Podcasts about Tempus

Christopher High and George Breden discuss a little bit of the history of shedding card games and their current Top 10. George also shares about a recent crowdfunding game he just received. Games discussed in this episode: Trouble on the Tempus, Tragedy Looper, Loop Inc., Mau-Mau, Whot!, Crazy 8s, War, Uno, Color8, LLAMA, Phase 10, The Yellow House, Who Did It, Dutch Blitz, Domino Train, Rummikub, Walkie Talkie, Haggis, Happy Mochi, Tichu, The Great Dalmutti, Fuji Flush, Linko, Things in Rings, Scout, Jungo, Nanatoridori, Planet Etuc (Ambient Abissal), Seven Prophecies, Order Overload Cafe, DNUP, Otter, 13 Leaves (I'm Out), Once Upon a Time, Don't LLAMA Dice, Frank's Zoo (Zoff im Zoo), Maskmen, We Need to Talk. Support the showWe talk about board games and tabletop games!Follow us to stay in touch: Youtube.com/boardagaingamesFacebook.com/boardagaingaming 

Are medical advancements closing or widening medical disparities? Eugene Manley, Jr., Ph.D., founder and CEO of the STEMM & Cancer Health Equity Foundation, breaks down why equity is still not completely measurable in clinical trials, what proper representation in studies is, and how certain demographics are at a disadvantage for biomarker tests compared to other groups with host Deborah Borfitz. Their conversation explores whether health equity in cancer trials is different compared to commonly occurring diseases and if basket and umbrella trials may help the move the needle. Plus, the latest news on a pioneering phage therapy service, a unique cardiac arrest pilot study, new primary endpoints for cancer trials, and trial disruptions threatening diversity. Listen and let us know in a review: where do you think our time and resources are most needed for equity? Show Notes News Roundup Compassionate use phage therapy Article in Nature Medicine Press release from Monash University   Sudden cardiac death research  Study in Prehospital Emergency Care News on the University of Cincinnati website New endpoints for cancer trials Consensus paper in The Lancet Oncology News on the Medical University of Vienna website USC and Tempus strategic collaboration News on the Keck School of Medicine of USC website Trial disruptions threaten diversity Article in the Journal of Medical Internet Research Misinterpreting effects of Alzheimer's drugs Research letter in JAMA Neurology News from Brown University School of Public Health  Guest Eugene Manley, Jr., Ph.D., founder and CEO of the STEMM & Cancer Health Equity Foundation The Scope of Things podcast explores clinical research and its possibilities, promise, and pitfalls. Clinical Research News senior writer, Deborah Borfitz, welcomes guests who are visionaries closest to the topics, but who can still see past their piece of the puzzle. Focusing on game-changing trends and out-of-the-box operational approaches in the clinical research field, the Scope of Things podcast is your no-nonsense, insider's look at clinical research today.  

 Clay Ramey, VP with Tempus Realty Partners discussing the commercial real estate market in NWA and nationally. 

Zaza leads Ibn the Scorcher, VS, Talsarian, and Eero in a nighttime exploration of the ruined Abbey of St Clewyd, also known as the Phantom Cloisters. They meet some ghost crow trappers, then enter the compound through a side entrance. In the herb garden, they meet a ghostly monk who tells Eero a secret, and in the cloisters, they meet another who wishes his bones to be properly buried - he also has a magic spear that Eero takes and some Devilweed Tabac that Ibn smokes. Exploring the ruined chapel, Tals immediately finds a key and the hidden altar compartment where the Battle Standard of Tempus is stored. Eero plays the organ and releases a murder of Ghost Crows that attack the party. They eventually defeat most of them and harvest a single Ghost Crow Quill for Tals. They discover the graveyard with some corpses missing teeth, and bury the bones of the other monk. They also see a small child there but avoid her, and move over to the bell tower. There, Zaza prays to St Woad of the Bread and decides that he is now the Abbot of St Woad. They encounter two other small children who speak highly of Mr Rag-n-Bones and show the adventurers his strange artworks. Zaza summons Mr Rag-n-Bones by tolling the bell but manages to avoid combat by complimenting his artistic style. Mr Rag-n-Bones tells the players about his past as a servant of the Dewdrop Man and how to find Dewdrop Manse in the heart of the Southwood. Before dawn breaks (possibly trapping them there), the party retreats back into the Southwood and makes their way back to Wildfire Caverns to plan their next move.

The Caravan Crew, led by Ibn the Scorcher and joined by wizard Tals (featuring Judd in his first DnDNerds appearance), visit the Abbey of the Broken Blade, a place for retired soldiers of war-god Tempus. Eero investigates whether Tempus is the god he's been searching for. They deliver some weapons and try to sell some armor, but instead are told some of the story of a mysterious site more than 150 miles to the west - the Phantom Cloister, also known as the Abbey of St. Clewweth, which only appears at night during the new moon. The party sets out to catch it by the next new moon in two weeks - along the way they battle fire beetles (which Tals successfully harvests fire glands from), stop to trade in Llorkh and at Zath Gor (formerly Oleg's Trading Post), and leave the caravan with Bariq at the Wildfire Caverns. They find some excellent hot springs, which ZaZa really enjoys. As the deadline approaches, they hear the unearthly wailing (or perhaps whaling?) associated with the site.

Dans lundimatin, on écrit et on parle trop. Parfois il y a un peu de dessin ou de peinture voir des bribes de cinéma, de la musique par contre, il n'y en a jamais assez. Alors quand nous avons croisé Laura Perrudin et sa harpe, nous l'avons immédiatement invitée et ça a donné cet entretien musical qui dit certainement plus, en tous cas largement tout autant, que beaucoup de nos mots. Et sans doute que certaines vibrations et mélodies déploient des dimensions de l'existence heureusement plus épaisses que ce que l'on appelle platement politique. Un petit extrait est disponible en attendant et en cliquant sur la vignette.Vous aimez ou au moins lisez lundimatin et vous souhaitez pouvoir continuer ? Ca tombe bien, pour fêter nos dix années d'existence, nous lançons une grande campagne de financement. Pour nous aider et nous encourager, C'est par ici.

Good morning from Pharma Daily: the podcast that brings you the most important developments in the pharmaceutical and biotech world. Today, we're diving into a series of compelling stories that highlight the intricate interplay of scientific innovation, regulatory dynamics, and strategic maneuvers shaping the industry.Starting with Moderna, the company has reached a pivotal resolution in a long-standing patent dispute involving its mRNA-based COVID-19 vaccine, Spikevax. This settlement involves a hefty $950 million payout to Genevant Sciences and Arbutus Biopharma, resolving claims of patent infringements. This agreement underscores the complex nature of intellectual property in the rapidly evolving mRNA landscape. Securing patent rights is crucial as new vaccines and therapies are developed, and this resolution not only clears a legal hurdle for Moderna but also exemplifies the industry trend towards resolving such disputes to foster continuous innovation.Sanofi has embarked on a significant strategic move by entering a $1.53 billion global licensing deal with Sino Biopharmaceutical. This agreement secures rights to a first-in-class JAK/ROCK inhibitor, which shows promise in treating hematological and immunological conditions. Such collaborations reflect the increasing focus on innovative therapies that target complex biological pathways, highlighting how companies are seeking unique assets to bolster their competitive edge.Regulatory scrutiny continues to be a formidable theme in the industry. The FDA has intensified its oversight on compounded GLP-1 drugs, issuing 30 warning letters to telehealth companies marketing unauthorized versions. This action highlights the agency's commitment to ensuring drug safety and efficacy while emphasizing the challenges companies face in navigating regulatory landscapes for compounded medications. Additionally, Novo Nordisk has been cautioned by the FDA regarding advertising practices for GLP-1 receptor agonists, illustrating the ongoing regulatory focus on pharmaceutical marketing strategies and compliance standards.Meanwhile, Bayer is experiencing a period of resilience in its pharmaceutical division, driven largely by its cancer drug Nubeqa and cardiovascular agent Kerendia. Despite these successes, Bayer faces challenges as revenues from older drugs like Xarelto and Eylea decline. This scenario reflects a broader industry challenge where companies must innovate while managing mature product lines facing generic competition.Teva Pharmaceuticals is making strategic strides by securing a $400 million deal with Blackstone to develop an anti-TL1A antibody for inflammatory bowel disease (IBD), in partnership with Sanofi. This investment highlights continued interest in autoimmune and inflammatory conditions as lucrative targets for novel therapies. Financial partnerships like Teva's substantial agreement with Blackstone illustrate how such collaborations can support sustained R&D efforts in chronic disease management.Technological integration into healthcare is expanding rapidly, with Nvidia collaborating with Droplet Biosciences to explore AI applications in medtech and cancer research. These partnerships illustrate an industry shift towards leveraging artificial intelligence to enhance diagnostic capabilities and accelerate research efforts. Moreover, collaborations leveraging AI/ML technologies across drug discovery pipelines are gaining traction; Earendil Labs partnering with WuXi XDC exemplifies this trend alongside Merck & Co.'s multi-year AI oncology data deal with Tempus—enhancing precision medicine capabilities while expediting therapeutic discoveries.In terms of funding new therapeutic areas, ARPA-H has announced a $158 million initiative aimed at developing medicines targeting the lymphatic system. This marks an exploration into less charted territories within physiological research that could yield transforSupport the show

Peu de rivalités ont autant marqué le monde et les mémoires que celles entre les USA et l'URSS. Débutée juste après la chute des nazis et de leurs alliés, elle est immédiatement baptisée “Guerre Froide” – et le nom veut tout dire. Script: Guilhem @DHistoiresenHistoire Adhérez à cette chaîne pour obtenir des avantages : https://www.youtube.com/channel/UCN4TCCaX-gqBNkrUqXdgGRA/join Pour soutenir la chaîne, au choix: 1. Cliquez sur le bouton « Adhérer » sous la vidéo. 2. Patreon: https://www.patreon.com/hndl Musique issue du site : epidemicsound.com Images provenant de https://www.storyblocks.com Abonnez-vous à la chaine: https://www.youtube.com/c/LHistoirenousledira Les vidéos sont utilisées à des fins éducatives selon l'article 107 du Copyright Act de 1976 sur le Fair-Use. Sources et pour aller plus loin: André FONTAINE, La guerre froide 1917-1991, Seuil, 2006. John LEWIS GADDIS, The Cold War. A New History, Penguin, 2006. Nicolas WERTH, Le cimetière de l'espérance, essais sur l'histoire de l'Union soviétique, 1914-1991, Tempus, 2019. Tony JUDT, Post War: A History of Europe Since 1945, Penguin, 2005. Pierre GROSSER, Les temps de la guerre froide, Complexe, 1995. Stanislas JEANNESSON, Sabine DULLIN, Atlas de la guerre froide, Autrement, 2017. Juliette BOURDIN, Entre portes ouvertes et portes fermées, la politique chinoise des États-Unis du XIXe au XXIe siècle, Paris, Presses Sorbonne nouvelle, 2013 Ian KERSHAW, L'âge global. L'Europe de 1950 à nos jours, Seuil, 2020. Serge BERSTEIN et Pierre MILZA, Histoire du XXe siècle – Tomes 2 (1945-1973) et 3 (1973-1990), éditions de 2006-2010 Juliette BOURDIN, Entre porte ouverte et porte fermée – La politique chinoise des États-Unis du XIXe au XXIe siècle, 2013 Pierre BROCHEUX (dir.), Les décolonisations au XXe siècle – La fin des empires européens et japonais, 2012 Hélène CARRÈRE-D'ENCAUSSE, Six années qui ont changé le monde (1985-1991) – La chute de l'empire soviétique, 2015 Jean CAZEMAJOU et Jean-Michel LACROIX (dir.), La guerre du Vietnam et l'opinion publique américaine (1961-1973), 1991 Sabine DULLIN et al., Atlas de la guerre froide (1947-1990) : un conflit global et multiforme, 2020 Catherine DURANDIN, La Guerre froide – « Que sais-je ? », 2023 Jacques GERNET, Le monde chinois – Tome 3 – L'époque contemporaine, édition de 2005 Bernard VINCENT, Histoire des États-Unis, édition de 2016 Michèle WEINACHTER (dir.), L'Est et l'Ouest face à la chute du Mur – Question de perspective, Travaux et documents du CIRAC, 2013 Nicolas WERTH, Histoire de l'Union Soviétique de Lénine à Staline (1917-1953) – “Que Sais-Je ?”, 6e édition de 2022 Nicolas WERTH, Histoire de l'Union Soviétique de Kroutchev à Gorbatchev – “Que Sais-Je ?”, 5e édition de 2023 Tessa Coombs, « Cold War », https://www.imdb.com/fr-ca/title/tt1282631/ MAD World - The History of the Cold War Episode 1/ Superpowers Free Documentary History https://youtu.be/cadWivTlj1A?si=fZ1liXpP3Px2PwXA The Cold War/ Seven Minutes to Midnight Documentary, WarsofTheWorld, 6 aout 2021 https://youtu.be/2336v76nEf8?si=E6VXmTLm7jPzn3hk John F. Kennedy's Speech at the Berlin Wall https://youtu.be/yBQvKXIDiuc?si=DPlhRN6vgfUbGNIJ Autres références disponibles sur demande. #histoire #documentaire

