutations and 16% having alterations in other HRR genes. Importantly, patients were stratified via CHAARTED disease volume, and outcomes were examined across treatment approaches, including ADT alone, doublet therapy, and triplet therapy. The prevalence of BRCA and HRR alterations were about similar between the metastatic hormone-sensitive prostate cancer and the metastatic castrate-resistant prostate cancer, with no differences observed, actually, between the patients with high volume versus low volume disease.  So, the key finding was that BRCA and HRR alterations were associated with poor clinical outcomes in metastatic hormone-sensitive prostate cancer. And notably, the impact of these alterations may actually be even greater in metastatic hormone-sensitive prostate cancer than previously reported in metastatic CRPC. So, the data showed that when BRCA mutations are present, the impact of the volume of disease is actually limited. So, poor outcomes were observed across the board for both high-volume and low-volume groups. So, the analysis showed that patients with HRR alterations had significantly worse outcomes compared to patients without HRR alterations. Median radiographic progression-free survival was about 20.5 months for the HRR-altered patients versus 30.6 months for the non-HRR patients, with a hazard ratio of 1.6. Median overall survival was 39 months for HRR-altered patients compared to 55.7 months for the non-HRR patients, with a hazard ratio of 1.5. Similar significant differences were observed when BRCA-mutant patients were compared with patients harboring non-BRCA HRR mutations. Overall, poor outcomes were independent of treatment of ARPI or taxanes. Dr. Neeraj Agarwal: Thank you, Jeanny. So, these data reinforce homologous recombination repair mutations as both a predictive and prognostic biomarker, not only in the mCRPC, but also in the metastatic hormone-sensitive setting as well. It also makes a strong case for incorporating genomic testing early in the disease course and not waiting until our patients have castration-resistant disease. Dr. Jeanny Aragon-Ching: Absolutely, Neeraj. And I think this really brings home the point and the lead up to the AMPLITUDE trial, which is LBA5006, a phase 3 trial that builds on this very concept of testing with a PARP inhibitor, niraparib, in the hormone-sensitive space. Can you tell us a little bit more about this abstract, Neeraj? Dr. Neeraj Agarwal: Sure. So, the AMPLITUDE trial, a phase 3 trial presented by Dr. Gerhardt Attard, enrolled 696 patients with metastatic hormone-sensitive prostate cancer and HRR gene alterations. 56% of these patients had BRCA1 and BRCA2 mutations. Patients were randomized to receive abiraterone with or without niraparib, a PARP inhibitor. The majority of patients, 78% of these patients, had high-volume metastatic hormone-sensitive prostate cancer, and 87% of these patients had de novo metastatic HSPC. And 16% of these patients received prior docetaxel, which was allowed in the clinical trial. So, with a median follow-up of nearly 31 months, radiographic progression-free survival was significantly prolonged with the niraparib plus abiraterone combination, and median was not reached in this arm, compared to abiraterone alone, which was 29.5 months, with a hazard ratio of 0.63, translating to a 37% reduction in risk of progression or death. This benefit was even more pronounced in the BRCA1 and BRCA2 subgroup, with a 48% reduction in risk of progression, with a hazard ratio of 0.52. Time to symptomatic progression also improved significantly across all patients, including patients with BRCA1, BRCA2, and HRR mutations. Although overall survival data remain immature, early trends favored the niraparib plus abiraterone combination. The safety profile was consistent with prior PARP inhibitor studies, with grade 3 or higher anemia and hypertension were more common but manageable. Treatment discontinuation due to adverse events remained low at 11%, suggesting that timely dose modifications when our patients experience grade 3 side effects may allow our patients to continue treatment without discontinuation. These findings support niraparib plus abiraterone as a potential new standard of care in our patients with metastatic hormone-sensitive prostate cancer with HRR alterations, and especially in those who had BRCA1 and BRCA2 mutations. Dr. Jeanny Aragon-Ching: Thank you, Neeraj. This trial is especially exciting because it brings PARP inhibitors earlier into the treatment paradigm. Dr. Neeraj Agarwal: Exactly. And it is exciting to see the effect of PARP inhibitors in the earlier setting.  So Jeanny, now let's switch gears a bit to bladder cancer, which also saw several impactful studies. Could you tell us about Abstract 4502, an exploratory analysis from the EV-302 trial, which led to approval of enfortumab vedotin plus pembrolizumab for our patients with newly diagnosed metastatic bladder cancer? So here, the authors looked at the outcomes in patients who achieved a confirmed complete response with EV plus pembrolizumab. Dr. Jeanny Aragon-Ching: Sure, Neeraj. So, EV-302 demonstrated significant improvements in progression-free and overall survival for patients previously treated locally advanced or metastatic urothelial cancer, I'll just call it metastatic UC, as a frontline strategy, establishing EV, which is enfortumab vedotin, plus pembro, with pembrolizumab as standard of care in this setting.  So, this year at ASCO, Dr Shilpa Gupta presented this exploratory responder analysis from the phase 3 EV-302 trial. Among 886 randomized patients, about 30.4% of patients, this is about 133, in the EV+P arm, and 14.5% of the patients in the chemotherapy arm, achieved a confirmed complete response. They call it the CCR rates. So for patients who achieved this, median PFS was not reached with EV+P compared to 26.9 months with chemotherapy, with a hazard ratio of 0.36, translating to a 64% reduction in the risk of progression. Overall survival was also improved. So the median OS was not reached in either arm, but the hazard ratio favored the EV+P at 0.37, translating to a 63% reduction in the risk of death. The median duration of complete response was not reached with EV+P compared to 15.2 months with chemotherapy. And among those patients who had confirmed CRs at 24 months, 78% of patients with the EV+P arm remained progression-free, and around 95% of the patients were alive, compared to 54% of patients who were progression-free and 86% alive of the patients in the chemotherapy arm. Safety among responders were also consistent with prior reports. Grade 3 or higher treatment-related adverse events occurred in 62% of EV+P responders and 72% of chemotherapy responders. Most adverse events were managed with dose modifications, and importantly, no treatment-related deaths were reported among those who were able to achieve complete response.  So these findings further reinforce EV and pembro as the preferred first-line therapy for metastatic urothelial carcinoma, offering a higher likelihood of deep, durable responses with a fairly manageable safety profile. Dr. Neeraj Agarwal: Thank you for the great summary, Jeanny. These findings underscore the depth and durability of responses achievable with this combination and also suggest that achieving a response may be a surrogate for long-term benefit in patients with metastatic urothelial carcinoma.  So now, let's move to Abstract 4503, an exploratory ctDNA analysis from the NIAGARA trial, which evaluated perioperative durvalumab, an immune checkpoint inhibitor, in muscle-invasive bladder cancer. So what can you tell us about this abstract? Dr. Jeanny Aragon-Ching: Absolutely, Neeraj. So, in NIAGARA, presented by Dr. Tom Powles, the addition of perioperative durvalumab to neoadjuvant chemotherapy, gem/cis, significantly improved event-free survival, overall survival, and pathologic complete response in patients with cisplatin-eligible muscle-invasive bladder cancer. Recall that this led to the U.S. FDA approval of this treatment regimen on March 28, 2025.  