Podcasts about Bruton

Year in Review: Clinical Investigator Perspectives on the Most Relevant New Datasets and Advances in Bruton Tyrosine Kinase Inhibitors for Chronic Lymphocytic Leukemia | Faculty Presentation 1: Role of Bruton Tyrosine Kinase (BTK) Inhibitors in Newly Diagnosed and Relapsed/Refractory Chronic Lymphocytic Leukemia (CLL) — Wojciech Jurczak MD, PhD CME information and select publications

Year in Review: Clinical Investigator Perspectives on the Most Relevant New Datasets and Advances in Bruton Tyrosine Kinase Inhibitors for Chronic Lymphocytic Leukemia | Faculty Presentation 2: Emerging BTK Inhibitor-Based Combination Approaches in CLL — Jennifer R Brown MD, PhD CME information and select publications

Proceedings from a webinar on March 11, 2026, moderated by Dr Neil Love, including the following topics: Introduction: I think I missed that day in med school (BTK biology) (0:00) First-Line Treatment (11:40) Relapsed/Refractory Disease (46:35) CME information and select publications

Have you ever realised a blazing row with your partner might actually have nothing to do with them… and everything to do with your sibling dynamic growing up? This week on Relatively, Catherine Carr is joined by therapist Lisa Bruton to unpack the huge, and often subconscious, impact our brothers and sisters have on every aspect of adult life. Lisa, the youngest of three girls (still known by her sisters as “Podgy Poo”), explains why people regularly walk into therapy wanting to discuss marriage, work stress, or relationships… only to spend the session untangling sibling history instead. From birth order and sibling rivalry to Family Systems Theory, Catherine and Lisa explore why family gatherings can instantly drag us back into childhood roles, whether you were “the responsible one”, “the messy one”, or the peacekeeper in the middle trying to disappear entirely. The episode also dives into the growing rise of sibling therapy, with more adult siblings choosing to work through past wounds together to improve their future relationships. At its emotional core, this conversation tackles sibling estrangement, the guilt, shame, and silence surrounding stepping away from toxic family dynamics. Lisa also shares a surprisingly simple way to start breaking free from the labels your family still places on you, without causing a full family fallout. Featuring brilliant archive moments from past guests including Caitlin Moran, Gok Wan, and Dan Snow, this is a funny, eye-opening, and deeply validating episode that may completely change how you see your family and yourself. If this one hit home, share it with your siblings. Subscribe to the Relatively Podcast channel so you never miss an episode: https://www.youtube.com/@relativelypodcast Listen to every episode here: https://pod.link/relatively Follow and connect with us: Facebook: @Relatively.pc Instagram: @relativelypodcast Website: https://www.relativelypodcast.com/ #Relatively #SiblingTherapy #FamilyDynamics