When Eric Lefkofsky's wife was diagnosed with breast cancer, it exposed how little technology and data were shaping cancer care, pushing the serial entrepreneur to build a different model.Lefkofsky is the founder and CEO of Tempus, now a $10B publicy traded health tech company, and previously founded Groupon. At Tempus, he's building a tech-first company applying multimodal data and AI to make diagnostics smarter and treatment decisions more tailored, starting in oncology and expanding across disease areas.We cover:What Tempus does in plain EnglishWhy Tempus built its own lab, and how it became one of the largest sequencers of cancer patients in the U.S.The hard part: extracting usable clinical data from EHRs and scaling to thousands of hospital connections and hundreds of petabytes of dataHow AI changes the patient-physician relationship, and why patients will increasingly arrive highly informedWhat Eric would change at CMS and HHS to responsibly pay for AI—About our guest: Eric Lefkofsky is the founder and CEO at Tempus, a leader in artificial intelligence and precision medicine. He is the co-founder and General Partner of Lightbank, a private venture capital firm specializing in investments in technology companies. He is also the co-founder of Pathos AI, a clinical stage biotechnology company focused on re-engineering drug development; Groupon (NASDAQ: GRPN), a global e-commerce marketplace; Mediaocean, a leading provider of integrated media procurement technology; Echo Global Logistics (NASDAQ: ECHO), a technology-enabled transportation and logistics outsourcing firm; and InnerWorkings (NASDAQ: INWK), a global provider of managed print and promotional solutions.He co-chairs the Lefkofsky Family Foundation with his wife Liz to advance high-impact initiatives that enhance lives in the communities served. Lefkofsky also serves on the board of directors of The Art Institute of Chicago and Northwestern Medicine. He holds a bachelor's degree from the University of Michigan and a J.D. from the University of Michigan Law School.—

Eero, Zaza, and VS hear rumors about the Monastery of the Broken Blade (from itinerant mendicant Brother Aerelm), the Black Cats reactions to being blamed for the (other PC's) heist (from aspiring fixer Narder), and something about the Black Network emptying some warehouses (from fish broker Vinchenziana Moory). In the Llodown neighborhood they stumble across some ghouls and get into a fight - Eero goes down multiple times but VS saves him multiple times, which Eero attributes to the favor of battle-god Tempus. They seek out Lord Harrand Tormblade, a patron of the Abbey of the Broken Blade, who gives them a consignment of weapons to deliver to the Abbey. On the way back, they encounter crazed hermit-priest Dintoven of Waukeen digging in a garbage heap, which VS and Zaza eagerly help him with. VS recovers his cursed tongue and is praised for his service to Waukeen, accidentally discovering that he is a vessel of divine will for the second time that day.

JCO PO author Dr. Foldi at UPMC Hillman Cancer Center and University of Pittsburgh School of Medicine shares insights into the JCO PO article, "Personalized Circulating Tumor DNA Testing for Detection of Progression and Treatment Response Monitoring in Patients With Metastatic Invasive Lobular Carcinoma of the Breast." Host Dr. Rafeh Naqash and Dr. Foldi discuss how serial ctDNA testing in patients with mILC is feasible and may enable personalized surveillance and real-time therapeutic monitoring. TRANSCRIPT Dr. Rafeh Naqash: Hello, and welcome to JCO Precision Oncology Conversations, where we bring you engaging conversations with authors of clinically relevant and highly significant JCO PO articles. I am your host, Dr. Rafeh Naqash, podcast editor for JCO Precision Oncology and Associate Professor at the OU Health Stephenson Cancer Center at the University of Oklahoma. Today, we are thrilled to be joined by Dr. Julia Foldi, Assistant Professor of Medicine in the Division of Hematology-Oncology at University of Pittsburgh School of Medicine and the Magee-Womens Hospital of the UPMC. She is also the lead and corresponding author of the JCO Precision Oncology article entitled "Personalized Circulating Tumor DNA Testing for Detection of Progression and Treatment Response Monitoring in Patients with Metastatic Invasive Lobular Carcinoma of the Breast." At the time of this recording, our guest's disclosures will be linked in the transcript. Julia, welcome to our podcast, and thank you for joining us today. Dr. Julia Foldi: Thank you so much for having me. It is a pleasure. Dr. Rafeh Naqash: Again, your manuscript and project address a few interesting things, so we will start with the basics, since we have a broad audience that comprises trainees, community oncologists, and obviously precision medicine experts as well. So, let us start with invasive lobular breast carcinoma. I have been out of fellowship for several years now, and I do not know much about invasive lobular carcinoma. Could you tell us what it is, what some of the genomic characteristics are, why it is different, and why it is important to have a different way to understand disease biology and track disease status with this type of breast cancer? Dr. Julia Foldi: Yes, thank you for that question. It is really important to frame this study. So, lobular breast cancers, which we shorten to ILC, are the second most common histologic subtype of breast cancer after ductal breast cancers. ILC makes up about 10 to 15 percent of all breast cancers, so it is relatively rare, but in the big scheme of things, because breast cancer is so common, this represents actually over 40,000 new diagnoses a year in the US of lobular breast cancers. What is unique about ILC is it is characterized by loss of an adhesion molecule, E-cadherin. It is encoded by the CDH1 gene. What it does is these tumors tend to form discohesive, single-file patterns and infiltrate into the tumor stroma, as opposed to ductal cancers, which generally form more cohesive masses. As we generally explain to patients, ductal cancers tend to form lumps, while lobular cancers often are not palpable because they infiltrate into the stroma. This creates several challenges, particularly when it comes to imaging. In the diagnostic setting, we know that mammograms and ultrasounds have less sensitivity to detect lobular versus ductal breast cancer. When it comes to the metastatic setting, conventional imaging techniques like CT scans have less sensitivity to detect lobular lesions often. One other unique characteristic of ILC is that these tumors tend to have lower proliferation rates. Because our glucose-based PET scans depend on glucose uptake of proliferating cells, often these tumors also are not avid on conventional FDG-PET scans. It is a challenge for us to monitor these patients as they go through treatment. If you think about the metastatic setting, we start a new treatment, we image people every three to four cycles, about every three months, and we combine the imaging results with clinical assessment and tumor markers to decide if the treatment is working. But if your imaging is not reliable, sometimes even at diagnosis, to really detect these tumors, then really, how are we following these patients? This is really the unique challenge in the metastatic setting in patients with lobular breast cancer: we cannot rely on the imaging to tell if patients are responding to treatment. This is where liquid biopsies are really, really important, and as the field is growing up and we have better and better technologies, lobular breast cancer is going to be a field where they are going to play an important role. Dr. Rafeh Naqash: Thank you for that easy-to-understand background. The second aspect that I would like to have some context on, to help the audience understand why you did what you did, is ctDNA, tumor informed and non-informed. Could you tell us what these subtypes of liquid biopsies are and why you chose a tumor informed assay for your study? Dr. Julia Foldi: Yes, it is really important to understand these differences. As you mentioned, there are two main platforms for liquid biopsy assays, circulating tumor DNA assays. I think what is more commonly used in the metastatic setting are non-tumor informed assays, or agnostic assays. These are generally next-generation sequencing-based assays that a lot of companies offer, like Guardant, Tempus, Caris, and FoundationOne. These do not require tumor tissue; they just require a blood sample, a plasma sample, essentially. The next-generation sequencing is done on cell-free DNA that is extracted from the plasma, and it is looking for any cell-free DNA and essentially, figuring out what part of the cell-free DNA comes from the tumor is done through a bioinformatics approach. Most of these assays are panel tests for cancer-associated mutations that we know either have therapeutic significance or biologic significance. So, the results we receive from these tests generally read out specific mutations in oncogenic genes, or sometimes things like fusions where we have specific targeted drugs. Some of the newer assays can also read out tumor fraction; for example, the newest generation Guardant assay that is methylation-based, they can also quantify tumor fraction. But the disadvantage of the tumor agnostic approach is that it is a little bit less sensitive. Opposed to that, we have our tumor informed tests, and these require tumor tissue. Essentially, the tumor is sequenced; this can either be whole exome or whole genome sequencing. The newer generation assays are now using whole genome sequencing of the tumor tissue, and a personalized, patient-specific panel of alterations is essentially barcoded on that tumor tissue. This can be either structural variants or it can be mutations, but generally, these are not driver mutations, but sort of things that are present in the tumor tissue that tend to stay unchanged over time. For each particular patient, a personalized assay, if you want to call it a fingerprint or barcode, is created, and then that is what then is used to test the plasma sample. Essentially, you are looking for that specific cancer in the blood, that barcode or fingerprint in the blood. Because of this, this is a much more sensitive way of looking for ctDNA, and obviously, this detects only that particular tumor that was sequenced originally. So, it is much more sensitive and specific to that tumor that was sequenced. You can argue for both approaches in different settings. We use them in different settings because they give us different information. The tumor agnostic approach gives us mutations, which can be used to determine what the next best therapy to use is, while the tumor informed assay is more sensitive, but it is not going to give us information on therapeutic targets. However, it is quantified, and we can follow it over time to see how it changes. We think that it is going to tell us how patients respond to treatment because we see our circulating tumor DNA levels rise and fall as the cancer burden increases or decreases. We decided to use the tumor informed approach in this particular study because we were really interested in how to determine if patients are having response to treatment versus if they are going to progress on their treatment, more so than looking for specific mutations. Dr. Rafeh Naqash: When you think about these tumor informed assays and you think about barcoding the mutations on the original tumor that you try to track or follow in subsequent blood samples, plasma samples, in your experience, if you have done it in non-lobular cancers, do you think shedding from the tumor has something to do with what you capture or how much you capture? Dr. Julia Foldi: Absolutely. I think there are multiple factors that go into whether someone has detectable ctDNA or not, and that has to do with the type of cancer, the location, right, where is the metastatic site? This is something that we do not fully understand yet: what are tumors that shed more versus not? There is also clearance of ctDNA, and so how fast that clearance occurs is also something that will affect what you can detect in the blood. ctDNA is very short-lived, only has a half-life of hours, and so you can imagine that if there is little shedding and a lot of excretion, then you are not going to be detecting a lot of it. In general, in the metastatic setting, we see that we can detect ctDNA in a lot of cases, especially when patients are progressing on treatment, because we imagine their tumor burden is higher at that point. Even with the non-tumor informed assays, we detect a lot of ctDNA. Part of this study was to actually assess: what is the proportion of patients where we can have this information? Because if we are only going to be able to detect ctDNA in less than 50 percent of patients, then it is not going to be a useful method to follow them with. Because this field is new and we have not been using a lot of tumor informed assays in the metastatic setting, we did not really know what to expect when we set out to look at this. We did not know what was going to be the baseline detection rate in this patient population, so that was one of the first things that we wanted to answer. Dr. Rafeh Naqash: Excellent. Now going to this manuscript in particular, what was the research question, what was the patient population, and what was the strategy that you used to investigate some of these questions? Dr. Julia Foldi: So, we partnered with Natera, and the reason was that their Signatera tumor-informed assay was the first personalized, tumor-informed, really an MRD assay, minimal residual disease detection assay. It has been around the longest and has been pretty widely used commercially already, even though some of our data is still lacking. but we know that people are using this in the real world. We wanted to gather some real-world data specifically in lobular patients. So, we asked Natera to look at their database of commercial Signatera testing and look for patients with stage 4 lobular breast cancer. The information all comes from the submitting physicians sending in pathologic reports and clinical notes, and so they have that information from the requisitions essentially that are sent in by the ordering physician. We found 66 patients who were on first-line or close to first-line endocrine-based therapies for their metastatic lobular breast cancer and had serial collections of Signatera tests. The way we defined baseline was that the first Signatera had to be sent within three months of starting treatment. So, it is not truly baseline, but again, this is a limitation of looking at real-world data is that you are not always going to get the best time point that you need. We had over 350 samples from those 66 patients, again longitudinal ctDNA samples, and our first question was what is the baseline detection rate using this tumor informed assay? Then, most importantly, what is the concordance between changes in ctDNA and clinical response to treatment? That is defined by essentially radiologic response to treatment. Dr. Rafeh Naqash: Interesting. So, what were some of your observations in terms of ctDNA dynamics, whether baseline levels made a difference, whether subsequent levels at different time points made a difference, or subsequent levels at, let us say, cycle three made a difference? Were there any specific trends that you saw? Dr. Julia Foldi: So, first, at baseline, 95 percent of patients had detectable ctDNA, which is, I think, a really important data point because it tells us that this can be a really useful test. If we can detect it in almost all patients before they start treatment, we are going to be able to follow this longitudinally. And again, these were not true baseline samples. So, I think if we look really at baseline before starting treatment, almost all patients will have detectable ctDNA in the metastatic setting. The second important thing we saw was that disease progression correlated very well with increase in ctDNA. So, in most patients who had disease progression by imaging, we saw increase in ctDNA. Conversely, in most patients who had clinical benefit from their treatment, so they had a response or stable disease, we saw decrease in ctDNA levels. It seems that what we call molecular response based on ctDNA is tracking very nicely along with the radiographic response. So, those were really the two main observations. Again, this is a small cohort, limited by its real-world nature and the time points that ctDNA assay was sent was obviously not mandated. This is a real-world data set, and so we could not really look at specific time points like you asked about, let us say, cycle three of therapy, right? We did not have all of the right time points for all of the patients. But what we were able to do was to graph out some specific patient scenarios to illustrate how changes in ctDNA correlate with imaging response. I can talk a little bit about that. Dr. Rafeh Naqash: That was going to be my question. Did you see patients who had serial monitoring using the tumor informed ctDNA assay where the assay became positive a few months before the imaging? Did you have any of those kinds of observations? Dr. Julia Foldi: Yes, so I think this is where the field is going: are we able to use this technology to maybe detect progression before it becomes clinically apparent? Of course, there are lots of questions about: does that really matter? But it seems like, based on some of the patient scenarios that we present in the paper, that this testing can do that. So, we had a specific scenario, and this is illustrated in a figure in the paper, really showing the treatment as well as the changes in ctDNA, tumor markers, and also radiographic response. So, this particular patient was on first-line endocrine therapy and CDK4/6 inhibitor with palbociclib. Initially, she had a low-level detectable ctDNA. It became undetectable during treatment, and the patient had a couple of serial ctDNA assays that were negative, so undetectable. And then we started, after about seven months on this combination therapy, the ctDNA levels started rising. She actually had three serial ctDNA assays with increasing level of ctDNA before she even had any imaging tests. And then around the time that the ctDNA peaked, this patient had radiographic evidence of progression. There was also an NGS-based assay sent to look for specific mutations at that point. The patient was found to have an ESR1 mutation, which is very common in this patient population. She was switched to a novel oral SERD, elacestrant, and the ctDNA fell again to undetectable within the first couple months of being on elacestrant. And then a very similar thing happened: while she was on this second-line therapy, she had three serial negative ctDNA assays, and then the fourth one was positive. This was two months before the patient had a scan that showed progression again. Dr. Rafeh Naqash: And Julia, like you mentioned, this is a small sample size, limited number of patients, in this case, one patient case scenario, but provides insights into other important aspects around escalation or de-escalation of therapy where perhaps ctDNA could be used as an integral biomarker rather than an exploratory biomarker. What are some of your thoughts around that and how is the breast cancer space? I know like in GI and bladder cancer, there has been a significant uptrend in MRD assessments for therapeutic decision making. What is happening in the breast cancer space? Dr. Julia Foldi: So, super interesting. I think this is where a lot of our different fields are going. In the breast cancer space, so far, I have seen a lot of escalation attempts. It is not even necessarily in this particular setting where we are looking at dynamics of ctDNA, but in the breast cancer world, of course, we have a lot of data on resistance mutations. I mentioned ESR1 mutation in a particular patient in our study. ESR1 mutations are very common in patients with ER-positive breast cancer who are on long-term endocrine therapy, and ESR1 mutations confer resistance to aromatase inhibitors. So, that is an area that there has been a lot of interest in trying to detect ESR1 mutations earlier and switching therapy early. So, this was the basis of the SERENA-6 trial, which was presented last year at ASCO and created a lot of excitement. This was a trial where patients had non-tumor-informed NGS-based Guardant assay sent every three to six months while they were on first-line endocrine therapy with a CDK4/6 inhibitor. If they had an ESR1 mutation detected, they were randomized to either continue the same endocrine therapy or switch to an oral SERD. The trial showed that the population of patients who switched to the oral SERD did better in terms of progression-free survival than those who stayed on their original endocrine therapy. There are a lot of questions about how to use this in routine practice. Of course, it is not trivial to be sending a ctDNA assay every three to six months. The rate of detection of these mutations was relatively low in that study; again, the incidence increases in later lines of therapy. So, there are a lot of questions about whether we should be doing this in all of our first-line patients. The other question is, even the patients who stayed on their original endocrine therapy were able to stay on that for another nine months. So, there is this question of: are we switching patients too early to a new line of therapy by having this escalation approach? So, there are a lot of questions about this. As far as I know, at least in our practice, we are not using this approach just yet to escalate therapy. Time will tell how this all pans out. But I think what is even more interesting is the de-escalation question, and I think that is where tumor informed assays like Signatera and the data that our study generated can be applied. Actually, our plan is to generate some prospective data in the lobular breast cancer population, and I have an ongoing study to do that, to really be able to tease out the early ctDNA dynamics as patients first start on endocrine therapy. So, this is patients who are newly diagnosed, they are just starting on their first-line endocrine therapy, and measure, with sensitive assays, measure ctDNA dynamics in the first few months of therapy. In those patients who have a really robust response, that is where I think we can really think about de-escalation. In the patients whose ctDNA goes to undetectable after just a few weeks of therapy with just an endocrine agent, they might not even need a CDK4/6 inhibitor in their first-line treatment. So, that is an area where we are very interested in our group, and I know that other groups are looking at this too, to try to de-escalate therapy in patients who clear their ctDNA early on. Dr. Rafeh Naqash: Thank you so much. Well, lots of questions, but at the same time, progress comes through questions asked, and your project is one of those which is asking an interesting question in a rarer cancer and perhaps will lead to subsequent improvement in how we monitor these individuals and how we escalate or de-escalate therapy. Hopefully, we will get to see more of what you are working on in subsequent submissions to JCO Precision Oncology and perhaps talk more about it in a couple of years and see how the space and field is moving. Thanks again for sharing your insights. I do want to take one to two quick minutes talking about you as an investigator, Julia. If you could speak to your career pathway, your journey, the pathway to mentorship, the pathway to being a mentor, and how things have shaped for you in your personal professional growth. Dr. Julia Foldi: Sure, yeah, that is great. Thank you. So, I had a little bit of an unconventional path to clinical medicine. I actually thought I was going to be a basic scientist when I first started out. I got a PhD in Immunology right out of college and was studying not even anything cancer-related. I was studying macrophage signaling in inflammatory diseases, but I was in New York City. This was right around the time that the first checkpoint inhibitors were approved. Actually, some of my friends from my PhD program worked in Jim Allison's lab, who was the basic scientist responsible for ipilimumab. So, I got to kind of first-hand experience the excitement around bringing something from the lab into the clinic that actually changed really the course of oncology. And so, I got very excited about oncology and clinical medicine. So, I decided to kind of switch gears from there and I went back to medical school after finishing my PhD and got my MD at NYU. I knew I wanted to do oncology, so I did a research track residency and fellowship combined at Yale. I started working early on with the breast cancer team there. At the time, Lajos Pusztai was the head of translational research there at Yale, and I started working with him early in my residency and then through my fellowship. I worked on several trials with him, including a neoadjuvant checkpoint inhibitor trial in triple-negative breast cancer patients. During my last year in fellowship, I received a Conquer Cancer Young Investigator Award to study estrogen receptor heterogeneity using spatial transcriptomics in this subset of breast cancers that have intermediate estrogen receptor expression. From there, I joined the faculty at the University of Pittsburgh in 2022. So, I have been there about almost four years at this point. My interests really shifted slowly from triple-negative breast cancers towards ER-positive breast cancers. When I arrived in Pittsburgh, I started working very closely with some basic and translational researchers here who are very interested in estrogen signaling and mechanisms of resistance to endocrine therapy, and there is a large group here interested in lobular breast cancers. During my training, I was not super aware even that lobular breast cancer was a unique subtype of breast cancers, and that is, I think, changing a little bit. There is a lot more awareness in the breast cancer clinical and research community about ILC being a unique subtype, but it is not even really part of our training in fellowship, which we are trying to change. But I have become a lot more aware of this because of the research team here and through that, I have become really interested also on the clinical side. And so, we do have a Lobular Breast Cancer Research Center of Excellence here at the University of Pittsburgh and UPMC, and I am the leader on the clinical side. We have a really great team of basic and translational researchers looking at different aspects of lobular breast cancers, and some of the work that I am doing is related to this particular manuscript we discussed and the next steps, as I mentioned, a prospective study of early ctDNA dynamics in lobular patients. I also did some more clinical research work in collaboration with the NSABP looking at long-term outcomes of patients with lobular versus ductal breast cancers in some of their older trials. And so, that is, in a nutshell, a little bit about how I got here and how I became interested in ILC. Dr. Rafeh Naqash: Well, thank you for sharing those personal insights and personal journey. I am sure it will inspire other trainees, fellows, and perhaps junior faculty in trying to find their niche. The path, as you mentioned, is not always straight; it often tends to be convoluted. And then finding an area that you are interested in, taking things forward, and being persistent is often what matters. Dr. Julia Foldi: Thank you so much for having me. It was great. Dr. Rafeh Naqash: It was great chatting with you. And thank you for listening to JCO Precision Oncology Conversations. Don't forget to give us a rating or review, and be sure to subscribe so you never miss an episode. You can find all ASCO shows at asco.org/podcasts. 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.  