So, a planned exploratory analysis evaluated the ctDNA dynamics and their association with clinical outcomes, which was the one presented recently at ASCO. So, the study found that the incidence of finding ctDNA positivity in these patients was about 57%. Following neoadjuvant treatment, this dropped to about 22%, with ctDNA clearance being more common in the durvalumab arm, about 41%, compared to the chemotherapy control arm of 31%. Notably, 97% of patients who remained ctDNA positive prior to surgery failed to achieve a pathologic CR. So, this indicates a strong association between ctDNA persistence and lack of tumor eradication. So, postoperatively, only about 9% of patients were ctDNA positive. So, importantly, durvalumab conferred an event-free survival benefit regardless of ctDNA status at both baseline and post-surgery. Among patients who were ctDNA positive at baseline, durvalumab led to a hazard ratio of 0.73 for EFS. So, this translates to a 27% reduction in the risk of disease recurrence, progression, or death compared to the control arm. In the post-surgical ctDNA-positive group, the disease-free survival was also improved with a hazard ratio of 0.49, translating to a 51% reduction in the risk of recurrence.  So, these findings underscore the prognostic value of ctDNA and suggest that durvalumab provides clinical benefit irrespective of molecular residual disease status. So, the data also supports that ctDNA is a promising biomarker for future personalized strategies in the perioperative treatment of muscle-invasive bladder cancer. Dr. Neeraj Agarwal: Thank you, Jeanny. It is great to see that durvalumab is improving outcomes in these patients regardless of ctDNA status. However, based on these data, presence of ctDNA in our patients warrants a closer follow-up with imaging studies, because these patients with positive ctDNA seem to have a higher risk of recurrence. Dr. Jeanny Aragon-Ching: I agree, Neeraj.  Let's round out the bladder cancer discussion with Abstract 4518, which reported the interim results of SURE-02, which is a phase 2 study evaluating neoadjuvant sacituzumab govitecan plus pembrolizumab in cisplatin-ineligible muscle-invasive bladder cancer. Can you tell us more about this abstract, Neeraj? Dr. Neeraj Agarwal: Sure, Jeanny. So, Dr Andrea Necchi presented interim results from the SURE-02 trial. This is a phase 2 study evaluating neoadjuvant sacituzumab govitecan plus pembrolizumab, followed by a response-adapted bladder-sparing treatment and adjuvant pembrolizumab in patients with muscle-invasive bladder cancer.  So, in this interim analysis, 40 patients were treated and 31 patients were evaluable for efficacy. So, the clinical complete response rate was 38.7%. All patients achieving clinical complete response underwent bladder-sparing approach with a repeat TURBT instead of radical cystectomy. Additionally, 51.6% of patients achieved excellent pathologic response with a T stage of 1 or less after neoadjuvant therapy. The treatment was well tolerated, with only 12.9% of patients experiencing grade 3 or higher adverse events without needing dose reduction of sacituzumab. Molecular profiling, interestingly, showed that clinical complete response correlated with luminal and genomically unstable subtypes, while high stromal gene expression was associated with lack of response.  These results suggest that sacituzumab plus pembrolizumab combination has promising activity in this setting, and tolerability, and along with other factors may potentially allow a bladder preservation approach in a substantial number of patients down the line. Dr. Jeanny Aragon-Ching: Yeah, agree with you, Neeraj. And the findings are very provocative and support completing the full trial enrollment and further exploration of this strategy in muscle-invasive bladder cancer in order to improve and provide further bladder-sparing strategies. Dr. Neeraj Agarwal: Agree. So, let's now turn to the kidney cancer, starting with Abstract 4505, the final overall analysis from CheckMate-214 trial, which evaluated nivolumab plus ipilimumab, so dual checkpoint inhibition strategy, versus sunitinib in our patients with metastatic clear cell renal cell carcinoma. Dr. Jeanny Aragon-Ching: Yeah, absolutely, Neeraj. So, the final 9-year analysis of the phase 3 CheckMate-214 trial confirms the long-term superiority of nivolumab and ipilimumab over sunitinib for first-line treatment of advanced metastatic renal cell carcinoma. So, this has a median follow-up of 9 years. Overall survival remains significantly improved with the combination. So, in the ITT patient population, the intention-to-treat, the hazard ratio for overall survival was 0.71. So, this translates to a 29% reduction in the risk of death. 31% of patients were alive at this 108-month follow-up compared to 20% only in those who got sunitinib. So, similar benefits were observed in the intermediate- and poor-risk groups with a hazard ratio of 0.69, and 30% versus 19% survival at 108 months.  Importantly, a delayed benefit was also seen in those favorable-risk patients. So, the hazard ratio for overall survival improved from 1.45 in the initial report and now at 0.8 at 9 years follow-up, with 35% of patients alive at 108 months compared to 22% in those who got sunitinib. Progression-free survival also favored the nivo-ipi arm across all risk groups. At 96 months, the probability of remaining progression-free was about 23% compared to 9% in the sunitinib arm in the ITT patient population, 25% versus 9% in the intermediate- and poor-risk patients, and 13% compared to 11% in the favorable-risk patients. Importantly, at 96 months, 48% of patients in the nivo-ipi responders remained in response compared to just 19% in those who got sunitinib. And in the favorable-risk group, 36% of patients who responded remained in response, although data were not available for sunitinib in this subgroup.  So, this data reinforces the use of nivolumab and ipilimumab as a durable and effective first-line effective strategy for standard of care across all risk groups for advanced renal cell carcinoma. Dr. Neeraj Agarwal: Thank you, Jeanny. And of course, since ipi-nivo data were presented, several other novel ICI-TKI combinations have emerged. And I'm really hoping to see very similar data with TKI-ICI combinations down the line. It is really important to note that we are not seeing any new safety signals with the ICI combinations or ICI-based therapies, which is very reassuring given the extended exposure. Dr. Jeanny Aragon-Ching: Absolutely agree with you there, Neeraj.  Now, going on and moving on to Abstract 4514, which is the KEYNOTE-564 trial, and they reported on the 5-year outcomes of adjuvant pembrolizumab in clear cell RCC in patients who are at high risk for recurrence. Can you tell us a little bit more about this abstract, Neeraj? Dr. Neeraj Agarwal: Sure. So, the KEYNOTE-564 trial established pembrolizumab monotherapy as the first adjuvant regimen to significantly improve both disease-free survival and overall survival compared to placebo after surgery for patients with clear cell renal cell carcinoma. So, Dr Naomi Haas presented the 5-year update from this landmark trial.  