There are many treatment options for people with relapsing MS. Patients should be carefully monitored to assess treatment response, and a change in treatment approach should be considered if safety concerns emerge. In this episode, Teshamae Monteith, MD, FAAN, speaks with Ellen M. Mowry, MD, MCR, and Daniel Ontaneda, MD, PhD, coauthors of the article "Treatment of Multiple Sclerosis" in the Continuum® April 2026 Multiple Sclerosis and Related Disorders issue. Dr. Monteith is the associate editor of Continuum® Audio and an associate professor of clinical neurology at the University of Miami Miller School of Medicine in Miami, Florida. Dr. Mowry is the director of the Multiple Sclerosis Experimental Therapeutics Program and a professor of neurology at The Johns Hopkins University School of Medicine in Baltimore, Maryland. Dr. Ontaneda is the director of research at the Mellen Center for Multiple Sclerosis and a professor of neurology at the Cleveland Clinic Lerner College of Medicine of Case Western Reserve University in Cleveland, Ohio. Additional Resources Read the article: Treatment of Multiple Sclerosis Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @headacheMD Guest: @EllenMowryMD Full episode transcript available here Dr. Monteith: There are so many new treatment strategies for multiple sclerosis, which is a blessing, but it does come with the complexity of really just trying to nail down the approach. I just got finished talking to Drs Ellen Mowry and Daniel Ontaneda about their article on treatment of multiple sclerosis. We discussed relapses, weighing escalation versus early high-effective treatment and progressive disease. This is a must-listen-to podcast. I hope you enjoy it as much as I enjoyed talking to them.  Dr. Jones: This is Dr. Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr. Monteith: This is Dr. Teshamae Monteith. Today, I'm interviewing Ds Ellen Mowry and Daniel Ontaneda about their article on treatment of multiple sclerosis, which they wrote with Dr. Darin Okuda. This article appears in the April 2026 Continuum issue on multiple sclerosis. Welcome, both of you. How are you?  Dr. Mowry: Great. And thank you so much for having us.  Dr. Monteith: Absolutely. So, why don't you both introduce yourself?  Dr. Ontaneda: All right. My name is Daniel Ontaneda. I'm a neurologist at the Cleveland Clinic. I spend the majority of my time doing research, but I still dedicate about a day a week to seeing people with MS in clinic.  Dr. Mowry: I'm Ellen Mowry. I'm also a neurologist, but practice at the Johns Hopkins University. And similar to Dan, I mostly work on research, but also have an active clinical care component, taking care of people with MS.  Dr. Monteith: Well, thank both of you for writing this article and being on our podcast. I assume you guys have probably known each other for quite a while now.  Dr. Mowry: Yes. Dr. Ontaneda: Yes. Dr. Monteith: What inspired you to get into multiple sclerosis research and then clinical care?  Dr. Ontaneda: I always loved neurology, and I think a lot of us who go into neurology are attracted to the complexity of the human brain and how the nervous system works. But what really hit home to me was a family member of mine who had multiple sclerosis, and he was being treated in a time where we really didn't have super effective disease-modifying medications. And so, as I went through my medical career, I always kind of kept an eye on what was happening with multiple sclerosis, and I started my training at a time where it was really flourishing in terms of the medications available, so that's what inspired me to go into MS. It's a disease that we can definitely treat, and you can change outcomes for people. So, that was it.  Dr. Monteith: Yeah, that personal experience can be very impactful.  Dr. Mowry: My journey started, actually, because I was thinking about whether I wanted to be a physician at all, and I happened to land, just after high school, a position with a neurologist who happened to mostly focus on multiple sclerosis and taking care of folks with multiple sclerosis. And by the end of the summer, I knew I wanted to go to med school and I wanted to be a neurologist and I wanted to work with people with MS. I thought I would be a clinician exclusively, but I think as time went on and I started to hear the consistent questions that people I served were asking in the clinic and realizing that those questions could be turned into research projects that could address their concerns, I moved more and more towards research. Dr. Monteith: Great. There are a lot of really detailed information in the article, so I think that research mind is very useful, and I see that in the writing. Why don't we talk about the goal of the article? Dr. Ontaneda: So, I think the goal of the article was to set out kind of what the large view of what treatment for multiple sclerosis looks like. And, you know, many times we divide the treatment of multiple sclerosis into these large pillars, and I think that's what we did in the article. The first was, you know, what do you do with a person who has an MS attack or relapse? The second is, what medications do we use to treat the relapsing forms of multiple sclerosis where there is a lot of acute inflammation, focal inflammatory lesions that are occurring? And then the final one is, what do you do with individuals who have a more progressive form of the disease where they're accruing disability slowly and gradually? Dr. Monteith: And what were some of the main points? Dr. Mowry: Dr. Okuda provided a really nice section on the treatment of acute relapses in multiple sclerosis, and it's important to understand what we talk about when we are saying "relapse". For people with MS, many symptoms can fluctuate and occur and then get better over time, and sometimes people with MS use the same term of "relapse" to describe those symptom fluctuations. As neurologists, when we're thinking about relapse, we're really trying to think about symptoms that can be attributed to new focal inflammatory events somewhere in the central nervous system. Typically, these are accompanied---if you were to get an MRI at the same time---by a new lesion or MS spot, as I like to call them, on MRI scan. And so, it's important to distinguish when somebody is talking about symptoms, whether they are true new symptoms that could be mapped to a place in the central nervous system. Because alternatively, a lot of people who've had attacks or relapses in the past can have what we call pseudo-relapses, and these are essentially recrudescence of old symptoms, typically in a similar pattern as what had occurred in the past. And these can be brought out by things like fever or infection, sometimes stress. And pseudo-relapses are not thought to be due to new development of immune system-induced injury and therefore would be less likely to respond to treatment; and in fact, treatment may be contraindicated for those events. We also talked a little bit in that article about how relapses are treated, talking about the use of high-dose steroids for true new relapses, but also kind of cautioning that those are not necessarily free of concerns, especially if you have a pseudo-relapse or there could be an infection going on. And that ultimately, the decision as to whether to treat a relapse really is a shared decision-making because it's thought that although the steroids can speed up recovery from a relapse, they may not have a major impact on ultimate recovery. And so, a lot of the shared decision-making comes in here because for a mild relapse, you might choose to forego a course of high-dose steroids.  Dr. Monteith: Daniel, any other main points?  Dr. Ontaneda: Yeah. On the side of treating relapses, I think one of the other things that probably has changed a lot, at least during the course of my training, is that in the past, whenever we had identified a relapse, as Dr. Mowry has clearly defined, we would typically treat with intravenous high-dose corticosteroids, typically with methylprednisolone. And that was kind of our go-to. We would either do it in an infusion center or we would set it up with home care. And I think one of the things that our field learned over, I would say, the last five or ten years is there's an abundance of studies that show that you can give that same dose of methylprednisolone. Rather than giving it IV, you can give it orally. No pun intended, as I tell my patients, a lot of pills to swallow because we use fifty-milligram prednisone pills, and they have to take 1,250 a day. The pharmacy always pushes back on that many pills, but really the advantage of being able to take steroids orally that way for three to five days is really, I think, one, better for people with MS because they can do it in the comfort of their own home, and two, I think also when you look at the costs associated with that treatment, it is the most cost-effective option. Dr. Monteith: And what are some of the latest developments that you're really excited about that weren't in the article?  