Lorem ipsum dolor sit amet consectetur adipiscing elit. Quisque faucibus ex sapien vitae pellentesque sem placerat. In id cursus mi pretium tellus duis convallis. Tempus leo eu aenean sed diam urna tempor. Pulvinar vivamus fringilla lacus nec metus bibendum egestas. Iaculis massa nisl malesuada lacinia integer nunc posuere. Ut hendrerit semper vel class aptent taciti sociosqu. Ad litora torquent per conubia nostra inceptos himenaeos.Lorem ipsum dolor sit amet consectetur adipiscing elit. Quisque faucibus ex sapien vitae pellentesque sem placerat. In id cursus mi pretium tellus duis convallis. Tempus leo eu aenean sed diam urna tempor. Pulvinar vivamus fringilla lacus nec metus bibendum egestas. Iaculis massa nisl malesuada lacinia integer nunc posuere. Ut hendrerit semper vel class aptent taciti sociosqu. Ad litora torquent per conubia nostra inceptos himenaeos.Lorem ipsum dolor sit amet consectetur adipiscing elit. Quisque faucibus ex sapien vitae pellentesque sem placerat. In id cursus mi pretium tellus duis convallis. Tempus leo eu aenean sed diam urna tempor. Pulvinar vivamus fringilla lacus nec metus bibendum egestas. Iaculis massa nisl malesuada lacinia integer nunc posuere. Ut hendrerit semper vel class aptent taciti sociosqu. Ad litora torquent per conubia nostra inceptos himenaeos.Lorem ipsum dolor sit amet consectetur adipiscing elit. Quisque faucibus ex sapien vitae pellentesque sem placerat. In id cursus mi pretium tellus duis convallis. Tempus leo eu aenean sed diam urna tempor. Pulvinar vivamus fringilla lacus nec metus bibendum egestas. Iaculis massa nisl malesuada lacinia integer nunc posuere. Ut hendrerit semper vel class aptent taciti sociosqu. Ad litora torquent per conubia nostra inceptos himenaeos.Lorem ipsum dolor sit amet consectetur adipiscing elit. Quisque faucibus ex sapien vitae pellentesque sem placerat. In id cursus mi pretium tellus duis convallis. Tempus leo eu aenean sed diam urna tempor. Pulvinar vivamus fringilla lacus nec metus bibendum egestas. Iaculis massa nisl malesuada lacinia integer nunc posuere. Ut hendrerit semper vel class aptent taciti sociosqu. Ad litora torquent per conubia nostra inceptos himenaeos.Questions or comments, we'd love to hear from you...send us a text!Record a question here so we can answer it on the next episode of Claim Your Confidence.To stay up to date with Claim Your Confidence and get all the behind-the-scenes content, follow us on Instagram and on YouTube.If you enjoyed this episode, please subscribe and leave a rating and review on Apple or Spotify or where ever you get your podcasts.Recorded at The Newsstand Studios at Rockefeller Center.Thank you for listening.