A total of 994 patients were randomized to receive either pembrolizumab or placebo. The median follow-up at the time of this analysis was approximately 70 months. Disease-free survival remained significantly improved with pembrolizumab. The median DFS was not reached with pembrolizumab compared to 68.3 months with placebo, with a hazard ratio of 0.71, translating to a 29% reduction in risk of recurrence. At 5 years, 60.9% of patients receiving pembrolizumab remained disease-free compared to 52.2% with placebo. Overall survival also favored pembrolizumab. The hazard ratio for OS was 0.66, translating to a 34% reduction in risk of death, with an estimated 5-year overall survival rate of 87.7% with pembrolizumab compared to 82.3% for placebo. Importantly, these benefits were consistent across all key subgroups, including patients with sarcomatoid features. In addition, no new serious treatment-related adverse events have been reported in the 3 years since treatment completion.  So, these long-term data confirm pembrolizumab as a durable and effective standard adjuvant therapy for patients with resected, high-risk clear cell renal cell carcinoma. Dr. Jeanny Aragon-Ching: Thank you for that wonderful summary, Neeraj. Dr. Neeraj Agarwal: That wraps up our kidney cancer highlights. Any closing thoughts, Jeanny, before we conclude? Dr. Jeanny Aragon-Ching: It's been so wonderful reviewing these abstracts with you, Neeraj. So, the 2025 ASCO Annual Meeting showcased a lot of transformative data across GU cancers, from first-in-class bispecifics to long-term survival in RCC. And these findings are already shaping our clinical practices. Dr. Neeraj Agarwal: I agree. And we have covered a broad spectrum of innovations in GU cancers with strong clinical relevance.  So, thank you, Jeanny, for joining me today and sharing your insights.  And thank you to our listeners for joining us. You will find links to the abstracts discussed today in the transcript of this episode. If you find these conversations valuable, please take a moment to rate, review, and subscribe to the ASCO Daily News Podcast wherever you listen. Thank you so much. 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. Find out more about today's speakers:    Dr. Neeraj Agarwal     @neerajaiims     Dr. Jeanny Aragon-Ching   Follow ASCO on social media:       @ASCO on Twitter       ASCO on Bluesky   ASCO on Facebook       ASCO on LinkedIn       Disclosures:   Dr. Neeraj Agarwal:   Consulting or Advisory Role: Pfizer, Bristol-Myers Squibb, AstraZeneca, Nektar, Lilly, Bayer, Pharmacyclics, Foundation Medicine, Astellas Pharma, Lilly, Exelixis, AstraZeneca, Pfizer, Merck, Novartis, Eisai, Seattle Genetics, EMD Serono, Janssen Oncology, AVEO, Calithera Biosciences, MEI Pharma, Genentech, Astellas Pharma, Foundation Medicine, and Gilead Sciences  Research Funding (Institution): Bayer, Bristol-Myers Squibb, Takeda, Pfizer, Exelixis, Amgen, AstraZeneca, Calithera Biosciences, Celldex, Eisai, Genentech, Immunomedics, Janssen, Merck, Lilly, Nektar, ORIC Pharmaceuticals, Crispr Therapeutics, Arvinas  Dr. Jeanny Aragon-Ching:   Honoraria: Bristol-Myers Squibb, EMD Serono, Astellas Scientific and Medical Affairs Inc., Pfizer/EMD Serono   Consulting or Advisory Role: Algeta/Bayer, Dendreon, AstraZeneca, Janssen Biotech, Sanofi, EMD Serono, MedImmune, Bayer, Merck, Seattle Genetics, Pfizer, Immunomedics, Amgen, AVEO, Pfizer/Myovant, Exelixis,    Speakers' Bureau: Astellas Pharma, Janssen-Ortho, Bristol-Myers Squibb, Astellas/Seattle Genetics

It's part 2 of our wild, unfiltered, and unexpectedly emotional episode when Carolyn Wiger returns to break down her time on The Traitors, share behind-the-scenes drama, and reflect on life, loyalty, and lips. Carolyn explains why she refused to eliminate Dorinda Medley early in the game—despite strategy and pressure—calling her a “badass bitch” and recognizing how much fans adore her. She also unleashes her honest take on Boston Rob Mariano, criticizing his overexposure and dominance, saying it made others feel like “pawns.” She calls out Bob the Drag Queen and Danielle Reyes for backstabbing her mid-game, which left her feeling betrayed and emotional. There's still no real resolution, and Carolyn opens up about how much it hurt—especially from people she expected more compassion from.

Dr. Vamsi Velcheti and Dr. Nate Pennell discuss novel treatment approaches in small cell and non-small cell lung cancer that were featured at the 2025 ASCO Annual Meeting. TRANSCRIPT Dr. Vamsi Velcheti: Hello, I'm Dr. Vamsi Velcheti, your guest host of the ASCO Daily News Podcast. I'm a professor of medicine and chief of hematology and oncology at the Mayo Clinic in Jacksonville, Florida. The 2025 ASCO Annual Meeting featured some exciting advancements in small cell lung cancer, targeted therapies for non-small cell lung cancer, and other novel [treatment] approaches. Today, I'm delighted to be joined by Dr. Nate Pennell to discuss some of the key abstracts that are advancing the lung cancer field. Dr. Pennell is the co-director of the Cleveland Clinic Lung Cancer Program and also the vice chair of clinical research at the Taussig Cancer Institute. Our full disclosures are available in the transcript of this episode. Nate, it's great to have you back on the podcast. Thanks so much for being here. Dr. Nate Pennell: Thanks, Vamsi. Always a pleasure. Dr. Vamsi Velcheti: Let's get started, and I think the first abstract that really caught my attention was Abstract 8516, “The Randomized Trial of Relevance of Time of Day of Immunotherapy for Progression-Free and Overall Survival in Patients With Non-Small Cell Lung Cancer.” What are your thoughts about this, Nate? Dr. Nate Pennell: I agree. I thought this was one of the most discussed abstracts, certainly in the lung cancer session, but I think even outside of lung cancer, it got some discussion. So, just to put this in perspective, there have been a number of publications that have all been remarkably consistent, and not just in lung cancer but across multiple cancer types, that immunotherapy, immune checkpoint inhibitors, are commonly used. And all of them have suggested, when looking at retrospective cohorts, that patients who receive immune checkpoint inhibitors earlier in the day – so in the morning or before the early afternoon – for whatever reason, appear to have better outcomes than those who get it later in the day, and this has been repeated. And I think many people just sort of assumed that this was some sort of strange association and that there was something fundamentally different from a prognostic standpoint in people who came in in the morning to get their treatment versus those who came later in the afternoon, and that was probably the explanation. The authors of this randomized trial actually decided to test this concept. And so, about 210 patients with previously untreated advanced non-small cell lung cancer were randomly assigned to get chemo and immune checkpoint inhibitor – either pembrolizumab or sintilimab – and half of them were randomly assigned to get the treatment before 3 PM in the afternoon, and half of them were assigned to get it after 3 PM in the afternoon. And it almost completely recapitulated what was seen in the retrospective cohorts. So, the median progression-free survival in those who got earlier treatment was 13.2 months versus only 6.5 months in those who got it later in the day. So, really enormous difference with a hazard ratio of 0.43, which was statistically significant. And perhaps even more striking, the median overall survival was not reached in the early group versus 17.8 months in the late group with a hazard ratio of 0.43, also highly statistically significant. Even the response rate was 20% higher in the early patients; 75% response rate compared to 56% in the late-time-of-day patients. So very consistent across all measures of efficacy with pretty good matched characteristics across the different groups. And so, I have to tell you, I don't know what to make of this. I certainly was a skeptic about the retrospective series, but now we have a