Dr. Mowry: A lot of the article focused on the approach to treatment of people with what we've traditionally called relapsing/remitting multiple sclerosis. So, this is the kind of MS that traditionally presents with a relapse or an attack initially, although some of that nomenclature is changing, actually. And the article focused a lot on the strategies surrounding treatment of somebody with newly diagnosed relapsing MS, and thinking about this vast number of disease-modifying therapies that are available to people with MS and their clinicians, and how to think about the strategy with respect to largely centered around the efficacy class of the medication, whether people should take an approach of using a higher-efficacy therapy---meaning a medicine that in clinical trials was more likely on average to suppress relapses as well as new lesions---or whether there's still a good argument for the case of using an escalation approach, using some of the more modest efficacy medications that also probably in general have lower risks, monitoring for response to treatment and changing if the medication isn't working. And so, there's still a lot of debate in the field, I would say, even though many people have moved towards a one-size-fits-all kind of approach. I think there's still a lot of debate in the field about the evidence underlying that. And, you know, full disclosure, Dr. Ontaneda and I are each running parallel and very complementary clinical trial programs to address this very question, the results of which should be available within the next year, year and a half.  Dr. Monteith: Well, we can't wait that long. Give me some clinical pearls to how we initiate these modifying therapies. Like, what are the pearls that we need to have in our mind?  Dr. Ontaneda: Yeah. I think when we think about starting the disease-modifying therapy in an individual who has an active form of multiple sclerosis, I think, you know, one of the cornerstones I would say of making that decision is shared decision-making. I think we tend to sit down with the patient and analyze the data that we have at hand, what we know about their multiple sclerosis, and we use several factors to inform how likely we think their disease is gonna be active or potentially might not respond to the initial treatment you give. And we look heavily at the MRI. The MRI is really a useful marker because it shows us, one, how many lesions a person might have---both, you know, where those lesions are and also kind of the amount of lesions. Lesions, certainly, that are in the spinal cord, a very large burden of diseases. A lot of active lesions, which we determine by the presence of contrast-enhancing lesions, really helps us inform on disease severity. I would say that was our number one tool that we use to decide and help us decide how we think that person's MS is gonna do over time. And then the second thing that we put into the equation also is, you know, how well do we think this person is going to tolerate our medications? All our disease-modifying medications act through suppression of the immune system, and we know that that carries some risks associated with it. Some of those risks are stuff like infections. Some of those can be simple infections that really don't have major consequences, but some of them can be quite serious, including the need for hospitalizations or prolonged antibiotic treatment courses. And so, we also look at what, you know, the underlying risk of a person has for infection. This kind of is determined by, one, A, how many infections they've had up to date, and also how much disability they had. I would say in our average patient who when we see them, they're probably typically pretty young, in their twenties, thirties, forties, they typically don't have a lot of infectious risks. And therefore, I think there's kind of a move to saying, "Well, actually their risk of infections is quite low." And we put that together with, you know, also what the preference of the patient might want. So, do they prefer to take a pill, for example? Do they prefer a medication where they receive that via infusion every six months and they don't really have to think about it? There are some people that don't like going into a hospital, and they might prefer an injection type of those medications. And so, after a complex discussion of all those factors, we take into consideration how much risk the patient wants to take as well, and we come up with a rational choice of a couple of medication options. So, I think it's challenging sometimes because we have over two dozen medications. There's the risk of you saying, "There are these twenty-four medications, you can pick one." And I think our job as neurologists is to kind of pare those down, talk about, in a person like yourself, these are the two or three medications that I would recommend using. Why don't you review them? And then we bring them back, and we kind of make a final decision with, one of the key factors that I think is important to remind people is that you're gonna start this medication, and we are gonna monitor to make sure it's working. We're gonna monitor to make sure you're tolerating it well. And although it's an important, the first decision you make, I think one key theme that we tell people is, we can revise our strategy whenever we like. We just have to think about it and do it in a way that we think is gonna make sure that their MS is under the best control. And then we think about the ultimate goal of treatment, which, in multiple sclerosis, is the absence of any attacks and also the absence of any new lesions on MRI. And that's where whether you are offering more of the high-effective medications or more moderate- or low-efficacy medications, that's where there's a little bit of controversy still in our field, and that's what our trials are trying to answer.  Dr. Monteith: Excellent. So now we've selected a particular option- and I love those points with shared decision-making, using the MRI to guide and then kind of risk tolerance related to infection. But now a patient's still having relapses, and I know the goal is zero, but, you know, there's some margin. What are the pearls to advance to more high-efficacy therapies?  Dr. Mowry: Yeah, that's a great question. Dr. Ontaneda in the article actually talked about the literature surrounding monitoring for breakthrough disease and when to say this much is too much, and there's actually not a definite right answer. It's clear that more active disease early in the course is probably more of concern than, say, developing, you know, a new spot in your fifties or something to that effect. So, different people have different thresholds. I know at our center, we tend to be pretty on top of making changes for breakthrough disease. So, what we typically do is reimage people about six months after they start a medication to establish a new baseline. And sometimes, because of delays in starting or because the medications take a while to kick in, there might be a new spot or two. So, if that's the case, I really only get concerned if the spots are also taking up the dye or enhancing to indicate they're really quite recent, and I think, "Ugh, that's not something I'd like to see six months after starting a medication." And so that otherwise is sort of the reference scan, moving forward, to evaluate the medication, and I have a very low threshold for changing, particularly if somebody is on a moderate-efficacy therapy. To me, I think, well, our goal of trying the moderate efficacy therapy is essentially to see if we could get away with a medicine that is probably, on average, safer and that will still work for your MS. But if the answer is no, I personally don't like to stick around too much on them. One caveat I would say is that if somebody develops what appears to be a new lesion or spot on higher-efficacy therapy, before presuming that that new area of activity is a definite new MS event, I always like to rethink carefully, did I get the diagnosis correct? Or could this be an early infection such as, you know, progressive multifocal leukoencephalopathy in people on natalizumab in particular? Because I see breakthrough activity so rarely in people on higher-efficacy therapies that I just like to rethink my diagnosis and the differential prior to making switches to, typically, another higher-efficacy therapy in that case. But that, again, is a little bit of shared decision-making. It's sometimes contextual. If a person is using a self-administered medication and they have a little breakthrough, sometimes you can solicit some history, saying, "Oh, I actually kind of stopped taking it for a few weeks because something was going on, and I really want to retry." And that's very reasonable as well. Dan, do you have any other thoughts?  