Mit einer etwas angeschlagenen Stimme knüpfe ich mit dem Thema der Perfektivität, also Konstruktionen, die Abgeschlossenheit markieren, direkt an die Diskussion zu Tempus und Temporalität an. Im Zentrum steht die Frage: Können wir adäquat die Verzahnung komplexer Konstruktionen beschreiben, die je auf unterschiedlichen Ebenen Abgeschlossenheit markieren? Konkreter blicken wir auf (1) telische Verben, (2) die aspektuelle Bedeutung des Perfektpartizips, (3) auf die Abgrenzung der Askription (traditionell Zustandspassiv) von Konstruktionen der Perfektivität mit _sein_ sowie (4) unterschiedliche Einbettungsverhältnisse von schematisch komplexen Konstruktionen. Präsentation (*.pdf): Alexander Lasch. 2025. Konstruktionsgrammatik. Zenodo. DOI: ⁠⁠⁠https://doi.org/10.5281/zenodo.17370032⁠⁠⁠. Videoaufzeichnungen: ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠https://youtube.com/@AlexanderLasch⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠. Informationen & Material zu allen Vorlesungen: ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠https://kurzelinks.de/fl7f⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠. Worksheet zu den Vorlesungen: ⁠⁠⁠⁠https://kurzlinks.de/WorksheetVorlesungen⁠⁠⁠⁠. Intro: "Reflections" von Scott Holmes (CC BY via ⁠⁠⁠⁠⁠⁠FMA⁠⁠⁠⁠⁠⁠).#Linguistik #OER #Sprache #Sprachwissenschaft #Grammatik #Konstruktionsgrammatik

In dieser Vorlesung stehen "Tempus(formen)" und "Temporalität" im Mittelpunkt. Ich diskutiere die Adaptation des traditionellen Systems der sechs Tempora des Lateinischen für das Deutsche kritisch und schlage stattdessen eine konstruktionsgrammatische Modellierung des kerngrammatischen Themas "Tempus" vor, das stärker auf Einbettungsverhältnissen und der Perspektivierungsleistung sprachlicher Muster basiert. Dabei werden zentrale Konzepte wie die Sprecherposition (Bühler), die Zeitlogik (Reichenbach / Thieroff), Dynamik der Zeitformen (Ballweg) sowie der Einfluss von Aktionsarten (Telizität) und Temporaladverbialen auf die Interpretation von Zeitstrukturen diskutiert.Präsentation (*.pdf): Alexander Lasch. 2025. Konstruktionsgrammatik. Zenodo. DOI: ⁠⁠https://doi.org/10.5281/zenodo.17370032⁠⁠. Videoaufzeichnungen: ⁠⁠⁠⁠⁠⁠⁠⁠⁠https://youtube.com/@AlexanderLasch⁠⁠⁠⁠⁠⁠⁠⁠⁠. Informationen & Material zu allen Vorlesungen: ⁠⁠⁠⁠⁠⁠⁠⁠⁠https://kurzelinks.de/fl7f⁠⁠⁠⁠⁠⁠⁠⁠⁠. Worksheet zu den Vorlesungen: ⁠⁠⁠https://kurzlinks.de/WorksheetVorlesungen⁠⁠⁠. Intro: "Reflections" von Scott Holmes (CC BY via ⁠⁠⁠⁠⁠⁠FMA⁠⁠⁠⁠⁠⁠).#Linguistik #OER #Sprache #Sprachwissenschaft #Grammatik #Konstruktionsgrammatik

Friends of the Rosary,The Holy Father's Intentions for the Month of January 2026 highlight a way of praying with the Word of God:"Let us pray that praying with the Word of God be nourishment for our lives and a source of hope in our communities, helping us to build a more fraternal and missionary Church."In January, the month dedicated to the Most Holy Name of Jesus, the first eleven days fall during the liturgical season of Christmas — until the feast of the Baptism of the Lord, this Sunday on the 11th, when we read that after Jesus was baptized, He saw the Spirit of God coming upon him.The remaining days of January are the beginning of the liturgical season of Tempus per Annum or Ordinary Time (formerly Time After Epiphany), which is represented by the liturgical color green.The remaining Feasts for January 2026 are:St. Anthony, Abbot (January 17),Sts. Fabian and Sebastian (January 20),St. Agnes (January 21),St. Francis de Sales (January 24),Sts. Timothy and Titus (January 26),St. Angela Merici (January 27),St. Thomas Aquinas (January 28)St. John Bosco (January 31)The Memorial of St. Elizabeth Ann Seton (January 4) and the Feast of the Conversion of St. Paul (January 25) are superseded by the Sunday liturgy.Come, Holy Spirit, come!To Jesus through Mary!Here I am, Lord; I come to do your will.Please give us the grace to respond with joy!+ Mikel Amigot w/ María Blanca | RosaryNetwork.com, New YorkEnhance your faith with the new Holy Rosary University app:Apple iOS | New! Android Google Play• ⁠January 9, 2026, Today's Rosary on YouTube | Daily broadcast at 7:30 pm ET

The guys recount the highlights of 2025 and wonder what even happened. Everyone gathers around for story time of Irish wishes and whimsical gifts. Ken and Aaron both receive gifts that help keep their minds stimulated and their reflexes sharp.

It's Christmas Day in 1066, and a new king is to be crowned. There will be all sorts of festive events: arrows in the eye, fires outside the church, and just a little holiday looting too. If you like what you hear and want to chip in to support the podcast, ⁠⁠⁠⁠⁠⁠⁠⁠my Patreon is here⁠⁠⁠⁠⁠⁠⁠⁠. I'm on BlueSky ⁠⁠⁠⁠⁠⁠⁠⁠@a-devon.bsky.social⁠⁠⁠⁠⁠⁠⁠⁠, and I have some things on ⁠⁠⁠⁠⁠⁠⁠⁠Redbubble⁠⁠⁠⁠⁠⁠⁠⁠. Sources: Guy Bishop of Amiens. The Carmen de Hastingae Proelio. Edited and translated by Frank Barlow. Oxford University Press, 1999. Lawson, M.K. The Battle of Hastings 1066. Tempus, 2002. Orderic Vitalis. The Ecclesiastical History of England and Normandy, Volume 1. Translated by Thomas Forester. H.G. Bohn, 1853. William of Poitiers. The Deeds of William. Oxford University Press, 1998. Learn more about your ad choices. Visit podcastchoices.com/adchoices

Merriam-Webster's Word of the Day for December 22, 2025 is: temporize • TEM-puh-ryze • verb To temporize is to avoid making a decision or giving a definite answer in order to have more time. // Pressured by voters on both sides of the issue, the congressman temporized. See the entry > Examples: "The question is, Did you eat the last piece of pie? And the politician who ate the last piece of pie doesn't want to say yes, because they might get in trouble. Doesn't want to say no, because that's an outright lie. So they waver, they equivocate, they temporize, they put things in context, and they talk like a politician." — David Frum, The Atlantic (The David Frum Show podcast), 21 May 2025 Did you know? Temporize comes from the Middle French word temporiser, which in turn likely traces back via Medieval Latin temporizāre, "to delay," to the Latin noun tempus, meaning "time." Tempus is also the root of such words as tempo, contemporary, and temporal. If you need to buy some time, you might resort to temporizing, but you probably won't win admiration for doing so, as the word typically carries a negative connotation. For instance, a political leader faced with a difficult issue might temporize by talking vaguely about possible solutions without actually doing anything. The point of such temporizing is to avoid taking definitive—and possibly unpopular—action, in hopes that the problem will somehow go away.

Peu de rivalités ont autant marqué le monde et les mémoires que celles entre les USA et l'URSS. Débutée juste après la chute des nazis et de leurs alliés, elle est immédiatement baptisée “Guerre Froide” – et le nom veut tout dire. Script: Guilhem  @DHistoiresenHistoire  00:00 Introduction 01:55 Idéologies et analyses concurrentes 07:26 Premières crises 15:01 Des escalades 18:39 Façades et réalités 21:59 Coexistence pacifique (1953-1963) 29:52 Détente (1963-1975) 34:12 Guerre fraîche (1975-1984) 38:28 Nouvelle détente 41:44 Effondrement de l'URSS 44:59 Conclusion Adhérez à cette chaîne pour obtenir des avantages : https://www.youtube.com/channel/UCN4TCCaX-gqBNkrUqXdgGRA/join Pour soutenir la chaîne, au choix: 1. Cliquez sur le bouton « Adhérer » sous la vidéo. 2. Patreon: https://www.patreon.com/hndl Musique issue du site : epidemicsound.com Images provenant de https://www.storyblocks.com Abonnez-vous à la chaine: https://www.youtube.com/c/LHistoirenousledira Les vidéos sont utilisées à des fins éducatives selon l'article 107 du Copyright Act de 1976 sur le Fair-Use. Sources et pour aller plus loin: André FONTAINE, La guerre froide 1917-1991, Seuil, 2006. John LEWIS GADDIS, The Cold War. A New History, Penguin, 2006. Nicolas WERTH, Le cimetière de l'espérance, essais sur l'histoire de l'Union soviétique, 1914-1991, Tempus, 2019. Tony JUDT, Post War: A History of Europe Since 1945, Penguin, 2005. Pierre GROSSER, Les temps de la guerre froide, Complexe, 1995. Stanislas JEANNESSON, Sabine DULLIN, Atlas de la guerre froide, Autrement, 2017. Juliette BOURDIN, Entre portes ouvertes et portes fermées, la politique chinoise des États-Unis du XIXe au XXIe siècle, Paris, Presses Sorbonne nouvelle, 2013 Ian KERSHAW, L'âge global. L'Europe de 1950 à nos jours, Seuil, 2020. Serge BERSTEIN et Pierre MILZA, Histoire du XXe siècle – Tomes 2 (1945-1973) et 3 (1973-1990), éditions de 2006-2010 Juliette BOURDIN, Entre porte ouverte et porte fermée – La politique chinoise des États-Unis du XIXe au XXIe siècle, 2013 Pierre BROCHEUX (dir.), Les décolonisations au XXe siècle – La fin des empires européens et japonais, 2012 Hélène CARRÈRE-D'ENCAUSSE, Six années qui ont changé le monde (1985-1991) – La chute de l'empire soviétique, 2015 Jean CAZEMAJOU et Jean-Michel LACROIX (dir.), La guerre du Vietnam et l'opinion publique américaine (1961-1973), 1991 Sabine DULLIN et al., Atlas de la guerre froide (1947-1990) : un conflit global et multiforme, 2020 Catherine DURANDIN, La Guerre froide – « Que sais-je ? », 2023 Jacques GERNET, Le monde chinois – Tome 3 – L'époque contemporaine, édition de 2005 Bernard VINCENT, Histoire des États-Unis, édition de 2016 Michèle WEINACHTER (dir.), L'Est et l'Ouest face à la chute du Mur – Question de perspective, Travaux et documents du CIRAC, 2013 Nicolas WERTH, Histoire de l'Union Soviétique de Lénine à Staline (1917-1953) – “Que Sais-Je ?”, 6e édition de 2022 Nicolas WERTH, Histoire de l'Union Soviétique de Kroutchev à Gorbatchev – “Que Sais-Je ?”, 5e édition de 2023 Tessa Coombs, « Cold War », https://www.imdb.com/fr-ca/title/tt1282631/ MAD World - The History of the Cold War Episode 1/ Superpowers Free Documentary History https://youtu.be/cadWivTlj1A?si=fZ1liXpP3Px2PwXA The Cold War/ Seven Minutes to Midnight Documentary, WarsofTheWorld, 6 aout 2021 https://youtu.be/2336v76nEf8?si=E6VXmTLm7jPzn3hk John F. Kennedy's Speech at the Berlin Wall https://youtu.be/yBQvKXIDiuc?si=DPlhRN6vgfUbGNIJ Autres références disponibles sur demande. #histoire #documentaire #guerrefroide #guerre #urss #usa #staline #marshall #russie #russia

Send us a textWhat if the biggest transformation in digital pathology this year had nothing to do with new hardware—and everything to do with how we think about value, workflow, and readiness?In this year-end recap livestream from the 11th Digital Pathology & AI Congress in London, I break down what truly mattered in 2025. Instead of focusing on buzzwords or hype cycles, this episode highlights the practical advances shaping diagnostics, patient care, and drug development—and the mindset shift our field must embrace to move forward.Digital pathology is no longer “early adoption.” It's becoming essential infrastructure. And yet the biggest barrier isn't scanners or algorithms—it's the knowledge and confidence needed to use them well.Key Highlights & Timestamps0:00 — Setting the Stage from LondonAn overview of the forces that shaped digital pathology in 2025: workflow integration, clinical readiness, and the move from theory to operational reality.1:45 — Leica's Expanded Portfolio & FDA-Cleared CollaborationsA look at Leica's updated scanner lineup and co-developed, FDA-cleared solutions with Indicollabs. These launches reflect a broader industry trend toward highly specialized, clinically validated digital tools designed for end-to-end workflows.4:12 — The Acceleration of Companion DiagnosticsFrom Artera's de novo–approved prostate prognostic test to AstraZeneca's TROP2 scoring efforts, 2025 pushed computational pathology directly into therapeutic decision-making.6:20 — Why Workflow Integration Became the Theme of 2025Partnerships like BioCare + Hamamatsu + Visgen and Zeiss + MindPeak show where the field is heading: full-stack solutions, not isolated tools. Labs want interoperability, reliability, and simplified digital workflows.9:10 — Adoption Challenges: ROI, Education & AI UncertaintyWe explore the realities slowing digital transformation: – ROI is real, but requires workflow change – AI anxiety persists among clinicians and patients – Education is still the strongest driver of adoption12:00 — 2025's Innovation HighlightsBreakthroughs shaping the next phase of digital pathology include: – emerging agentic AI platforms – voice-enabled image management systems – improved multiplexing technologies like Hamamatsu's Moxiplex15:40 — The Growing Intersection of Pathology & GenomicsAI models predicting genomic alterations from H&E images gained traction, especially for cases with minimal tissue. Tempus acquiring Paige signals the deepening connection between digital workflows and molecular data.18:30 — What 2026 Will RequirePriorities for the coming year include: – building agentic AI solutions capable of real workflow orchestration – strengthening validation and QC – sharing real-world deployment case studies – expanding training and hands-on learningRESOURCES:1. The Lucerne Toolbox 3: digital health and artificial intelligence to optimise the patient journey in early breast cancer-a multidisciplinary consensus2. Artificial intelligence (AI) molecular analysis tool assists in rapid treatment decision in lung cancer: a case reportSupport the showGet the "Digital Pathology 101" FREE E-book and join us!