prospective randomized trial that shows essentially the same thing. So, maybe there is a difference between getting treated in the morning, although I have yet to hear someone give a very good mechanistic explanation as to why this would be. What were your thoughts on this? Dr. Vamsi Velcheti: It's indeed fascinating, Nate, and I actually think this was a very interesting abstract. Really, I was caught off guard looking at the data. I mean, if it were a drug, we would be so excited, right? I mean, with those kind of survival benefits. I don't know. I think circadian rhythm probably has something to do with it, like different cytokine profiles at the time of administration. I mean, who knows? But I think it's a randomized trial, and I think I would expect to see a mad rush for treatment appointments early in the morning given this, and at least I want my patients to come in first thing in the morning. It'll be interesting to see. Dr. Nate Pennell: It's important to point out that in this study, everyone got chemo and immunotherapy. And, at least in our cancer center, most patients who are getting platinum-doublet chemotherapy and immunotherapy actually do get treated earlier in the day already, just because of the length of the infusion appointment that's needed. So it really is oftentimes people getting single-agent immunotherapy who are often getting the later, shorter visits. But if you have a choice, I think it would be very reasonable to have people treated earlier in the day. And I do think most of the impressions that I got from people about this is that they would like to see it reproduced but certainly well worth further investigation. And I personally would like to see more investigation into what the rationale would be for this because I still can't quite figure out, yes, if you got it at, say, you know, 5 PM, that's later in the day and I can understand that maybe your immune system is somewhat less receptive at that point than it would be in the morning. But because these checkpoint inhibitors have such long half-lives, it's still in your system the next morning when your immune system is supposedly more receptive. So I don't quite understand why that would be the case. Well, let's move on to the next study. I would like to hear your thoughts on Abstract 8515, “Plasma-Guided, Adaptive First-Line Chemoimmunotherapy for Non-Small Cell Lung Cancer.” Dr. Vamsi Velcheti: Yeah, this was another abstract that seems to be really interesting in my opinion. I think there's kind of a lot of emphasis lately on ctDNA and MRD-based assays to monitor disease. In the lung cancer space, we haven't had a lot of clinical trials looking at this prospectively, and this was one of those pilot studies where they looked at circulating free DNA (cfDNA)-based response-adaptive strategy for frontline patients who are PD-L1 positive. So, patients started with pembrolizumab monotherapy, and based on plasma molecular response after 2 cycles, those patients without response received early treatment intensification with a platinum doublet. So the approach essentially was to reduce the chemotherapy exposure in patients who respond to immunotherapy. And only about 17.5% of the patients on the trial received chemotherapy based on lack of molecular response. So, in this trial, what they found was patients with the cfDNA response had a markedly improved PFS of 16.4 months versus 4.8 months. So essentially, like, this is a really nice study to set a foundation on which we have to do larger studies to incorporate molecular markers trying to look at cfDNA response to inform treatment strategy, either escalation or de-escalation strategies. So, I thought it was a very interesting study. Dr. Nate Pennell: Yeah. I mean, we always have this question for patients, “Should they get immunotherapy alone or combined with chemo?” and I think this certainly is intriguing, suggesting that there may be ways you can monitor people and perhaps rescue those that aren't going to respond to single agent. I'd like to see a randomized trial against, you know, this strategy, perhaps against everyone getting, say, chemoimmunotherapy or make sure that you're not potentially harming people by doing this strategy. But I agree, it's time to move beyond just observing that cell-free DNA is prognostic and important and start using it to actually guide treatment. Dr. Vamsi Velcheti: Yeah, and I would just caution though, like, you know, I think we need more data, but, however, it's certainly a very interesting piece of data to kind of help inform future trials. So, there was another abstract that caught my attention, and I think this would be a very interesting abstract in the EGFR space. Abstract 8506, "Patritumab Deruxtecan (HER3-DXd) in Resistant EGFR-Mutant Advanced Non-Small Cell Lung Cancer Patients After Third-Generation EGFR TKI," it's the HERTHENA-Lung02 study. What do you think about the results of this study? Dr. Nate Pennell: Yeah, this was, I would say, very widely anticipated and ultimately a little disappointing, despite being a positive trial. So, these are patients with EGFR-mutant non-small cell lung cancer who have progressed after a third-generation EGFR TKI like osimertinib. This is really an area of major unmet need. We do have drugs like amivantamab in this space, but still definitely an area where essentially patients move from having a highly effective oral therapy to being in the realm of chemotherapy as their best option. So, this HER3 antibody-drug conjugate, patritumab deruxtecan, had some good single-arm data for this. And we're sort of hoping this would become an available option for patients. This trial was designed against platinum-doublet chemotherapy in this setting and with a primary endpoint of progression-free survival. And it actually was positive for improved progression-free survival compared to chemo with a hazard ratio of 0.77. But when you look at the medians, you can see that the median PFS was only 5.8 versus 5.4 months. It was really a modest difference between the two arms. And on the interim analysis, it appeared that there will not be a difference in overall survival between the two arms. In fact, the hazard ratio at the interim analysis was 0.98 for the two arms. So based on this, unfortunately, the company that developed the HER3-DXd has withdrawn their application to the FDA for approval of the drug, anticipating that they probably wouldn't get past approval without that overall survival endpoint. So, unfortunately, probably not, at least for the near future, going to be a new option for these patients. Dr. Vamsi Velcheti: Yeah, I think this is a space that's clearly an unmet need, and this was a big disappointment, I should say. I think all of us were going into the meeting anticipating some change in the standard of care here. Dr. Nate Pennell: Yeah, I agree. It was something that I was telling patients, honestly, that I was expecting this to be coming, and so now, definitely a bit of a disappointment. But it happens and, hopefully, it will still find perhaps a role or other drugs with a similar target. Certainly an active area. Well, let's leave the EGFR-mutant space and move into small cell. There were a couple of very impactful studies. And one of them was Abstract 8006, “Lurbinectedin Plus Atezolizumab as First-Line Maintenance Treatment in Patients With Extensive-Stage Small Cell Lung Cancer, Primary Results from the Phase III IMforte Trial.” So, what was your impression of this? Dr. Vamsi Velcheti: Yeah, I think this is definitely an interesting study, and small cell, I remember those days when we had barely any studies of small cell at ASCO, and now we have a lot of exciting developments in the small cell space. It's really good to see. The IMforte trial is essentially like a maintenance