Dr. Ontaneda: No, I think I agree. That's really close to how I practice myself as well, and the majority of people at my center. I think that we are learning that when you start a treatment, many times---depending on how deeply you look---you can find evidence of ongoing disease, and that's something that we struggle with. It's almost like we have tools to treat inflammation in terms of new MS lesions and new relapses. And so, when those are present, it's pretty clear that you probably have to switch medication. I think a slightly trickier issue is when, for example, you have a person who might be stable. They don't have an attack. But you notice that they're worsening, and they tell you they're worsening. I think our ability and tools for that is a little bit harder, and we recognize that that can actually happen fairly early in the disease. And that's why we're trying to rethink this mantra that we've had for many years, where we kind of divide MS up into relapsing and progressive, and we see people develop progressive MS 10 to 15 years after they've had a relapsing form of the disease. So, I think that's just a reality of clinical practice. And we don't have as many tools to treat that gradual worsening, which is kind of what the rest of our article spent some time talking about. Dr. Monteith: You've also written about the clinical trial long-term extension studies. And what are the few points that you take away from the emergence of these types of publications over the past few years? Dr. Mowry: Yeah, well, long-term extension studies can be really helpful to understand whether the findings that are evidenced during the randomized portion of trials themselves continue into a longer term. And for people with MS, understanding these data can be really helpful because, particularly when we're looking for impact of a given treatment or a strategy on disability worsening, often it takes longer than the short-term portion of the trial to truly understand if the medication or strategy has an impact on insidious worsening that Dan is speaking about. Many trials have demonstrated a short-term benefit, but we think a lot of times that benefit is probably because of the reduction in relapses, which sometimes leave a permanent mark on neurologic function. But the extension studies are trying to understand a little bit more about whether the effect on disability worsening is sustained, and also to look a little bit more deeply at long-term safety, especially when it comes to medications that do increase the risk of infection. The caveats, though, in interpreting those types of studies are that people drop out, and so probably the people who drop out of those studies are really different. They may be either less disabled and they think, "Oh, you know, I'm done. I feel good." Or potentially more disabled and they think, "Ugh, I have more things to do I've got to take care of. What's going on?" And so that kind of dropout can produce some bias in interpreting the results. Dan, any other thoughts?  Dr. Ontaneda: No, I think that's spot on. I mean, I think that when we're trying to decide on what general philosophy to use, right? Like, you're seeing a patient for the first time. They've recently been diagnosed with MS, and you have... you know, I kind of bin them into three options. You can start a low-efficacy, a moderate, or a high-efficacy medication. And the first piece of information you could use is clinical trials, and Dr Mowry very clearly identified why some of that data might be a little bit biased and isn't, you know, completely applicable to the patient who's in front of you. The second thing that we might look at is observational data, and there's a wealth of observational data that shows that, in general, people on higher-efficacy medications tend to do better over time. But one of the challenges we have is that there's always biases related to those observational study designs. And so, I think you have to interpret them with a little bit of caution because there are reasons people start specific medications in people. And when you look at them in a purely observational study, even if you do some fancy way of addressing those biases, such as propensity, there always is the possibility of some residual bias. You know, that's part of the reason why we're doing the trials that Dr Mowry described, because we really need kind of long-term evidence to show that these medications actually can affect disability ten, twelve years after started. And I think pragmatic clinical trials, like the ones we're running, are really gonna be the key to answer those questions. We all have our favorite approaches right now, but I think that the data to actually demonstrate what's best for people with MS is really needed.  Dr. Monteith: Great, and there's so much in this article. I mean, we didn't even touch on radiological isolated syndrome, monitoring MS therapeutically, and treatment of progressive MS. Any final take-home points?  Dr. Ontaneda: Yeah. Maybe I will touch a little bit on the side of progressive MS, because it has been, you know, the MS that we historically have not been able to treat as much. So, we described there's over two dozen therapies approved for relapsing forms of MS. For purely progressive forms of MS that don't have any evidence of activity, we really only have one approved therapy, and it appears that that therapy actually does work through active inflammation anyway. And in the article, we highlighted examples of studies that have been negative, but also some recent examples of studies that have been positive, specifically with a new class of medication called BTKI, or Bruton tyrosine kinase inhibitors. We just recently heard of a second molecule that also had positive results in this realm. So, we're excited that, you know, in the next four to five years-  Dr. Monteith: I'm sorry. Can you just go ahead and say what that molecule...You're leaving people hanging.  Dr. Ontaneda: One molecule is tolebrutinib, which already has a positive study in secondary progressive MS in individuals without activity. And then the second compound that has been studied with positive trial results, we only have summary results from that, is a medication called fenobrutinib. And we think these two compounds that are part of a single class, the hope is that maybe they can address some of that gradual worsening that occurs in MS. And then the question comes whether we should use those from the get-go or if we should just use them later. So, a whole sort of variety of different questions. But I think important to call out for clinicians that this area where we had no available treatments for so many years might be changing.  Dr. Monteith: Well, thank you both. I really loved this conversation. I learned a lot listening to both of you, and I look forward to your clinical trial results.  Dr. Mowry: Thank you so much for having us. Dr. Ontaneda: Thanks so much. It was our pleasure. Dr. Monteith: Again, today I've been interviewing Doctors Ellen Mowry and Daniel Ontaneda about their article on treatment of multiple sclerosis, which they wrote with Dr. Darin Okuda. This article appears in the April 2026 Continuum issue on multiple sclerosis. Be sure to check out Continuum Audio episodes from this and other issues. And thank you to our listeners for joining today. Dr. Monteith: This is Dr. Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