Host Anthony Desiato and guests Rob O'Connor (All Star Superfan Podcast) & Chris Fuchs (Always Hold On To Star Wars) "draft" their favorite villains from LOIS & CLARK: THE NEW ADVENTURES OF SUPERMAN — including Tempus, Lord Nor, Jason Trask, and more — as they compete to form the best "Superman Revenge Squad." Listen to the draft, then be sure to head on over to social media to vote on the best lineup!Support the show and receive exclusive podcast content at Patreon.com/AnthonyDesiato, including the spinoff podcasts BEYOND METROPOLIS and DIGGING FOR JUSTICE!Visit BCW Supplies and use promo code FSP to save 10% on your next order of comics supplies. Get your DFK merch at the podcast's TeePublic storefront!FACEBOOK GROUP: Digging for Kryptonite: A Superman Fan GroupFACEBOOK PAGE: @diggingforkryptonitepodINSTAGRAM: @diggingforkryptonitepodTWITTER: @diggingforkrpodBLUESKY: @diggingforkrpod.bsky.socialEMAIL: flatsquirrelproductions@gmail.comWEBSITE: FlatSquirrelProductions.com Digging for Kryptonite is a Flat Squirrel Production. Theme music by Dan Pritchard. Key art by Isaiah Simmons. Mentioned in this episode:Single Bound PodcastThis Podcast Will Never DieAlways Hold On To SmallvilleHang On To Your Shorts Film FestivalFat Moose ComicsAw Yeah Comics

2025-12-05 Hosts Dr. Amir Kalali, Craig Lipset, and Jane Myles were joined by Noelle Gaskill and Karla Polk from Tempus AI to unpack how DCTs are expanding access and accelerating research, especially in oncology. They explored how Tempus' data-connected site network, genomics capabilities, and operational model help match patients faster, streamline startup timelines, and support community practices in running complex trials.The conversation covers real-world strategies for patient activation, managing variability across sites, partnering with CROs, and enabling rural and community-based providers to participate in research. They also touched on the future: global expansion plans and how DCT approaches could extend beyond oncology into other therapeutic areas.You can join TGIF-DTRA Sessions live on LinkedIn Live on Friday's at 12:00 PM ET by checking out our LinkedIn. Follow the Decentralized Trials & Research Alliance (DTRA) on LinkedIn and X. Learn more about Membership options and our work at www.dtra.org.

Invité : Jean-Dominique Merchet, auteur de «Sommes-nous prêts pour la guerre ?», aux éditions Tempus, sur le retour du service militaireHébergé par Audiomeans. Visitez audiomeans.fr/politique-de-confidentialite pour plus d'informations.

Invités : Jean-Dominique Merchet, auteur de «Sommes-nous prêts pour la guerre ?», aux éditions Tempus, sur le retour du service militaireChristian Saint-Etienne, économiste, sur le budget et le MercosurFrançois-Guillaume Lorrain, historien, pour «Ces lieux qui ont fait la France » aux éditions TempusHébergé par Audiomeans. Visitez audiomeans.fr/politique-de-confidentialite pour plus d'informations.

Mes chers camarades, bien le bonjour !Il y a des sujets qui sont plus simples que d'autres à aborder quand on fait des vidéos sur YouTube. Les morts insolites des rois, les jobs nuls, les inventions dues au hasard… C'est passionnant mais niveau terrain glissant, ça va, je ne me mouille pas trop ! Aujourd'hui, je vous propose de faire l'inverse : on va parler d'un des sujets les plus difficiles que j'ai eu à aborder sur la chaîne, toutes époques confondues. Tout simplement parce que c'est un sujet sensible au cœur même d'un autre sujet sensible : les Harkis et la guerre d'Algérie. Qui étaient véritablement les Harkis ? Pourquoi se battaient-ils, et quel a été leur sort ? Bonne écoute !➤ Retrouvez nos épisodes sur l'Algérie en podcast et sur YouTube : https://www.youtube.com/playlist?list=PLgLm3t2YjNL3QGojxMN66eKvBe-TYrtLW➤ Cet épisode a été réalisé en collaboration avec la CNIH : https://bit.ly/Harkis_CNIH_NB

En 1936, l'Espagne est profondément divisée par la victoire aux élections du Front Populaire. Le gouvernement de gauche est visé par un coup d'Etat de généraux conservateurs. Parmi eux se trouve Franco. Après avoir pris la tête des troupes basées au Maroc, il a besoin d'avions pour faire passer ses hommes en Espagne. Hitler et Mussolini se chargent de les lui fournir. Ce sont les débuts de la guerre civile. Les troupes de Franco, désormais leader des généraux rebelles, multiplient les exactions.En nouveau chef suprême, Franco commence à diffuser son image et à mettre en place le culte de sa personnalité. La victoire sur les Républicains est pourtant loin d'être acquise. La guerre civile s'achève en 1939. L'Espagne est franquiste, mais l'Europe bascule la même année dans la Seconde Guerre mondiale. Franco reste à l'écart, trop attaché à son rêve de restaurer la grandeur de l'Espagne. Au retour à la paix, Franco est certes toujours là, mais, muré dans le passé, le pays sombre dans la pauvreté.Dans la suite de ce récit, Virginie Girod vous raconte comment il s'est emparé du pouvoir et l'a conservé par la force. (rediffusion)Au Cœur de l'Histoire est un podcast Europe 1.- Auteure et Présentatrice : Virginie Girod - Production : Caroline Garnier- Réalisation : Nicolas Gaspard- Direction artistique : Julien Tharaud- Composition de la musique originale : Julien Tharaud et Sébastien Guidis- Edition et Diffusion : Nathan Laporte et Clara Ménard- Visuel : Sidonie Mangin- Patrimoine sonore : Sylvaine Denis, Laetitia Casanova et Antoine ReclusBibliographie :- Bartolomé Bennassar, Franco, Perrin coll. Tempus, 2002. Ressources en ligne :- https://www.eldiario.es/comunitat-valenciana/informacion-alemana-masones-franco-espanoles-gestapo_1_1271932.html - https://historia.nationalgeographic.com.es/a/entrevista-franco-y-hitler-estacion-hendaya_17306 - https://www.retronews.fr/conflits-et-relations-internationales/interview/2023/05/30/guerre-civile-espagnole-interview-franco - https://www.persee.fr/doc/casa_0076-230x_1994_num_30_3_2722Hébergé par Audiomeans. Visitez audiomeans.fr/politique-de-confidentialite pour plus d'informations.

Au Cœur de l'Histoire est un podcast Europe 1. - Auteure et Présentatrice : Virginie Girod  - Production : Caroline Garnier - Réalisation : Nicolas Gaspard - Direction artistique : Julien Tharaud - Composition de la musique originale : Julien Tharaud et Sébastien Guidis - Edition et Diffusion : Nathan Laporte et Clara Ménard - Visuel : Sidonie Mangin - Patrimoine sonore : Sylvaine Denis, Laetitia Casanova et Antoine Reclus Bibliographie : - Bartolomé Bennassar, Franco, Perrin coll. Tempus, 2002.  Ressources en ligne : - https://www.eldiario.es/comunitat-valenciana/informacion-alemana-masones-franco-espanoles-gestapo_1_1271932.html  - https://historia.nationalgeographic.com.es/a/entrevista-franco-y-hitler-estacion-hendaya_17306  - https://www.retronews.fr/conflits-et-relations-internationales/interview/2023/05/30/guerre-civile-espagnole-interview-franco  - https://www.persee.fr/doc/casa_0076-230x_1994_num_30_3_2722   Hébergé par Audiomeans. Visitez audiomeans.fr/politique-de-confidentialite pour plus d'informations.

Presented in partnership with Cancer Wellness Center, Tempus, and TriCan Health Artificial Intelligence (AI) is reshaping healthcare — helping patients and providers make smarter, more personalized decisions. In this Wellness Wednesday program, experts from Tempus and TriCan Health will explore how AI is being used to support cancer care, enhance communication between patients and doctors, and make clinical trials more accessible.Whether you're newly diagnosed, supporting a loved one, or simply curious about how technology can drive progress, this discussion will break down complex topics in clear, empowering ways.What You'll Learn: How AI tools help physicians and patients analyze complex data and uncover insightsWays technology personalizes care and improves outcomesHow AI is simplifying the process of finding and joining clinical trials

Au Cœur de l'Histoire est un podcast Europe 1. - Auteur et présentation : Jean des Cars - Production : Timothée Magot - Réalisation : Christophe Daviaud  - Diffusion et édition : Clémence Olivier, Salomé Journo et Clara Ménard Ressources bibliographiques : - Michel Meyer, Histoire secrète de la chute du Mur de Berlin (Odile Jacob, 2009, nouvelle édition, 2014) - Henry Bogdan, Histoire des pays de l'Est (Perrin, 1991, réédition actualisée collection Tempus, 2008)   Hébergé par Audiomeans. Visitez audiomeans.fr/politique-de-confidentialite pour plus d'informations.

Dans la nuit du 9 au 10 novembre 1989, les "piverts" et leurs burins commencent à s'attaquer au mur de Berlin, un événement couvert en direct par les médias du monde entier. Jean des Cars achève son récit sur la chute du mur de Berlin qui a séparé la capitale allemande pendant 28 ans. (rediffusion)Au Cœur de l'Histoire est un podcast Europe 1.- Auteur et présentation : Jean des Cars- Production : Timothée Magot- Réalisation : Christophe Daviaud - Diffusion et édition : Clémence Olivier, Salomé Journo et Clara MénardRessources bibliographiques :- Michel Meyer, Histoire secrète de la chute du Mur de Berlin (Odile Jacob, 2009, nouvelle édition, 2014)- Henry Bogdan, Histoire des pays de l'Est (Perrin, 1991, réédition actualisée collection Tempus, 2008)Hébergé par Audiomeans. Visitez audiomeans.fr/politique-de-confidentialite pour plus d'informations.

ReferencesKant, I Critique of Pure Reason. 2nd Edition 1787.Kierkegaard, S. 1849. The Sickness unto Death. Guerra 2025 Notes and thoughts on a Tuesday afternoon. UnpublishedHayward, J and J Lodge. 1967. Tuesday Afternoon. Moody Blues https://music.youtube.com/watch?v=jmMPBQ4kYKk&si=QqYC7kv_gQQw86K2Haydn, FJ. 1794. Symphony 101 in D Major "The Clock" Hob1/101https://music.youtube.com/watch?v=fAfs5Ic0Uwc&si=uHNcXktvM8_mjL_s

-what if im already dead. -Im trying to be the person others think I am. -fake cocaine addiction. -top 5 dirty crack house movies. -the uncification of hiphop. -Politically weve been here before. -Society is an act of violence. -they mad at us. Youtube: https://youtu.be/wb4t71ZdwuE Patreon: https://homie.gives/ Merch: https://www.redbubble.com/people/HomiesOnly/shop?asc=u Other stuff: https://linktr.ee/OccultnicHomie Discord: https://discord.gg/ua6FjftA5w PO Box: (host name) Care of: IvyCorp PO Box 57 carrboro, NC 27510

Feliciter nobis, Ilsae Andreaeque, accidit ut cum amica nobis carissima atque etiam doctissima conveniremus ut antiquitatis conventiculum celebraremus. Tempus et datum est nobis ut Latine loqueremur. En plura de ea: https://www.binghamton.edu/cemers/people/profile.html?id=tchronopPlacuitne sermo? Plura talia audire vultis? Nos certiores facere potestis per habesnelac.com/contact

Stéphane Bern nous invite au Congrès de Vienne, le "festival de la paix" tel qu'on l'a surnommé à l'époque, orchestré par les vainqueurs de Napoléon 1er qui ont oeuvré, entre 1814 et 1815, pour redessiner la carte de l'Europe diaboliquement bouleversée par l'Empereur déchu qui va pourtant tenter un “célèbre” retour qui ne va durer que cent jours…Quels étaient les enjeux du Congrès de Vienne ? Quelles en ont été les conséquences ? En quoi cette réunion diplomatique, considérée comme la plus grande de l'Histoire, a-t-elle posé les premières bases du droit international ?Pour en parler, Stéphane Bern reçoit Thierry Lentz, historien, spécialiste des questions napoléoniennes et auteur de l'ouvrage de référence « Le Congrès de Vienne » (ED. Perrin, collection Tempus). (rediffusion)Au Coeur de l'Histoire est un podcast Europe 1. - Présentation : Stéphane Bern - Réalisation : Guillaume Vasseau- Rédaction en chef : Benjamin Delsol- Auteur du récit : Simon Veille- Journaliste : Clara LegerHébergé par Audiomeans. Visitez audiomeans.fr/politique-de-confidentialite pour plus d'informations.