lurbinectedin trial with atezolizumab maintenance. And the study was a positive trial. The primary endpoint was a PFS, and the study showed improvement in both PFS and OS with the addition of lurbinectedin to atezolizumab maintenance. And definitely, it's a positive trial, met its primary endpoint, but I always am a little skeptical of adding maintenance cytotoxic therapies here in this setting. In my practice, and I'd like to hear your opinion, Nate, most patients with small cell after 4 cycles of a platinum doublet, they're kind of really beaten up. Adding more cytotoxic therapy in the maintenance space is going to be tough, I think, for a lot of patients. But also, most importantly, I think this rapidly evolving landscape for patients with small cell lung cancer with multiple new, exciting agents, actually like some FDA-approved like tarlatamab, also like a lot of these emerging therapeutics like I-DXd and other ADCs in this space. You kind of wonder, is it really optimal strategy to bring on like another cytotoxic agent right after induction chemotherapy, or do you kind of delay that? Or maybe have like a different strategy in terms of maintenance. I know that the tarlatamab maintenance trial is probably going to read out at some point too. I think it's a little challenging. The hazard ratio is also 0.73. As I said, it's a positive trial, but it's just incremental benefit of adding lurbi. And also on the trial, we need to also pay attention to the post-progression second-line treatments, number of patients who received tarlatamab or any other investigational agents.  So I think it's a lot of questions still. I'm not quite sure I'd be able to embrace this completely. I think a vast majority of my patients might not be eligible anyway for cytotoxic chemotherapy maintenance right away, but yeah, it's tough. Dr. Nate Pennell: Yeah. I would call this a single and not a home run. It definitely is real. It was a real overall survival benefit. Certainly not surprising that a maintenance therapy would improve progression-free survival. We've known that for a long time in small cell, but first to really show an overall survival benefit. But I completely agree with you. I mean, many people are not going to want to continue further cytotoxics after 4 cycles of platinum-doublet chemo. So I would say, for those that are young and healthy and fly through chemo without a lot of toxicity, I think certainly something worth mentioning. The problem with small cell, of course, is that so many people get sick so quickly while on that observation period after first-line chemo that they don't make it to second-line treatment. And so, giving everyone maintenance therapy essentially ensures everyone gets that second-line treatment. But they also lose that potentially precious few months where they feel good and normal and are able to be off of treatment. So, I would say this is something where we're really going to have to kind of sit and have that shared decision-making visit with patients and decide what's meaningful to them. Dr. Vamsi Velcheti: Yeah, I agree. The next abstract that was a Late-Breaking Abstract, 8000, “Overall Survival of Neoadjuvant Nivolumab Plus Chemotherapy in Patients With Resectable Non-Small Cell Lung Cancer in CheckMate-816.” This was a highly anticipated read-out of the OS data from 816. What did you make of this abstract? Dr. Nate Pennell: Yeah, I thought this was great. Of course, CheckMate-816 changed practice a number of years ago when it first reported out. So, this was the first of the neoadjuvant or perioperative chemoimmunotherapy studies in resectable non-small cell lung cancer. So, just to review, this was a phase 3 study for patients with what we would now consider stage II or stage IIIA resectable non-small cell lung cancer. And they received three cycles of either chemotherapy or chemotherapy plus nivolumab, and that was it. That was the whole treatment. No adjuvant treatment was given afterwards. They went to resection. And patients who received the chemoimmunotherapy had a much higher pathologic complete response rate and a much better event-free survival. And based on this, this regimen was approved and, I think, at least in the United States, widely adopted.  Now, since the first presentation of CheckMate 816, there have been a number of perioperative studies that have included an adjuvant component of immunotherapy – KEYNOTE-671, the AEGEAN study – and these also have shown improved outcomes. The KEYNOTE study with pembrolizumab also with an overall survival benefit. And I think people forgot a little bit about CheckMate-816. So, this was the 5-year overall survival final analysis. And it did show a statistically and, I think, clinically meaningful difference in overall survival with the 3 cycles of neoadjuvant chemo-nivo compared to chemo with a hazard ratio of 0.72. The 5-year overall survival of 65% in the chemo-IO group versus 55% with the chemo alone. So a meaningful improvement. And interestingly, that hazard ratio of 0.72 is very similar to what was seen in the peri-operative pembro study that included the adjuvant component. So, very much still relevant for people who think that perhaps the value of those neoadjuvant treatments might be really where most of the impact comes from this type of approach. They also gave us an update on those with pathologic complete response, showing really astronomically good outcomes. If you have a pathologic complete response, which was more than a quarter of patients, the long-term survival was just phenomenal. I mean, 95% alive at 5 years if they were in that group and suggesting that in those patients at least, the adjuvant treatment may not be all that important.  So, I think this was an exciting update and still leaves very much the open question about the importance of continuing immunotherapy after surgery after the neoadjuvant component. Dr. Vamsi Velcheti: Yeah, I completely agree, Nate. I think the million-dollar question is: “Is there like a population of patients who don't have complete response but like maybe close to complete response?” So, would you like still consider stopping adjuvant IO? I probably would not be comfortable, but I think sometimes, you know, we all have patients who are like very apprehensive of continuing treatments. So, I think that we really need more studies, especially for those patients who don't achieve a complete CR. I think trying to find strategies for like de-escalation based on MRD or other risk factors. But we need more trials in that space to inform not just de-escalation, but there are some patients who don't respond at all to a neoadjuvant IO. So, there may be an opportunity for escalating adjuvant therapies. So, it is an interesting space to watch out for. Dr. Nate Pennell: No, absolutely. Moving to KRAS-mutant space, so our very common situation in patients with non-small cell lung cancer, we had the results of Abstract 8500, “First-Line Adagrasib With Pembrolizumab in Patients With Advanced or Metastatic KRASG12C-Mutated Non-Small Cell Lung Cancer” from the phase 2 portion of the KRYSTAL-7 study. Why was this an interesting and important study? Dr. Vamsi Velcheti: First of all, there were attempts to kind of combine KRASG12C inhibitors in the past with immune checkpoint inhibitors, notably sotorasib with pembrolizumab. Unfortunately, those trials have led to like a lot of toxicity, with increased especially liver toxicity, which was a major issue. This is a phase 2 study of adagrasib in combination with pembrolizumab, and this is a study in the frontline setting in patients with the G12C-mutant metastatic non-small cell lung cancer. And across all the PD-L1 groups, the ORR was 44%, and the median PFS was 11 months, comparable to the previous data that we have seen with