I knew Higher Farm as a place just outside Bruton that did an amazing breakfast. However, it wasn't long before I started to hear about the two brothers behind the brand and their ambition, energy and passion about growing food. They are on a mission to support the movement for regenerative food and farming. And it is Ketchup that is at the epicentre of their aspirations to change the way we eat. I sat down with Matteo and Giacomo, in their kitchen dining room at Higher Farm and talked about how they came together in business, their vision, approach, and their regenerative standards. In their individual ways, the brothers behind Higher Farm are bold, deep thinking and have great fervor. @higher_farmhigher-farm.co.uk Hosted on Acast. See acast.com/privacy for more information.

Darren Bailey displays his newfound love for Chicago by eating pizza and not putting catsup on a hot dog. Ben riffs. Paul Bruton tells you everything you need to know about the last vestiges of Chicago's Democratic Machine. A subject he knows quite well as he had the audacity to run against Alderman Marty Quinn, Michael Madigan's guy in the 13th Ward. He's also a University of Chicago graduate in history, so he knows a thing or two or three about American politics.See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

In this episode of Treating Together, host Marc Braunstein, MD, PhD, associate professor of medicine at the NYU Perlmutter Cancer Center, sits down with Adam Kittai, MD, associate professor and director of the CLL and Lymphoma programs at NYU Perlmutter Cancer Center, for a deep dive into the rapidly evolving frontline treatment landscape in chronic lymphocytic leukemia (CLL). As chemotherapy continues to give way to targeted and time-limited therapies, clinicians face an increasingly complex array of choices, each influenced by disease biology, patient preferences, and emerging clinical trial data. Key Discussion PointsThe episode focuses on the evolving frontline management of CLL and how clinicians can individualize therapy in an era of expanding options. Highlights include: Patient Evaluation and Diagnosis Considerations: Beyond traditional risk factors such as TP53 mutation and IGHV status, importance is also being placed on patient preference, comorbidities, and treatment goals (eg, time-limited vs continuous therapy) to guide treatment decisions. Therapy Selection and Sequencing Strategy: Dr Kittai offers his view on sequencing decisions in the front line: given the lack of robust comparative data, current evidence supports prioritizing the most appropriate upfront regimen rather than relying on uncertain sequencing strategies across agents. Insights From the AMPLIFY Trial (NCT03836261): With the recent February 2026 FDA approval of acalabrutinib (Calquence) plus venetoclax (Venclexta) in the front line, the discussion highlights progression-free survival (PFS) benefits seen in the AMPLIFY trial and favorable safety of the doublet. The Growing Role of Minimal Residual Disease (MRD): The discussion briefly pivots to the use of MRD testing in the clinic today, including data from trials like GLOW (NCT03462719) and FLAIR (EudraCT: 2013-001944-76), and its potential to guide treatment duration. Emerging Therapeutic Strategies in the Pipeline: The conversation looks to the future of CLL care, including Bruton tyrosine kinase (BTK) degraders, next-generation BCL-2 inhibitors, and novel combinations currently under investigation. Managing Richter's Transformation: Dr Kittai covers evolving combination approaches for this aggressive cancer that aim to target both CLL and lymphoma biology, moving beyond chemoimmunotherapy.

Finally, we have talked long time show cohost Kent Wolverton to sit in the hot seat to talk about his life and career. You have heard him for years now give small peeks into his life, offer wise cracks, and hint at some struggles in his life and career. This episode will have a much deeper look at who Kent Wolverton is as a person, professional, and friend. He walks us through the beginning of his career in 2003, and we will dissect his first critical incident in 2005 that nearly ended his Dallas PD career. Kent's complex journey has many twists and turns that has built a level of resilience that he still works on to this day. Sit back and take a rare closer look at one of the cohosts lives as he shows vulnerability and honesty in hopes others may use his story to help or inspire others. Special guest cohost Dallas SWAT Matt Smith   Critical Incidents :   Sept 23, 2005, pedestrian struck: Kent was responding to cover officers in South Dallas and accidently struck a pedestrian with his police vehicle.   December 2005: Discussion on two separate vehicle incidents that he was a part of. Hostage Rescue on Bruton and High Crest while Sgt in SWAT. 2020 George Floyd Riots and aftermath.  

Dr Hanny Al-Samkari from Massachusetts General Hospital in Boston discusses recent developments from the ASH 2025 Annual Meeting involving the use of Bruton tyrosine kinase inhibitors and BAFF-R antagonists in the treatment of immune thrombocytopenia.CME information and select publications here.

Fellow ex-MP and former health minister Steve Brine sends in a question asking Ed Balls and George Osborne how we judge the performance of a health secretary, and in particular Wes Streeting. They lay out the historical challenges of the role, and where Streeting has risen or succumbed to them thus far.A colleague of Ed's from King's College then asks how useful it is for benefits to be so conditional, in particular for care leavers. They debate the fairness in having conditional benefits systems, and why people are more sympathetic to care leavers than other disadvantaged groups. They then discuss the perks of pedestrianising Bruton, George's stomping ground, in a manner similar to Paris. Would George lead the campaign to see this through? Or is it an enticing but unrealistic idea? Finally, a former Tory parliamentary candidate raises his concerns around Nick Timothy's controversial comments on a Ramadan event in London. They discuss the dangerous direction these comments represent for both the Tories, and British politics more widely. We love hearing from you, so please don't forget to send all your EMQs to questions@politicalcurrency and make sure to include a voice note of your question.This podcast is sponsored by Chip. Join 400,000 customers building long term wealth. T&Cs apply, you must be a new Chip customer, over 18, a UK tax resident, and it's app only. Chip is a trading name of Chip Financial Limited. Savings products are provided by Clearbank and are protected up to the FSCS limit. When investing, your capital is at risk.Thanks for listening. To get episodes early and ad- free join Political Currency Gold or our Kitchen Cabinet. If you want even more perks including our exclusive newsletter, join our Kitchen Cabinet today:

I am yet to walk passed Briar and not see someone I recognise seated at a table! Since opening the doors, not even two years ago, this beautiful restaurant is hot on the lips of locals and visitors to Bruton. Housed in Number One, a Georgian townhouse hotel, Briar is a Michelin Bib Gourmand restaurant, recognised for exceptional food that does not break the bank.Chef Sam Lomas is warm, generous and unassuming. With an amazing background working at River Cottage and Glebe House, he has brought his passion for old school craft cooking, and his appreciation for what the season's bring us, to Briar. With a small team working besides him, he talks about them being the backbone to the business and we share in talking how food brings an indescribable connection to our lives. numberonebruton.com/briar@briar_restaurant Hosted on Acast. See acast.com/privacy for more information.

Dr Hanny Al-Samkari from Massachusetts General Hospital in Boston discusses recent developments from the ASH 2025 Annual Meeting involving the use of Bruton tyrosine kinase inhibitors and BAFF-R antagonists in the treatment of immune thrombocytopenia.CME information and select publications here.