In the 2025 Payer Oncology Trend Report, we analyze how health plans and PBMs are navigating the shifting landscape of branded cancer drug management. To deepen our findings, we spoke with industry experts Michael Kolodziej, MD, and Ira Klein, Vice President, Medical Affairs & Payer Relations at Tempus, who shared their perspectives on the data, key trends, and what these insights mean for manufacturers moving forward.

JCO PO authors Dr. Abhishek Tripathi and Dr. Salvador Jaime-Casas at City of Hope Comprehensive Cancer Center share insights into their article, “Comparative Genomic Characterization of Small Cell Carcinoma of the Bladder Compared With Urothelial Carcinoma and Small Cell Lung Carcinoma.”  Host Dr. Rafeh Naqash and Drs. Tripathi and Jaime-Casas discuss a novel understanding of the genomic alterations underlying SCBC, revealing actionable mutations that could serve as potential targets for improved clinical outcomes. TRANSCRIPT Dr. Rafeh Naqash: Hello and welcome to JCO Precision Oncology Conversations, where we bring you engaging conversations with authors of clinically relevant and highly significant JCO PO articles. I am your host, Dr. Dr. Rafeh Naqash, Podcast Editor for JCO Precision Oncology and Associate Professor at the OU Health Stephenson Cancer Center at the University of Oklahoma. Today, I am thrilled to be joined by Dr. Abhishek Tripathi, Associate Professor in the Department of Medical Oncology and Experimental Therapeutics Research at the City of Hope Comprehensive Cancer Center, as well as his mentee, Dr. Salvador Jaime-Casas, postdoctoral research fellow and first author of the JCO Precision Oncology article entitled "Comparative Genomic Characterization of Small Cell Carcinoma of the Bladder Compared with Urothelial Carcinoma and Small Cell Lung Carcinoma". At the time of this recording, our guest disclosures will be linked in the transcript. Abhishek and Salvador, welcome to our podcast and thank you for joining us today. This is a very interesting topic given that at least the landscape for neuroendocrine carcinomas, where small cell lung cancer is on one end of the spectrum, has been changing, at least on the lung cancer side, with recent approvals and some new ADCs. So, of course, understanding the genomic and transcriptomic similarities or differences between pulmonary small cell and extrapulmonary small cell is of huge interest. Could you tell us a little bit about small cell bladder cancer, current approaches to treatment of small cell bladder cancer, and then why you wanted to investigate that in this project as far as the genomic differences or similarities are concerned? Dr. Salvador Jaime-Casas: Well, first of all, thank you very much for having me. I am very excited to be here. And really what served as backbone for this research project was the notion that there is a currently evolving genomic landscape in the area of bladder cancer. We know this is a highly heterogeneous disease when it comes to molecular underpinnings and mutational profile. Specifically, we know that the most common histologic subtype is urothelial carcinoma. Small cell bladder cancer represents a histology that is found in less than 1% of all bladder cancer cases. However, it is one of the most aggressive histologies. It presents with a very poor prognosis to patients and very poor response to treatment, which is why we attempted to really elucidate what is the mutational profile behind this and provide a comparison contrast between small cell bladder cancer, small cell lung cancer, and conventional urothelial carcinoma. As your question mentioned, in terms of treatment, the conventional urothelial carcinoma and small cell bladder cancer are two distinct pathways when it comes to treatment algorithms. We know that in the current era there are newer and newer drugs being developed for conventional urothelial carcinoma. We have perioperative immunotherapy in the context of metastatic disease. We have antibody-drug conjugates such as enfortumab vedotin. But really, this amazing track record of drug development hasn't been mirrored in small cell bladder cancer. And here most of the therapy is usually extrapolated from studies from other small cell histologies like you mentioned earlier, small cell lung cancer has given some form of background in terms of what therapies are used here. Cytotoxic chemotherapy, for some patients with localized disease and small cell bladder cancer, concurrent chemotherapy and radiotherapy or perioperative cytotoxic chemotherapy have been the cornerstone of treatment for many years now. However, like I mentioned, the oncologic outcomes are very suboptimal when it comes to comparing it with other disease histologies, which is why we really wanted to describe the landscape here and provide this comparison across three different groups. For this particular study, we leveraged the Tempus dataset. So, include patients with urothelial carcinoma with small cell bladder cancer and small cell lung cancer. We included their demographic information, as well as the frequency of most common genomic alterations identified. And really, it was a very comparable Table 1. We see the demographic data across the three groups was very similar. One key thing that we identified was the female prevalence was a little bit lower in patients with small cell bladder cancer when compared to small cell lung cancer. But other than that, the age, race, ethnicity, was comparable across groups, and even the smoking history. Most of the patients in this cohort were former smokers, which we believe comes to explain that regardless of any mutational profile that we talked about in a few minutes, there are shared commonalities between these histologies and shared environmental exposures and risk factors that are going to be implicated in the disease biology for these three histologies. Dr. Rafeh Naqash: Thank you so much, Salvador, for that useful background. I would like to shift to Abhishek real quick. Abhishek, you are a practicing clinician, you have led several studies in the GU space, especially bladder. Based on what you see in the small cell lung cancer space, how drug development is shaping up, which aligns with what you are trying to evaluate in this paper as targets, how do you see some of that being implemented for small cell bladder cancer in the current era and age? Abhishek Tripathi: Thanks so much for the excellent question, Rafeh. As a GU investigator, small cell bladder cancer has always lagged behind in some regards regarding enrollment abilities for the novel clinical trials. And small cell lung cancer has paved the way and led the development of a lot of these drugs across the board. With the most recent sort of drugs targeting DLL3 already approved and several antibody-drug conjugates currently in development. That actually translates really well to how we should approach drug development in bladder cancer. What we saw in the study is that although there are overlaps and similarities between small cell lung cancer and small cell bladder cancer, there are also certain differences. So the long-term assumption that all therapies for small cell bladder cancer can be extrapolated to small cell bladder], may or may not be true, and I think it is high time that we specifically investigate these novel agents in tissue-specific small cell carcinomas. To that effect, we are excited to be participating in trials that are looking at some of the novel DLL3 targeted agents, specifically bispecific antibodies and T cell engagers so to speak, and antibody-drug conjugates that are now starting to open enrollment specifically in non-lung cancer cohorts to evaluate its efficacy. So overall, I think studies like this have the opportunity to identify more putative targets for organ-specific development of these novel agents. Dr. Rafeh Naqash: Absolutely, I could not agree more. I think tumor-agnostic therapies definitely have a place, but not all therapies work the same in different tumors with a similar histological or genomic background because there are definitely differences. So now going to the comparison that Salvador, you guys did in this project, could you help us understand what are some of the things you looked at, what were some of the commonalities and the differences, and what were some of the conceptual thoughts that come out from those results? Dr. Salvador Jaime-Casas: Of course. So, the first thing that we identified was which were the most frequent molecular alterations across these histologies. We actually provided a table showcasing how the most common mutations that we identified were TP53, TERT, RB1. However, like Dr. Tripathi mentioned, the distinction between these histologies is notable in the sense that some are more predominant in small cell-pertaining cancers such as bladder cancer and lung cancer. While some others are more common in bladder-pertaining malignancies like urothelial carcinoma and small cell bladder cancer. For instance, we saw that TP53 and RB1 were significantly more evident in small cell histologies, both small cell bladder cancer and small cell lung cancer, as opposed to conventional urothelial carcinoma, which really this mirrors what is known about these mutations and what has been published. These are markers associated with more aggressive disease with a worse prognosis and even to resistance to treatment. We also identified how TERT mutations were characteristically more prevalent in small cell bladder cancer as opposed to small cell lung cancer, as well as in urothelial carcinoma. TERT mutations were more commonly identified than in small cell lung cancer. And we give a long list of these mutations that we identified, but really what we wanted to underscore here was, A, the most common mutations across histologies; B, the most common co-occurring mutations where we saw that these are not mutually exclusive. A lot of patients had co-occurring TP53 and RB1 or RB1 and TERT or RB1 and ARID1A, really elucidating how heterogeneous this molecular landscape is across histologies. And the third one that we believe really brings down the clinical impact of this research was evidencing the idea of clinically actionable mutations. We also provided a table here showcasing how mutations like FGFR, DLL notch pathway, HER2, were evident in these histologies, and what is the current status of some clinical trials evaluating different drug designs for these mutations. Like Dr. Tripathi mentioned in the context of FGFR, approximately 6% of our cohort with small cell bladder cancer showcased mutations in FGFR3. However, up to 14% of them had mutations in any FGFR gene, which really underscores the notion that drugs like erdafitinib, which have been introduced in the market in recent years, could potentially showcase some response in the space of small cell bladder cancer. We actually provide the description of two trials, phase two, phase three trials, that are evaluating erdafitinib in the context of high-risk non-muscle invasive bladder cancer and even metastatic urothelial carcinoma. Like Dr. Tripathi mentioned as well, antibody-drug conjugates, another very interesting area of drug development targeting HER2, we included evidence on how disitamab vedotin and trastuzumab deruxtecan are currently being explored across different phase two and phase three clinical trials, both as part of basket trial designs for solid malignancies expressing HER2, but also for patients with urothelial carcinoma where there is evidence of HER2 expression. So, we believe that the landscape is shifting in the right direction in the sense that therapies are becoming much more personalized and targeted against these known molecular profiles. Dr. Rafeh Naqash: Thank you, Salvador, for summarizing some of those very interesting results and providing a very unique conceptual context to that. I would like to go to Abhishek this last portion. Of course, I am sure you guys will expand on this work and there are a lot of other interesting things that will likely come out from this work and hopefully you will publish that in JCO PO. But one of the very important things that I wanted to highlight from this podcast specifically was the science is obviously very interesting, but I feel the more important interesting aspect is giving trainees and fellows, residents, mentorship opportunities, mentoring them and giving them lead roles in projects like this, which is what Dr. Tripathi has successfully done for you in this project, Salvador. So, Abhishek, as somebody I have known for a couple of years now, more than a couple of years, as a very successful clinical translational investigator in the GU space in the early phase setting, Abhishek, really briefly, within a minute, could you tell us about your journey and what are some of the things that have worked for you as an early career investigator that you have learned from, and then your journey of mentorship, how has that been for you and what are some of the things that you take home from your mentorship role? Abhishek Tripathi: Absolutely. And as you mentioned, mentorship has been pivotal for all early career investigators for them to really succeed. So, my journey, as you know, I started off as an early career investigator at another institution, and I think I owe it to my mentors even at that time and even now who are helping me develop some of these newer translational and clinical trial ideas, creating opportunities where we could really showcase some of the interesting work that we are doing. That actually goes a long way in terms of creating independence as an established investigator. And I think the sooner we start off with mentorship prospects, I think the better it is. And paying it forward, I think I have been lucky to have mentees like Salvador who are just extremely talented, really committed, and goal-oriented. He really led the project right from the beginning in terms of initial analyses and looking up all the sort of correlative studies that we could do and the contextual data between small cell lung cancer and bladder cancer that we have delved into for the past several years. And it really showcases the ability of young mentees like Salvador to really excel given the right guidance and the support. As a mentor, it has been a really rewarding experience. It is really helpful to actually learn from some of these mentees as well as to approach the same problem from a different angle and different thought process and guide them through the study. So, it has been incredibly helpful and rewarding both being a mentee and a mentor over the past several years as I have transitioned. Dr. Rafeh Naqash: Thank you, Abhishek, for those very insightful comments on how both being a mentee and being a mentor helps shape you as an individual as well. And then you take a lot of pride in the success of your mentees. Now real quick, Salvador, could you tell us a little bit about yourself, you know, how you ended up at City of Hope under Dr. Tripathi's mentorship and what are some of the next important things that you are looking forward to doing? Dr. Salvador Jaime-Casas: So, a little bit about who I am. I did medical school in Mexico City. I was born and raised there, and towards the end of my medical training, I started to be engaged in research projects. And through one of my mentors in Mexico, I was actually introduced to the team here at City of Hope, including Dr. Tripathi. And through this, we got the opportunity to have some conversations about what I wanted to do, become a physician-researcher in the area of genitourinary oncology and hopefully my transition to residency in a few years. And that is how I came to be his mentee here at City of Hope. I think it has been a very rewarding experience, like Dr. Tripathi said, having such an incredible mentor and really being with him both in the academic setting and in the clinical setting, in patients with clinic, seeing this curiosity and all these clinical trials, all of this evidence that we have coming together to generate this insight. Dr. Rafeh Naqash: Thank you so much for both the scientific insights, as well as the journey of being a mentee for you, Salvador, and as a mentor for you, Abhishek. I really enjoyed talking to you guys about both aspects here today and hopefully we will see more of your work, Abhishek and Salvador, as far as understanding the transcriptomic heterogeneity in neuroendocrine tumors or neuroendocrine cancers of the bladder. Dr. Salvador Jaime-Casas: Thank you very much. Thank you for having us. Dr. Rafeh Naqash: Thank you for listening to JCO Precision Oncology Conversations. Do not forget to give us a rating or review and be sure to subscribe so you never miss an episode. You can find all ASCO shows at ASCO.org/podcasts. 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.   Dr. Abhishek Tripathi Disclosures Consulting or Advisory Role:  Company: Aadi biosciences, Seattle Genetics/Astellas, Exelixis, Bayer, Gilead Sciences, Pfizer, Deka biosciences Speakers' Bureau: Company: Sanofi

Tempus AI's (TEM) RNA-based vitro diagnostic device got clearance from the FDA for use. The company reached record highs on Monday's session but pulled back by the closing bell. George Tsilis talks more about the development and why he believes Tempus experienced a pullback.======== Schwab Network ========Empowering every investor and trader, every market day. Subscribe to the Market Minute newsletter - https://schwabnetwork.com/subscribeDownload the iOS app - https://apps.apple.com/us/app/schwab-network/id1460719185Download the Amazon Fire Tv App - https://www.amazon.com/TD-Ameritrade-Network/dp/B07KRD76C7Watch on Sling - https://watch.sling.com/1/asset/191928615bd8d47686f94682aefaa007/watchWatch on Vizio - https://www.vizio.com/en/watchfreeplus-exploreWatch on DistroTV - https://www.distro.tv/live/schwab-network/Follow us on X – https://twitter.com/schwabnetworkFollow us on Facebook – https://www.facebook.com/schwabnetworkFollow us on LinkedIn - https://www.linkedin.com/company/schwab-network/ About Schwab Network - https://schwabnetwork.com/about

Crain's commercial real estate reporter Rachel Herzog talks with host Amy Guth about the Chicago-area apartment market.Plus: As Trump steps up Fed attacks, Chicago finance execs weigh in; Tempus gets FDA OK for AI-driven cardiac image analysis; former Mars Wrigley exec pleads guilty to $28 million in fraud charges; and GTCR buys SimpliSafe in deal expanding its home security portfolio. Hosted by Simplecast, an AdsWizz company. See pcm.adswizz.com for information about our collection and use of personal data for advertising.