adagrasib in this setting. So it's not like a major improvement in clinical efficacy. However, I think the toxicity profile that we were seeing was slightly better than the previous trials in combination with sotorasib, but you still have a fair amount of transaminitis even in the study. At this point, this is not ready for clinical primetime. I don't think we should be using sotorasib or adagrasib in the frontline or even in the second line in combination with checkpoint inhibitors. Combining these drugs with checkpoint inhibitors in the clinical practice might lead to adverse outcomes. So, we need to wait for more data like newer-generation G12C inhibitors which are also being studied in combination, so we'll have to kind of wait for more data to emerge in this space. Dr. Nate Pennell: I agree, this is not immediately practice changing. This is really an attempt to try to combine targeted treatment with immune checkpoint inhibitor. And I agree with you that, you know, it does appear to be perhaps a little bit better tolerated than some of the prior combinations that have tried in this space. The outcomes overall were not that impressive, although in the PD-L1 greater than 50%, it did have a better response rate perhaps than you would expect with either drug alone. And I do think that the company is focusing on that population for a future randomized trial, which certainly would inform this question better. But in the meantime, I agree with you, there's a lot of newer drugs that are coming along that potentially may be more active and better tolerated. And so, I'd say for now, interesting but we'll wait and see. Dr. Vamsi Velcheti: Yeah, so now moving back again to small cell. So, there was a Late-Breaking Abstract, 8008. This is a study of tarlatamab versus chemotherapy as second-line treatment for small cell lung cancer. They presented the primary analysis of the phase III DeLLphi-304 study. What do you think about this? Dr. Nate Pennell: Yeah, I thought this was really exciting. This was, I would say, perhaps the most important lung study that was presented. Tarlatamab is, of course, the anti-DLL3 bispecific T-cell engager compound, which is already FDA approved based on a prior single-arm phase II study, which showed a very nice response rate as a single agent in previously treated small cell lung cancer and relatively manageable side effects, although somewhat unique to solid tumor docs in the use of these bispecific drugs in things like cytokine release syndrome and ICANS, the neurologic toxicities. So, this trial was important because tarlatamab was approved, but there were also other chemotherapy drugs approved in the previously treated space. And so, this was a head-to-head second-line competition comparison between tarlatamab and either topotecan, lurbinectedin, or amrubicin in previously treated small cell patients with a primary endpoint of overall survival. So, a very well-designed trial. And it did show, I think, a very impressive improvement in overall survival with a median overall survival in the tarlatamab group of 13.6 months compared to 8.3 months with chemotherapy, hazard ratio of 0.6. And progression-free survival was also longer at 4.2 months versus 3.2 months, hazard ratio of 0.72. In addition to showing improvements in cancer-related symptoms that were improved in tarlatamab compared to chemotherapy, there was actually also significantly lower rates of serious treatment-related adverse events with tarlatamab compared to chemotherapy. So, you do still see the cytokine release syndrome, which is seen in most people but is manageable because these patients are admitted to the hospital for the first two cycles, as well as a significant number of patients with neurologic side effects, the so-called ICANS, which also can be treated with steroids. And so, I think based upon the very significant improvement in outcomes, I would expect that this should become our kind of standard second-line treatment since it seems to be much better than chemo. However, tarlatamab is definitely a new drug that a lot of places are not used to using, and I think a lot of cancer centers, especially ones that aren't tied to a hospital, may have questions about how to deal with the CRS. So, I'm curious your thoughts on that. Dr. Vamsi Velcheti: Yeah, thank you, Nate. And I completely agree. I think the data looked really promising, and I've already been using tarlatamab in the second-line space. The durability of response and overall, having used tarlatamab quite a bit - like, I participated in some of the early trials and also used it as standard of care - tarlatamab has unique challenges in terms of like need for hospitalization for monitoring for the first few treatments and make sure, you know, we monitor those patients for CRS and ICANS. But once you get past that initial administration and monitoring of CRS, these patients have a much better quality of life, they're off chemotherapy, and I think it's really about the logistics of actually administering tarlatamab and coordination with the hospital and administration in the outpatient setting. It's definitely challenging, but I think it definitely can be done and should be done given what we are seeing in terms of clinical efficacy here. Dr. Nate Pennell: I agree. I think hospital systems now are just going to have to find a way to be able to get this on formulary and use it because it clearly seems to be more effective and generally better tolerated by patients. So, should move forward, I think. Finally, there's an abstract I wanted to ask you about, Abstract 8001, which is the “Neoadjuvant osimertinib with or without chemotherapy versus chemotherapy alone in resectable epidermal growth factor receptor-mutated non-small cell lung cancer: The NeoADAURA Study”. And this is one that I think was also fairly highly anticipated. So, what are your thoughts? Dr. Vamsi Velcheti: You know, I wasn't probably surprised with the results, and I believe we were all expecting a positive trial, and we certainly were handed a positive trial here. It's a phase III trial of osimertinib and chemotherapy or osimertinib in the neoadjuvant space followed by surgery, followed by osimertinib. It's a global phase 3 trial and very well conducted, and patients with stage II to stage IIIB were enrolled in the study. And in the trial, patients who had a neoadjuvant osimertinib with or without chemotherapy showed a significant improvement in major pathologic response rates over chemotherapy alone. And the EFS was also positive for osimertinib and chemotherapy, osimertinib monotherapy as well compared to chemotherapy alone. So overall, the study met its primary endpoint, and I think it sheds light on how we manage our patients with early-stage lung cancer. I think osimertinib, we know that osimertinib is already FDA approved in the adjuvant space, but what we didn't really know is how was osimertinib going to work in the neoadjuvant space. And there are always situations, especially for stage III patients, where we are on the fence about, are these patients already close to being metastatic? They have, like, almost all these patients have micrometastatic disease, even if they have stage III. As we saw in the LAURA data, when you look at the control arm, it was like a very short PFS. Chemoradiation does nothing for those patients, and I think these patients have systemic mets, either gross or micrometastatic disease at onset. So, it's really important to incorporate osimertinib early in the treatment course. And I think, especially for the locally advanced patients, I think it's even more important to kind of incorporate osimertinib in the neoadjuvant space and get effective local control with surgery and treat them with adjuvant. I'm curious to hear your thoughts, Nate. Dr. Nate