Featuring a slide presentation and related discussion from Prof Constantine Tam, including the following topics: Fixed-duration versus continuous targeted treatment for previously untreated chronic lymphocytic leukemia (CLL): Results from the randomized CLL17 trial (0:00) Six-year follow-up data from the Phase III SEQUOIA trial of zanubrutinib for patients with treatment-naïve CLL and those with del(17p) CLL not randomly assigned (4:59) Primary endpoint analysis of the randomized STAIR trial of time-limited acalabrutinib monotherapy for frail patients with previously untreated CLL (7:25) Safety analyses of acalabrutinib/venetoclax (AV) or AV in combination with obinutuzumab for previously untreated CLL (10:50) Three-year results with zanubrutinib combined with venetoclax in arm D of the Phase III SEQUOIA trial for treatment-naïve CLL (17:15) Early-phase data with sonrotoclax combinations as front-line treatment of CLL (19:12) Pirtobrutinib for treatment-naïve and relapsed/refractory CLL/small lymphocytic lymphoma: Results from the Phase III BRUIN CLL-314 and BRUIN CLL-313 trials (23:27) Long-term extension (LTE1) results from the Phase III ALPINE trial of zanubrutinib versus ibrutinib in patients with relapsed/refractory CLL or small lymphocytic lymphoma (R/R CLL/SLL) (28:53) Updated efficacy and safety results of the Bruton tyrosine kinase degrader BGB-16673 in patients with R/R CLL/SLL from the ongoing phase 1 CaDAnCe-101 study (30:35) Real-world outcomes of lisocabtagene maraleucel in CLL (33:04) CME information and select publications

Featuring an interview with Dr Hanny Al-Samkari, including the following topics: VAYHIT1: A multicenter randomized, double-blind, Phase III trial evaluating ianalumab versus placebo in addition to first-line corticosteroids for patients with primary immune thrombocytopenia (ITP) (0:00) Secondary analysis results from VAYHIT3, a Phase II study of ianalumab for patients with primary ITP previously treated with at least 2 lines of therapy (8:15) Improved health-related quality of life and bleeding scores with the oral Bruton tyrosine kinase inhibitor rilzabrutinib in the open-label period of the multicenter Phase III LUNA 3 study for adults with ITP (12:23) Romiplostim for chemotherapy-induced thrombocytopenia in patients with colorectal, gastroesophageal and pancreatic cancer: A global Phase III randomized, placebo-controlled trial (16:01) CME information and select publications

Dr Hanny Al-Samkari from Massachusetts General Hospital in Boston discusses recent developments from the ASH 2025 Annual Meeting involving the use of Bruton tyrosine kinase inhibitors and BAFF-R antagonists in the treatment of immune thrombocytopenia.CME information and select publications here.

Dr Hanny Al-Samkari from Massachusetts General Hospital in Boston discusses recent developments from the ASH 2025 Annual Meeting involving the use of Bruton tyrosine kinase inhibitors and BAFF-R antagonists in the treatment of immune thrombocytopenia.CME information and select publications here.

There isn't a broadsheet or glossy mag that hasn't featured this man's name across their pages. Merlin Labron-Johnson's, chef and owner of Osip, the Michelin starred restaurant in Bruton, has a reputation for quietly refined and deeply seasonal food that is rooted in the land has led to a foundation that is authentic and revered by many. This sense of identity is delivered not only in his culinary creations but also in his considered eye when it comes to aesthetic and artistry. We met in his restaurant at the end of the breakfast service so you'll hear the lovely clattering of background noise. Hosted on Acast. See acast.com/privacy for more information.

Featuring an interview with Dr Hanny Al-Samkari, including the following topics: Mechanism of action and toxicity of the monoclonal antibody ianalumab (0:00) Primary results from VAYHIT2, a randomized, double-blind Phase III trial of ianalumab with eltrombopag for patients with primary immune thrombocytopenia (ITP) after failure of first-line corticosteroid treatment (7:32) Mechanism of action and toxicity of the Bruton tyrosine kinase inhibitor rilzabrutinib (11:52) Reduction in corticosteroid use with rilzabrutinib and sustained response in adults with persistent or chronic ITP in the long-term extension period of the Phase III LUNA3 study (18:46) CME information and select publications

Transforming CLL care: measurable residual disease (MRD) guided stopping, smart triplet selection, and next‑gen Bruton tyrosine kinase (BTKs)—practical insights.   Credit available for this activity expires: 02/19/27 Earn Credit / Learning Objectives & Disclosures: https://www.medscape.org/viewarticle/chronic-lymphocytic-leukemia-cll-review-combination-2026a10004ku?ecd=bdc_podcast_libsyn_mscpedu    

In this episode of Manufacturing Unscripted, host Peter Parsons sits down with Nelson Bruton, President of Manufacturing Chats, to discuss the growing role of chat bots in manufacturing websites and digital strategy. Nelson and Peter explore why chat bots are becoming an important tool for manufacturers, how they can improve customer engagement, and where companies need to be careful not to lose the human touch. They dive into finding the “sweet spot” — giving chat bots enough information to be useful without removing meaningful human interaction from the sales and support process. The conversation also covers who the ideal customer is for chat bots, where they add the most value, and how manufacturers can use them to better qualify leads, answer questions faster, and enhance the overall website experience.  Watch on YouTube: https://www.youtube.com/watch?v=sYOOA58YcZ0  @peter parsons @nelson bruton  #ManufacturingUnscripted #ChatBotsInManufacturing #ManufacturingChats #DigitalManufacturing #ManufacturingMarketing #AIinManufacturing #CustomerExperience #SmartManufacturing #PeterParsons #ManufacturingPodcast 

On this week's special mini-sode Cal Bruton joins us to discuss the Allen Iverson Inner Circle and Masterclass events that he is hosting this January across Brisbane, Sydney and Melbourne.Tickets are still available and available Tickify!

Australian basketball legend Cal Bruton joins the show to discuss his upcoming Q&A tour with Hall of Famer Allen Iverson.Presented by Global Tours and Entertainment, Allen Iverson brings his Inner Circle Experience to Australia, appearing in Brisbane on January 18 and Sydney on January 20. The tour concludes with the Allen Iverson Master Class Experience in Melbourne on January 22. Tickets, including General Admission and VIP packages, are available now via Tickify.io.Unwrapped is presented by C2C Sport. Get 10% exclusive discount on your initial order, use code PICKROLL on the checkout page at c2csport.com.au. Valid for custom orders. Contact sales@c2csport.com or call 02 6581 1558 if you need help. Hosted on Acast. See acast.com/privacy for more information.