The Department of Homeland Security says its Chicago immigration crackdown, which many anticipated for weeks, has begun. Crain's reporter John Pletz discusses with host Amy Guth.Plus: Chicago Fed chief wants inflation data before making rate call, Chicago investor sells Park Forest apartments for $23 million, ex-Mayer Brown attorneys launch Akin Gump's Chicago office and Northwestern first to integrate Tempus' AI assistant into health records system.

Dr. Pedro Barata and Dr. Rana McKay discuss the integration of innovative advances in molecular imaging and therapeutics to personalize treatment for patients with renal cell and urothelial carcinomas. TRANSCRIPT Dr. Pedro Barata: Hello, I'm Dr. Pedro Barata, your guest host of By the Book, a podcast series featuring insightful conversations between authors and editors of the ASCO Educational Book. I'm a medical oncologist at University Hospitals Seidman Cancer Center and an associate professor of medicine at Case Western Reserve University in Cleveland, Ohio. I'm also an associate editor of the ASCO Educational Book. Now, we all know the field of genitourinary cancers (GU) is evolving quite rapidly, and we have new innovations in molecular imaging as well as targeted therapeutics. Today's episode will be exploring novel approaches that are transforming the management of renal cell and urothelial carcinomas and also their potential to offer a more personalized treatment to patients. For that, joining for today's discussion is Dr. Rana McKay, a GU medical oncologist and professor at University of California San Diego. Dr. McKay will discuss her recently published article titled, “Emerging Paradigms in Genitourinary Cancers: Integrating Molecular Imaging, Hypoxia-Inducible Factor-Targeted Therapies, and Antibody-Drug Conjugates in Renal Cell and Urothelial Carcinomas.”  Our full disclosures are available in the transcript of this episode.  And with that, Rana McKay, great to have you on the podcast today. Dr. Rana McKay: Oh, thank you so much, Dr. Barata. It's really wonderful to be here with you. So, thanks for hosting. Dr. Pedro Barata: No, thanks for taking the time, and I'm looking forward to this conversation. And by the way, let me start by saying congrats on a great article in the Educational Book. Really super helpful paper. I'm recommending it to a lot of the residents and fellows at my own institution. I would like to first ask you to kind of give our listeners some context of how novel approaches in the molecular imaging as well as targeted therapeutics are actually changing the way we're managing patients with GU, but specifically with renal cell carcinoma and urothelial carcinoma. So, what are the areas you would call out as like being big areas for innovation in this context, and why are they important? Dr. Rana McKay: Very good question. And I think this is really what this article highlights. It highlights where are we going from an imaging diagnostics standpoint? Where are we going from a therapeutic standpoint? And I think if we have to step back, from the standpoint of diagnostics, we've seen PET imaging really transform diagnostics in prostate cancer with the advent of PSMA PET imaging, and now PSMA PET imaging is used as a biomarker for selection for theranostics therapy. And so, we're starting to see that enter into the RCC landscape, enter into the urothelial cancer landscape to a lesser extent. And I think it's going to potentially be transformative as these tools get more refined. I think when we think about therapeutics, what's been transformative most recently in the renal cell carcinoma landscape has been the advent of HIF2α inhibition to improve outcomes for patients. And we have seen the approval of belzutifan most recently that has reshaped the landscape. And now there's other HIF2α inhibitors that are being developed that are going to be further important as they get refined. And lastly, I think when we think about urothelial carcinoma, the greatest transformation to treatment in that context has been the displacement of cisplatin and platinum-based chemotherapy as a frontline standard with the combination of enfortumab vedotin plus pembrolizumab. And we've seen antibody-drug conjugates really reshape treatment and tremendously improve outcomes for patients. So, I think those are the three key areas of interest. Dr. Pedro Barata: So with that, let's focus first on the imaging and then we'll get to the therapeutic area. So, we know there's been a paradigm shift, really, when prostate-specific targets emerged as tracers for PET scanning. And so, we now commonly use prostate-specific membrane antigen, or PSMA-based PET scanning, and really transform how we manage prostate cancer. Now, it appears that we're kind of seeing a similar wave in renal cell carcinoma with the new radiotracer against the target carbonic anhydrase IX. What can you tell us about this? And is this going to be available to us anytime soon? And how do you think that might potentially change the way we're managing patients with RCC today? Dr. Rana McKay: First, I'll step back and say that in the context of PSMA PET imaging, we have actually been able to better understand RCC as well. So, we know that PSMA is expressed in the neovasculature of tumors, and it can actually be used to detect renal cell carcinoma tumors. It has a detection rate of about 84% when used for detection. And so, you know, I don't think it's just restricted to carbonic anhydrase IX, but we will talk about that. So, PSMA expressed in the neovasculature has a detection rate of around 84%, particularly if we're looking at clear cell RCC. CAlX is overexpressed in clear cell RCC, and it's actually used in diagnosing renal cell carcinoma when we think of CAlX IHC for diagnosing clear cell RCC. And now there are CAlX PET tracers. The first foray was with the ZIRCON study that was actually an interestingly designed study because it was designed to detect the likelihood of PET imaging to identify clear cell RCC. So, it was actually used in the early diagnostics setting when somebody presents with a renal mass to discriminate that renal mass from a clear cell versus a non-clear cell, and it was a positive study. But when I think about the potential application for these agents, you know, I think about the entire landscape of renal cell carcinoma. This is a disease that we do treat with metastasis-directed therapy. We have certainly seen patients who've undergone metastasectomy have long, durable remissions from such an approach. And I think if we can detect very early onset oligometastatic disease where a metastasis-directed therapy or SABR could be introduced - obviously tested in a trial to demonstrate its efficacy - I think it could potentially be transformative. Dr. Pedro Barata: Wonderful. It's a great summary, and I should highlight you are involved in some of those ongoing studies testing the performance of this specific PET scanning for RCC against conventional imaging, right? And to remind the listeners, thus far, for the most part, we don't really do FDG-PET for RCC. There are some specific cases we do, but in general, they're not a standard scanning. But maybe that will change in the future. Maybe RCC will have their own PSMA-PET. And to your point, there's also emerging data about the role of PSMA-PET scanning in RCC as well, as you very elegantly summarized. Wonderful. So, let me shift gears a little bit because you did, in your introduction, you did highlight a novel MOA that we have in renal cell carcinoma, approved for use, initially for VHL disease, and after that for sporadic clear cell renal cell carcinoma. We're talking about hypoxia-inducible factor 2-alpha inhibitors, or HIF2α inhibitors, such as belzutifan. But there's also others coming up. So, as a way to kind of summarize that, what can you tell us about this breakthrough in terms of therapeutic class, this MOA that got to our toolbox of options for patients with advanced RCC? Tell us a little bit what is being utilized currently in the management of advanced RCC. And where do you see the future going, as far as, is it moving early on? Is it getting monotherapy versus combinations? Maybe other therapies? What are your thoughts about that? What can you tell us about it? Dr. Rana McKay: Belzutifan is a first-in-class HIF2α inhibitor that really established clinical validation for HIF2α as a therapeutic target. When we think about the activity of this agent, the pivotal LITESPARK-005 trial really led to the approval of belzutifan in patients who were really heavily pretreated. It was patients who had received prior IO therapy, patients who had received prior VEGF-targeted therapy. And in the context of this study, we saw a median PFS of 5.6 months, and there did seem to be a tail on the curve when you looked at the 12-month PFS rate with belzutifan. It was 33.7% compared to 17.6% with everolimus. And then when we look at the response rate, it was higher with belzutifan on the order of 22-23%, and very low with everolimus, as we've previously seen. I think one of the Achilles heels of this regimen is the primary PD rate, which was 34% when used in later line. There are multiple studies that are testing belzutifan in combination across the treatment landscape. So, we have LITESPARK-011, which is looking at the combination of belzutifan plus lenvatinib in the second-line setting. We've got the MK-012 [LITESPARK-012] study, which is looking at belzutifan in various combinations in the frontline setting. So there is a combination with IO plus belzutifan. And so this is also being looked at in that context. And then we also have the LITESPARK-022 study, which is looking at pembrolizumab with belzutifan in the adjuvant setting. So there's a series of studies that will be exploring belzutifan really across the treatment landscape. Many of these studies in combination. Additionally, there are other HIF2α inhibitors that are being developed. We have casdatifan, which is another very potent HIF2α inhibitor. You know, I think pharmacologically, these are different agents. There's a different half-life, different dosing. What is going to be the recommended phase 3 dose for both agents, the EPO suppression levels, the degree of EPO suppression, and sustainability of EPO suppression is very different. So, I think we've seen data from casdatifan from the ARC-20 trial from monotherapy with a respectable response rate, over 30%, primary PD rate hovering just around 10%.  And then we've also seen data of the combination of casdatifan with cabozantinib as well that were recently presented this year. And that agent is also being tested across the spectrum of RCC. It's being looked at in combination with cabozantinib in the PEAK-1 study, and actually just at the KCRS (Kidney Cancer Research Summit), we saw the unveiling of the eVOLVE-RCC trial, which is going to be looking at a volrustomig, which is a PD-1/CTLA-4 inhibitor plus casdatifan compared to nivo-ipi in the frontline setting.  So, we're going to see some competition in this space of the HIF2α inhibitors. I think when we think of mechanism of action in that these are very potent, not a lot of off-target activity, and they target a driver mutation in the disease. And that driver mutation happens very early in the pathogenesis. These are going to be positioned much earlier in the treatment landscape. Dr. Pedro Barata: All these studies, as you're saying, look really promising. And when we talk about them, you mentioned a lot of combinations. And to me, when I think of these agents, it makes a lot of sense to combine because there's not a lot of overlapping toxicities, if you will. But perhaps for some of our listeners, who have not used HIF2α inhibitors in practice yet, and they might be thinking about that, what can you tell us about the safety profile? How do you present it to your patients, and how do you handle things like hypoxia or anemia? How do you walk through the safety profile and tolerability profile of those agents like belzutifan? Dr. Rana McKay: I think these drugs are very different than your traditional TKIs, and they don't cause the classic symptoms that are associated with traditional TKIs that many of us are very familiar with like the rash, hand-foot syndrome, hypertension, diarrhea. And honestly, these are very nuanced symptoms that patients really struggle with the chronicity of being on a chronic daily TKI. The three key side effects that I warn patients about with HIF2α inhibitors are: (1) fatigue; (2) anemia; and (3) hypoxia and dysregulation in the ability to sense oxygen levels. And so, many of these side effects - actually, all of them - are very dose-dependent. They can be very well-managed. So, we can start off with the anemia. I think it's critically important before you even start somebody on belzutifan that you are optimizing their hemoglobin and bone marrow function. Make sure they don't have an underlying iron deficiency anemia. Make sure they don't have B12 or folate deficiency. Check for these parameters. Many patients who have kidney cancer may have some hematuria, other things where there could be some low-level blood loss. So, make sure that those are resolved or you're at least addressing them and supplementing people appropriately. I monitor anemia very closely every 3 to 4 weeks, at least, when people start on these medications. And I do initiate EPO, erythropoietin, should the anemia start to worsen. And I typically use a threshold of around 10g/dL  for implementing utilization of an EPO agent, and that's been done very safely in the context of the early studies and phase 3 studies as well. Now, with regards to the hypoxia, I think it's also important to make sure that you're selecting the appropriate individual for this treatment. People who have underlying COPD, or even those individuals who have just a very high burden of disease in their lung, lymphangitic spread, pleural effusions, maybe they're already on oxygen - that's not an ideal candidate for belzutifan. Something that very easily can be done in the clinic before you think about initiating somebody on this treatment, and has certainly been integrated into some of the trials, is just a 6-minute walk test. You know, have the patient walk around the clinic with one of the MAs, one of the nurses, put the O2 sat on [measuring oxygen saturation], make sure they're doing okay. But these side effects, like I said, are very dose-dependent. Typically, if a patient requires, if the symptoms are severe, the therapy can be discontinued and dose reduced. The standing dose is 120 mg daily, and there's two dose reductions to 80 mg and 40 mg should somebody warrant that dose modification. Dr. Pedro Barata: This is relatively new, right? Like, it was not that we're used to checking oxygen levels, right? In general, we're treating these patients, so I certainly think there's a learning curve there, and some of the points that you highlight are truly critical. And I do share many of those as well in our practice. Since I have you, I want to make sure we touch base on antibody-drug conjugates as well. It's also been a hot area, a lot of developments there. When I think of urothelial carcinoma and renal cell carcinoma, I see it a little bit different. I think perhaps in urothelial carcinoma, antibody-drug conjugates, or ADCs, are somewhat established already. You already mentioned enfortumab vedotin. I might ask you to expand a little bit on that. And then in renal cell carcinoma, we have some ADCs as well that you include in your chapter, and that I would like you to tell us what's coming from that perspective. So, tell us a little bit about how do you see ADCs in general for GU tumors, particularly UC and RCC? Tell us a little bit about the complexity or perhaps the challenges you still see. At the same time, tell us about the successes. Dr. Rana McKay: Stepping back, let's just talk about like the principles and design of ADCs. So, most ADCs have three components. There's a monoclonal antibody that typically targets a cell surface antigen, which is conjugated by a linker, which is the second component, to a payload drug. And typically, that payload drug has been chemotherapy, whether it be topoisomerase or whether it be MMAE or other chemotherapeutic. We can start in the RCC space. There's been multiple antibody-drug conjugates that have been tested. There's antibody-drug conjugates to CD70, which is expressed on clear cell RCC. There's been antibody-drug conjugates to ENPP3, which is also expressed on RCC. There's antibody-drug conjugates to CDH6. And they have different payloads, like I said, whether it be topoisomerase I or other microtubule inhibitors. Now, when we think about kidney cancer, we don't treat this disease with chemotherapy. This disease is treated with immunotherapy. It is treated with treatments that target the VEGF pathway and historically has not been sensitive to chemo. So, I think even though the targets have been very exciting, we've seen very underwhelming data regarding activity, and in some context, seen increased toxicity with the ADCs. So, I think we need to tread lightly in the context of the integration and the testing of ADCs in RCC. We just came back from the KCRS meeting, and there was some very intriguing data about a c-Kit ADC that's being developed for chromophobe RCC, which is, you know, a huge unmet need, these variant tumors that really lack appropriate therapeutics. But I just caution us to tread lightly around how can we optimize the payload to make sure that the tumor that we're treating is actually sensitive to the agent that's targeting the cell kill. So, that's a little bit on the ADCs in RCC. I still think we have a long way to go and still in early testing. Now, ADCs for UC are now the standard of care. I think the prototypical agent, enfortumab vedotin, is a nectin-4-directed ADC that's conjugated to an MMAE payload and was the first ADC approved for advanced urothelial, received accelerated approval following the EV-201 trial, which was basically a multicenter, single-arm study that was investigating EV in cisplatin-ineligible patients with advanced urothelial carcinoma, and then ultimately confirmed in the EV-301 study as well. And so, that study ended up demonstrating the support superiority of EV from an overall survival standpoint, even PFS standpoint. Building on that backbone is the EV-302 study, which tested EV in combination with pembrolizumab versus platinum-based chemotherapy in the frontline setting. And that was a pivotal, landmark study that, like I said, has displaced platinum therapy as a frontline treatment for people with advanced urothelial carcinoma. And when we think about that study and the median overall survival and just how far we've come in urothelial cancer, the median OS with EV-pembro from that trial was 31 and a half months. I mean, that's just incredible. The control arm survival was 16 and a half months. The hazard ratio for OS, 0.47. I mean this is why when this data was presented, it was literally a standing ovation that lasted for several minutes because we just haven't seen data that have looked that good. And there are other antibody-drug conjugates that are being tested. We've all been involved in the saga with sacituzumab govitecan, which is a trophoblast cell surface antigen 2 (Trop-2) targeted ADC with a topoisomerase I payload. It was the second ADC to receive approval, but then that approval was subsequently withdrawn when the confirmatory phase 3 was negative, the TROPiCS-04 trial. So, approval was granted based off of the TROPHY-U-01, single-arm, phase 2 study, demonstrating a response rate of around 28% and a PFS of, you know, about 5 and a half months. But then failure to show any benefit from an OS standpoint. And I think there's a lot of controversy in the field around whether this agent still has a role in advanced urothelial carcinoma. And I think particularly for individuals who do not have molecular targets, like they're not HER2-amplified or have HER2-positivity or FGFR or other things like that. Dr. Pedro Barata: Fantastic summary, Rana. You were talking about the EV, and it came to mind that it might not be over, right, for the number of ADCs we use in clinical practice in the near future. I mean, we've seen very promising data for ADC against the HER2, right, and over-expression. It also can create some challenges, right, in the clinics because we're asking to test for HER2 expression. It's almost like, it's not exactly the same to do it in breast cancer, but it looks one more time that we're a little bit behind the breast cancer field in a lot of angles. And also has vedotin as a payload. Of course, I'm referring to disitamab vedotin, and there's very elegant data described by you in your review chapter as well. And it's going to be very interesting to see how we sequence the different ADCs, to your point as well. So, before we wrap it up, I just want to give you the opportunity to tell us if there's any area that we have not touched, any take-home points you'd like to bring up for our listeners before we call it a day. Dr. Rana McKay: Thank you so much. I have to say, you know, I was so excited at ASCO this year looking at the GU program. It was fantastic to see the progress being made, novel therapeutics that really there's a tremendous excitement about, not just in RCC and in UC, but also in prostate cancer, thinking about the integration of therapies, not just for people with refractory disease that, even though our goal is to improve survival, our likelihood of cure is low, but also thinking about how do we integrate these therapies early in the treatment landscape to enhance cure rates for patients, which is just really spectacular. We're seeing many of these agents move into the perioperative setting or in combination with radiation for localized disease. And then the special symposium on biomarkers, I mean, we've really come a long, long way. And I think that we're going to continue to evolve over the next several years. I'm super excited about where the field is going in the treatment of genitourinary malignancies. Dr. Pedro Barata: Oh, absolutely true. And I would say within the Annual Meeting, we have outstanding Educational Sessions. And just a reminder to the listeners that actually that's where the different teams or topics for the Educational Book chapters come from, from actually the educational sessions from ASCO. And your fantastic chapter is an example of that, right, focusing on advanced GU tumors. So, thank you so much, Rana, for taking the time, sharing your insights with us today on the podcast. It was a fantastic conversation as always. Dr. Rana McKay: My pleasure. Thanks so much for having me, Dr. Barata. Dr. Pedro Barata: Of course.  And thank you to our listeners for your time today. You will find the link to the article discussed today in the transcript of this episode. I also encourage you to check out the 2025 ASCO Educational Book. You'll find an incredible wealth of information there. It's free, available online, and you'll find, hopefully, super, super important information on the key science and issues that are shaping modern oncology, as we've heard from Dr. McKay and many other outstanding authors. So, thank you, everyone, and I hope to see you soon. 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. Pedro Barata @PBarataMD Dr. Rana McKay @DrRanaMcKay Follow ASCO on social media:        @ASCO on X (formerly Twitter)        ASCO on Bluesky       ASCO on Facebook        ASCO on LinkedIn        Disclosures:     Dr. Pedro Barata: Stock and Other Ownership Interests: Luminate Medical Honoraria: UroToday Consulting or Advisory Role: Bayer, BMS, Pfizer, EMD Serono, Eisai, Caris Life Sciences, AstraZeneca, Exelixis, AVEO, Merck, Ipson, Astellas Medivation, Novartis, Dendreon Speakers' Bureau: AstraZeneca, Merck, Caris Life Sciences, Bayer, Pfizer/Astellas Research Funding (Inst.): Exelixis, Blue Earth, AVEO, Pfizer, Merck  Dr. Rana McKay: Consulting or Advisory Role: Janssen, Novartis, Tempus, Pfizer, Astellas Medivation, Dendreon, Bayer, Sanofi, Vividion, Calithera, Caris Life Sciences, Sorrento Therapeutics, AVEO, Seattle Genetics, Telix, Eli Lilly, Blue Earth Diagnostics, Ambrx, Sumitomo Pharma Oncology, Esiai, NeoMorph, Arcus Biosciences, Daiichi Sankyo, Exelixis, Bristol Myers Squibb, Merck, Astrazeneca, Myovant Research Funding (Inst.): Bayer, Tempus, AstraZeneca, Exelixis, Bristol Myers Squibb, Oncternal Therapeutics, Artera    