Pennell: I am a believer and have long been a believer in targeted adjuvant treatments, and, you know, it has always bothered me somewhat that we're using our far and away most effective systemic therapy; we wait until after they go through all their pre-op treatments, they go through surgery, then they go through chemotherapy, and then finally months later, they get their osimertinib, and it still clearly improves survival in the adjuvant setting. Why not just start the osimertinib as soon as you know that the patient has EGFR-mutant non-small cell lung cancer, and then you can move on to surgery and adjuvant treatment afterwards? And I think what was remarkable about this study is that all of these patients almost - 90% in each arm - went to surgery. So, you weren't harming them with the neoadjuvant treatment. And clearly better major pathologic response, nodal downstaging, event-free survival was better. But I don't know that this trial is ever going to show an overall survival difference between neoadjuvant versus just surgery and adjuvant treatment, given how effective the drug is in the adjuvant setting. Nonetheless, I think the data is compelling enough to consider this, certainly for our N2-positive, stage IIIA patients or a IIIB who might be otherwise surgical candidates. I think based on this, I would certainly consider that. Dr. Vamsi Velcheti: Yeah, and especially for EGFR, like even for stage IIIB patients, in the light of the LAURA study, those patients who do not do too well with chemoradiation. So you're kind of delaying effective systemic therapy, as you said, waiting for the chemoradiation to finish. So I think probably time to revisit how we kind of manage these locally advanced EGFR patients. Dr. Nate Pennell: Yep, I agree. Dr. Vamsi Velcheti: Nate, thank you so much for sharing your fantastic insights today on the ASCO Daily News Podcast. It's been an exciting ASCO again. You know, we've seen a lot of positive trials impacting our care of non-small cell lung cancer and small cell lung cancer patients. Dr. Nate Pennell: Thanks for inviting me, Vamsi. Always a pleasure to discuss these with you. Dr. Vamsi Velcheti: And thanks to our listeners for your time today. You will find links to all of the abstracts discussed today in the transcript of the episode. Finally, if you value the insights that you hear from the ASCO Daily News Podcast, please take a moment to rate, review, subscribe wherever you get your podcast. 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. More on today's speakers:    Dr. Vamsi Velcheti   @VamsiVelcheti    Dr. Nathan Pennell   @n8pennell   Follow ASCO on social media:     @ASCO on Twitter     ASCO on Facebook     ASCO on LinkedIn   ASCO on BlueSky   Disclosures:   Dr. Vamsi Velcheti:   Honoraria: ITeos Therapeutics   Consulting or Advisory Role: Bristol-Myers Squibb, Merck, Foundation Medicine, AstraZeneca/MedImmune, Novartis, Lilly, EMD Serono, GSK, Amgen, Elevation Oncology, Taiho Oncology, Merus   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. Nathan Pennell:     Consulting or Advisory Role: AstraZeneca, Lilly, Cota Healthcare, Merck, Bristol-Myers Squibb, Genentech, Amgen, G1 Therapeutics, Pfizer, Boehringer Ingelheim, Viosera, Xencor, Mirati Therapeutics, Janssen Oncology, Sanofi/Regeneron    Research Funding (Inst): Genentech, AstraZeneca, Merck, Loxo, Altor BioScience, Spectrum Pharmaceuticals, Bristol-Myers Squibb, Jounce Therapeutics, Mirati Therapeutics, Heat Biologics, WindMIL, Sanofi 

In tonight’s podcast, we give the latest updates regarding the ongoing war in the Middle East between Israel and Iran. The Supreme Leader of Iran has just rejected Trump’s request to surrender and has made new threats against US interests in the Mideast. Will Trump take the final step and use the M.O.A.B. to be […]

The globalist resistance, pro-America, media has been completely exposed as nothing more than a new form of mockingbird press. The big patriot leaders are in unison calling for the end of “third world immigration” and even “non-white immigration,” becoming the very thing the left accused them of all along - while ignoring the fact that Asians, for example, commit little crime, use few drugs, and are some of the top earners and contributors to the country. All the hopes and dreams of “promises made, promises kept,” are evaporating in real time, with few able to further justify the increasingly obvious: the downfall of the Republic has been monetized and archetypically framed. With riots all across the country, fears of a black and white racial war have instead manifested as Mexican and American; the fear of outright civil war has manifested as a problem-reaction-solution of absolute information control and military martial law in the name of defending the country. Now the “No Kings” movement has nationwide protests planned for June 14th, 2025, the day of Saturn. Rather than arresting the organizers behind that, and the riots via the communist Indivisible, the AG has instead sued a coffee shop for antisemitism. The protests are meant to resist the massive military parade and presidential birthday parade in Washington on the same day. Don't like it? You will be met with “very big force,” says the President, if you don't like his “big parade.” BIG beautiful bill anyone? Not even Roman emperors held military parades for their birthdays, but they did hold them for victories in battle. So either the Trump camp is totally delusional, considering nationwide civil war as victory, or the display is meant to put the final nail in the Constitutional coffin. It all culminates with the US suddenly pulling all nonessential staff from embassies across the Middle East and putting the country on high alert the same week. The word is Iran is prepared to strike Israel's nuclear sites and Israel is fully poised to strike Iran (thus, the Houthis are warning of war too), and regardless of what the fake Donald-Benjamin feud suggests, the US will sacrifice its own citizens for the jewish state, which itself will, under the Samson Option, destroy the entire world if it doesn't get its way. Hence, the fake (maybe real) threat of Benjamin Netanyahu circulating the Internet: “if we do fall, many parts of the world will fall with us.” *The is the FREE archive, which includes advertisements. If you want an ad-free experience, you can subscribe below underneath the show description.-FREE ARCHIVE (w. ads)SUBSCRIPTION ARCHIVEX / TWITTER FACEBOOKYOUTUBEMAIN WEBSITECashApp: $rdgable Paypal email rdgable1991@gmail.comEMAIL: rdgable@yahoo.com / TSTRadio@protonmail.comBecome a supporter of this podcast: https://www.spreaker.com/podcast/the-secret-teachings--5328407/support.

When was Checkpoint Charlie created in Berlin? What triggered Stalin to enact a blockade on West Berlin? And how did the Western powers airlift over 2.3 million tons of supplies to their occupied zone of the city from 1948 to 1949? William and Anita are joined once again by Giles Milton, author of Checkmate in Berlin: The Cold War Showdown That Shaped the Modern World, to discuss the Berlin Blockade, the Berlin Airlift, and the way in which the Iron Curtain hardened towards the end of the 1940s. ----------------- Empire Club: Become a member of the Empire Club to receive early access to miniseries, ad-free listening, early access to live show tickets, bonus episodes, book discounts, our exclusive newsletter, and access to our members' chatroom on Discord! Head to empirepoduk.com to sign up. For more Goalhanger Podcasts, head to www.goalhanger.com.  ----------------- Email: empire@goalhanger.com Instagram: @empirepoduk  Blue Sky: @empirepoduk  X: @empirepoduk Assistant Producer: Becki Hills Producer: Anouska Lewis Senior Producer: Callum Hill Learn more about your ad choices. Visit podcastchoices.com/adchoices