It's the last BEHIND THE LENS for 2025! And this week, we shine a light on producer, director, writer, and actor RYAN FRANCIS and his latest film, SPEED TRAIN. I have had the pleasure of knowing Ryan for more than two decades. I reviewed his first directorial short film and multiple feature films thereafter, and interviewed him. And over the years, he has moved from being an actor in front of the camera to going behind the camera into directing and, most recently, also producing. And now he brings us a fast-paced, entertaining futuristic film that posits some interesting questions for us as individuals and a society – SPEED TRAIN. In this very candid, fun, and unfettered exclusive interview, writer/director RYAN FRANCIS discusses his career growth from acting to directing, highlighting his recent film SPEED TRAIN, as well as discussing at length some of his prior films of late in which he only acts or serves an Executive Producer versus directing; notably, "Reverence", "The Jurassic Games: Extinction", "Trail of Vengeance", "The Flood", and "3 Days in Malay". He also discusses two upcoming films he's excited about, "Bruton" and "Bring the Law." As we specifically dig into the making of SPEED TRAIN, Ryan shares the challenges of directing a futuristic sci-fi film in 12 days with a small budget, praising his team, including DP Nico De La Fere and editor Austin Nordell, as well as producer Daemon Hillin and his Thailand team. A large portion of our conversation also discusses the film's themes of AI and human reliance on technology. An interesting aspect of our discussion revolved around the challenges of the film industry, the importance of maintaining a passion for making movies, and the need to bring audiences back to the theater experience. As you'll hear, Ryan speaks with a mix of candor, humor, and hard-earned perspective about a career that has quietly but decisively evolved. Once primarily known as an actor, Ryan has increasingly stepped behind the camera, carving out a space as a filmmaker unafraid of ambition—or of admitting when that ambition nearly outruns the clock. http://eliasentertainmentnetwork.com