The pivot began when Jim Rogers raised his hand. Groupon was shifting from mobile daily deals to a goods business in Europe, and—still early in his career—he volunteered to help lead the finance work. That step, he tells us, bridged his path from technical accounting into FP&A and set a pattern: seek out the build stage, then make finance a partner to the business.Rogers started in audit at Ernst & Young before moving through technical accounting and controllership into planning. He earned a master's in accounting at Northern Illinois University to qualify for the CPA, he tells us. At Groupon, he advanced to head of FP&A for North America, experience that informed his philosophy at Tempus AI: “we're not here to report the news,” he says—finance should enable decisions.Joining Tempus in 2017 as the first finance hire—when the company was pre-revenue, he tells us—Rogers built the function, became CFO in 2021, and helped steer the company public. He also stood up investor relations, initially outsourcing the function before bringing it in-house by the end of 2021, he tells us, investing time to educate analysts on a business that spans multiple categories.AI runs through Tempus's work. Externally, a physician portal (“positive”) and the researcher tool “Lens” aim to make diagnostics and data more useful. Internally, large language models sift “hundreds of petabytes of data,” Rogers tells us, and surface real-time finance insights. The strategic throughline is discipline: double down on oncology, keep pilots siloed, and expand only when the core is ready—because, as he notes, “no two days are alike.”

In this episode, Scott Becker highlights major market moves with updates on Tempus AI, Marvel Technologies, Dick's Sporting Goods, Astera Labs, and Palantir.

In this episode, Scott Becker highlights major market moves with updates on Tempus AI, Marvel Technologies, Dick's Sporting Goods, Astera Labs, and Palantir.

In this episode, Scott Becker explores how Tempus AI is supporting oncologists and health systems with predictive analytics and data-driven insights, filling critical gaps as physicians face increasing demands and overwhelming workloads.

In this episode, Scott Becker explores how Tempus AI is supporting oncologists and health systems with predictive analytics and data-driven insights, filling critical gaps as physicians face increasing demands and overwhelming workloads.

In this episode, Scott Becker explores how Tempus AI is supporting oncologists and health systems with predictive analytics and data-driven insights, filling critical gaps as physicians face increasing demands and overwhelming workloads.

In this episode, Scott Becker discusses Tempus AI's rapid growth, recent market moves, and its impact on oncology care.

In this episode, Scott Becker discusses Tempus AI's rapid growth, recent market moves, and its impact on oncology care.

Tonight on Market Mondays, we broke down the truth about the DeepSeek situation and shared our thoughts on the developments since last week. We also discussed six stocks that could be DeepSeek-proof for those concerned about a potential AI or chip sector crash. With Nvidia's earnings on the horizon, we explored whether the company needs to blow out expectations to keep the stock market afloat.We also took a deep dive into Tempus as a long-term investment, especially now that Nancy Pelosi has revealed she's trading it. The conversation then shifted to the impact of tariffs on the market, particularly semiconductor stocks, and which companies could benefit from these changes. As AI and tech continue to evolve, we discussed how we can better prepare our youth to compete in this rapidly changing space. Another key topic was the recent wave of hedge funds selling off stocks—what it means and how investors should respond. Additionally, we highlighted a few stocks we like under $100 and addressed the burning question: Should investors consider selling Nvidia?To close out the episode, we sat down with Timbaland for a powerful conversation about the state of music, AI's growing influence in the industry, the importance of independence, and key lessons from some of the greatest artists of all time.#MarketMondays #DeepSeek #AIStocks #Nvidia #StockMarket #Investing #TechStocks #HedgeFunds #Timbaland #MusicIndustry #AI #FinanceSupport this podcast at — https://redcircle.com/marketmondays/donationsAdvertising Inquiries: https://redcircle.com/brandsPrivacy & Opt-Out: https://redcircle.com/privacy