MeidasTouch host Ben Meiselas reports on Donald Trump getting easily outmaneuvered, outplayed, and mocked by world leaders and often to his face. Dose: Save 30% on your first month of subscription by going to https://dosedaily.co/MEIDAS or entering MEIDAS at checkout. Visit https://meidasplus.com for more! Remember to subscribe to ALL the MeidasTouch Network Podcasts: MeidasTouch: https://www.meidastouch.com/tag/meidastouch-podcast Legal AF: https://www.meidastouch.com/tag/legal-af MissTrial: https://meidasnews.com/tag/miss-trial The PoliticsGirl Podcast: https://www.meidastouch.com/tag/the-politicsgirl-podcast The Influence Continuum: https://www.meidastouch.com/tag/the-influence-continuum-with-dr-steven-hassan Mea Culpa with Michael Cohen: https://www.meidastouch.com/tag/mea-culpa-with-michael-cohen The Weekend Show: https://www.meidastouch.com/tag/the-weekend-show Burn the Boats: https://www.meidastouch.com/tag/burn-the-boats Majority 54: https://www.meidastouch.com/tag/majority-54 Political Beatdown: https://www.meidastouch.com/tag/political-beatdown On Democracy with FP Wellman: https://www.meidastouch.com/tag/on-democracy-with-fpwellman Uncovered: https://www.meidastouch.com/tag/maga-uncovered Coalition of the Sane: https://meidasnews.com/tag/coalition-of-the-sane Learn more about your ad choices. Visit megaphone.fm/adchoices

What was life like in Berlin in the immediate aftermath of the Second World War? Why did the Red Army steal taps from Berlin houses when they reached the city? Was the famous photo of the red flag on the Reichstag staged or authentic? Anita and William are joined by Giles Milton, author of Checkmate in Berlin: The Cold War Showdown That Shaped the Modern World, to discuss the division and destitution of the capital city after the Second World War.  ----------------- Empire Club: Become a member of the Empire Club to receive early access to miniseries, ad-free listening, early access to live show tickets, bonus episodes, book discounts, our exclusive newsletter, and access to our members' chatroom on Discord! Head to empirepoduk.com to sign up. For more Goalhanger Podcasts, head to www.goalhanger.com.  ----------------- Email: empire@goalhanger.com Instagram: @empirepoduk  Blue Sky: @empirepoduk  X: @empirepoduk Assistant Producer: Becki Hills Producer: Anouska Lewis Senior Producer: Callum Hill Learn more about your ad choices. Visit podcastchoices.com/adchoices

Keith Murphy and Andy Fales recap the eventful weekend before discussing the Pacers-Thunder matchup in the NBA Finals, and Magnus Carlsen losing. OTD in history, ThrowDowns and MORE! Presented by Ramsey Subaru. Learn more about your ad choices. Visit megaphone.fm/adchoices

How God 'flipped the script' on Haman; learning that God will give victory no matter what it takes; a summary of Esther chapters 5-7. To support this ministry financially, visit: https://www.oneplace.com/donate/1213/29

In a legal sleight of hand, Republicans want to strip judges of their power to enforce rulings — because holding Trump in contempt might actually work…See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

On a stormy night filled with board games and boredom, two siblings answer a knock at the door — only to find two very strange visitors whose motives are anything but clear.FREE Word Search and Crossword puzzles, plus a fun Q&A for you and your kids to see how closely they were paying attenetion to the story! https://weirddarkness.com/mt-checkmateFind more family-friendly frights and creepy games to play on our website at http://MicroTerrors.com!Facebook page: https://www.facebook.com/microterrorsOther stories, novels, and more from author Scott Donnelly: https://amzn.to/3LymHaUOther narrations, podcasts, and audiobooks from voice artist Darren Marlar: https://WeirdDarkness.com= = = = = = = = = = = = = = = = = = = = = = = = = = = = = =Weird Darkness©, 2025Micro Terrors: Scary Stories for Kids™, 2025

Watch The X22 Report On Video No videos found (function(w,d,s,i){w.ldAdInit=w.ldAdInit||[];w.ldAdInit.push({slot:17532056201798502,size:[0, 0],id:"ld-9437-3289"});if(!d.getElementById(i)){var j=d.createElement(s),p=d.getElementsByTagName(s)[0];j.async=true;j.src="https://cdn2.decide.dev/_js/ajs.js";j.id=i;p.parentNode.insertBefore(j,p);}})(window,document,"script","ld-ajs");pt> Click On Picture To See Larger Picture As time goes on the people now can see the green new scam was a hoax, Bernie Sanders flies on private jet and Hawaii sues oil industry but spares refinery because they donate to the D party. Inflation is down, the fake news and the Fed were wrong. Trump once again calls on the Fed, he has now boxed them in.Transition to a people's economy is happening. The [DS] has lost all power. Trump has now signaled that he has the power and that the old guard has failed and it in the process of being replaced. What we are witnessing the forced exposure of the corrupt system, the people are seeing it. Now the offensive begins and those who were treasonous to this country will be held accountable. Checkmate. Economy https://twitter.com/mkhammer/status/1921181550239993909 https://twitter.com/libsoftiktok/status/1922302004904280481 https://twitter.com/thehill/status/1922270983534129248 (function(w,d,s,i){w.ldAdInit=w.ldAdInit||[];w.ldAdInit.push({slot:18510697282300316,size:[0, 0],id:"ld-8599-9832"});if(!d.getElementById(i)){var j=d.createElement(s),p=d.getElementsByTagName(s)[0];j.async=true;j.src="https://cdn2.decide.dev/_js/ajs.js";j.id=i;p.parentNode.insertBefore(j,p);}})(window,document,"script","ld-ajs");   https://twitter.com/WSJ/status/1922270583930167754 The inflation rate in the United States for April 2021, as measured by the Consumer Price Index (CPI), was 4.2% over the 12 months from April 2020 to April 2021 TRUMP ECONOMIC UPDATE: Inflation Drops to 2.3%, Lowest Since 2021, and US Treasury Records Second Biggest Surplus in History Thanks to Trump's Record Tariff Revenues  https://twitter.com/KobeissiLetter/status/1922268438912798730   https://twitter.com/RapidResponse47/status/1922277662560526415?ref_src=twsrc%5Etfw%7Ctwcamp%5Etweetembed%7Ctwterm%5E1922277662560526415%7Ctwgr%5E9a0647d641b176e03f79d37607411d8da3baf9a9%7Ctwcon%5Es1_c10&ref_url=https%3A%2F%2Fwww.thegatewaypundit.com%2F2025%2F05%2Ftrump-economy-update-inflation-drops-2-3-lowest%2F   Source: thegatewaypundit.com https://twitter.com/Peoples_Pundit/status/1922021412983730442 https://twitter.com/charliekirk11/status/1922286454119829804 https://twitter.com/TrumpWarRoom/status/1908318952838594601 @Taylor47 political class didn't do anything about it—they allowed it to happen!" @USTradeRep"The goal very clearly was to remove U.S. tariffs and trade barriers to make it easier for people to outsource to China." TAKE A LISTEN Trump Just Got Britain To Hit China, UK Politicians Say  British politicians are expressing alarm that the new U.S.–UK trade deal gives President Donald Trump the power to block Chinese investments in critical British infrastructure. The deal announced last week requires the UK to “promptly meet U.S. requirements” to shield supply chains and “relevant production facilities” from foreign investment. If the European country does not meet these requirements, the U.S. can reimpose tariffs, effectively using trade pressure to dictate which countries can invest in the UK's core infrastructure. That clause triggered immediate backlash from British lawmakers and media, who say the U.S. now has a de facto “veto” over foreign investment — specifically Chinese money flowing into the UK's steel and aluminum sectors.   “Washington wants the UK and others to peel away from Chinese trade and investment, especially in sensitive areas like steel,” said Allie Renison, a former trade official, speaking to the FT. Source: dailycaller.com