JCO Editor-in-Chief Dr. Jonathan Friedberg is joined by colleagues Dr. Jennifer Woyach, Dr. Wojciech Jurczak, and Dr. Matthew Davids to discuss simultaneous publications presented at ASH 2025 on pertibrutinib, a new upfront treatment option for patients with chronic lymphocytic leukemia. TRANSCRIPT The disclosures for guests on this podcast can be found in the show notes. Dr. Jonathan Friedberg: I'm Jonathan Friedberg, editor of Journal of Clinical Oncology, and welcome to JCO After Hours, where we are covering two manuscripts that were presented at the American Society of Hematology meeting 2025 in Orlando, Florida. I am delighted to be joined by colleagues on this call to discuss these pivotal manuscripts which cover the topic of pirtobrutinib, a new upfront treatment option for patients with chronic lymphocytic leukemia. I will first just introduce our guests, Dr. Woyach. Dr. Jennifer Woyach: Hi, my name is Jennifer Woyach. I am from the Ohio State University. Dr. Wojciech Jurczak: Hello, I am Wojciech Jurczak, working at the National Research Institute of Oncology in Krakow, Poland. Dr. Matthew Davids: Hi, I am Matthew Davids from Dana-Farber Cancer Institute in Boston. Dr. Jonathan Friedberg: We are going to start by just learning a little bit about these two trials that were both large, randomized phase 3 studies that I think answered some definitive questions. We will start with your study, Jennifer. If you could just describe the design of your study and the patient population. Dr. Jennifer Woyach: Absolutely. So this is the BRUIN CLL-314 study, and this is a phase 3 randomized trial of pirtobrutinib versus ibrutinib in patients with CLL or SLL who had not previously been treated with a covalent BTK inhibitor. The patients were both treatment-naive and relapsed/refractory, about one-third of the patients treatment-naive, the rest relapsed/refractory, and they were stratified based upon 17p deletion and the number of prior lines of therapy. The primary objective was looking at non-inferiority of overall response rate over the entire treated population as well as the relapsed/refractory patient population. Key secondary objectives included progression-free survival in the intention-to-treat and the smaller relapsed/refractory and treatment-naive populations. Dr. Jonathan Friedberg: And just comment a little bit on the risk of the patients. Dr. Jennifer Woyach: This study was fairly typical of this cohort of patients. Within the relapsed/refractory patient population, there was a median of one prior line of therapy in each of the groups, up to nine prior lines of therapy in the patients included on the study. For the overall cohort, about two-thirds of the patients were IGHV unmutated, about 15% had 17p deletion, 30% had TP53 mutations, and about 35% to 40% had a complex karyotype, which is three or more abnormalities. Dr. Jonathan Friedberg: And what were your findings? Dr. Jennifer Woyach: Regarding the primary outcome, which is the focus of the publication, we did find that pirtobrutinib was indeed non-inferior and actually superior to ibrutinib for overall response rate throughout the entire patient population and in both the relapsed/refractory and treatment-naive cohorts. PFS is a little bit immature at this time but is trending towards also being significantly better in pirtobrutinib-treated patients compared with ibrutinib-treated patients. Probably most significantly, we found this to be the case in the treatment-naive cohort where there was a striking trend to an advantage of pirtobrutinib versus ibrutinib. Dr. Jonathan Friedberg: And the follow-up that you have on that progression-free survival? Dr. Jennifer Woyach: So we have about 18 months follow-up on progression-free survival. Dr. Jonathan Friedberg: The second study, Wojciech, can you just go through the design and patient population that you treated? Dr. Wojciech Jurczak: Thank you, Dr. Friedberg, for this question. So the BRUIN CLL-313 study was, in fact, the first phase 3 study with pirtobrutinib in exclusively untreated CLL patients. It was a randomized study where we challenged pirtobrutinib versus bendamustine-rituximab. At the time we designed the protocol, bendamustine-rituximab was an option as a standard of care, and Bruton tyrosine kinase monotherapy was used far more commonly than nowadays. The primary target of the study was progression-free survival. We took all untreated patients except for those with 17p deletions. Therefore, it is a good representation for intermediate risk. We had about 60% of the population, 56 to be precise, which was unmutated, evenly distributed into two treatment arms. 17p deleted cases were excluded, but we had about 7% and 8% of TP53 mutated patients as well as about 11% and 7%, respectively, in the pirtobrutinib and bendamustine-rituximab arm of patients with complex karyotype. The progression-free survival was in favor of pirtobrutinib and was assessed by an independent review committee. What is important is that the progression-free survival of the bendamustine-rituximab arm was actually similar to the other studies addressing the same questions, like the comparison with ibrutinib in the ALLIANCE study or zanubrutinib in the SEQUOIA study. What was different was the hazard ratio. In our study, it was 0.20. It was one of the longest effect sizes noted in the frontline BTK study. It represented an 80% reduction in progression-free survival or death. If we compare it to ibrutinib or zanubrutinib, it was 0.39 and 0.42 respectively. Presumably, this great effect contributed towards a trend of overall survival difference. Although survival data are not mature enough, there is a clear trend represented by three patients we lost in the pirtobrutinib arm versus 10 patients lost in the bendamustine-rituximab arm. This trend in overall survival is becoming statistically significant despite the fact that there was a possibility of crossover, and effectively 52.9 patients, which means 18 out of 34 patients relapsing in the bendamustine-rituximab arm, were treated by pirtobrutinib. Dr. Jonathan Friedberg: I am going to turn it over to Matt. The question is: why study pirtobrutinib in this patient population? And then with these two studies, how do you find the patients that were treated, are they representative of people who you see? And do you see this maybe being approved and more widely available? Dr. Matthew Davids: I think in terms of the first question, why study this in a frontline population, we have seen very impressive data with pirtobrutinib in a very difficult-to-treat population of CLL patients. This was from the original BRUIN phase 1/2 study where most of the patients had at least two or three lines of therapy, often both a covalent BTK inhibitor and the BCL2 inhibitor venetoclax, and yet they were still responding to pirtobrutinib. The drug was also very well tolerated in that early phase experience. And actually, we have seen phase 3 data from the BRUIN 321 study comparing pirtobrutinib to bendamustine and rituximab in a relapse population as well. So I think that really motivated these studies to look at pirtobrutinib as a first therapy. You know, often in other cancers of course, we want to use our best therapy first, and I think these studies are an initial step at looking at that. In terms of the second question around the patient population, these are pretty representative patient populations, I would say, for most frontline CLL studies. We see patients who are a bit younger and fitter than sort of the general population of CLL patients who are treated in clinical practice, and I think that is true here as well. Median age in the sort of mid-60s here is a bit younger than the typical patients we are treating in practice. But that is not different from other CLL frontline studies that we have seen recently, so I think it makes it a little bit easier as we kind of think across studies to feel comfortable that these are relatively similar populations. Dr. Jonathan Friedberg: How do you see this either getting regulatory approval or potentially being used compared to current standard of care options? Dr. Matthew Davids: So my understanding is that both of these trials were designed with registrational intent in the frontline setting, and they are both positive studies. That is certainly very encouraging in terms of the potential for an approval here. We have seen in terms of the FDA recently some concerns around the proportion of patients who are coming from North America, and my understanding is that is relatively low on these two studies. But nonetheless, the datasets are very impressive, and so I think it is certainly supportive of regulatory approval for frontline pirtobrutinib. Dr. Jonathan Friedberg: I will ask Jennifer a question. The control arm in your study was ibrutinib, and I think many in the audience may recognize that newer, second-generation BTK inhibitors like acalabrutinib and zanubrutinib are more frequently used now if monotherapy is decided. How do you respond to that, and how would you put your results in your pirtobrutinib arm in context with what has been observed with those agents? Dr. Jennifer Woyach: Yeah, that is a great question. Even though in the United States we are predominantly using acalabrutinib or zanubrutinib when choosing a monotherapy BTK inhibitor, this is actually not the case throughout the entire world where ibrutinib is still used very frequently. The head-to-head studies of both acalabrutinib and zanubrutinib compared to ibrutinib have shown us pretty well what the safety profile and efficacy profile of the second-generation BTK inhibitors is. So even though we do not have a head-to-head study of acalabrutinib or zanubrutinib versus pirtobrutinib, I think, given the entirety of data that we have with all of the covalent BTK inhibitors, I think we can safely look at the pirtobrutinib arm here, how the ibrutinib arm compares or performs in context with those other clinical trials. And though we really can not say anything about pirtobrutinib versus acalabrutinib or zanubrutinib, I think we can still get a good idea of what might be the clinical scenarios in which you might want to choose pirtobrutinib. Dr. Jonathan Friedberg: And Wojciech, do you agree with that? Obviously, I think you have acknowledged that chemoimmunotherapy is rarely used anymore as part of upfront treatment for CLL. So, I guess a similar question. If you were to put the pirtobrutinib result in your study in context with, I guess, more contemporary type controls, would you agree that it is competitive? Dr. Wojciech Jurczak: Well, I think that that was the last study ever where bendamustine-rituximab was used as a comparator arm. So we should notice that smashing difference. Because if we look at the progression-free survival at two years, we have 93.4% in pirtobrutinib arm versus 70.7% in bendamustine-rituximab arm. Bendamustine-rituximab arm did the same as in the other trials, like ALLIANCE or SEQUOIA. Pirtobrutinib did exceptionally well, as pirto is not just the very best BTK inhibitor overcoming the resistance, but perhaps even more important for the first line, it is very well tolerated and is a very selective drug. Now, if we look at treatment-related adverse events, the discontinuation rate, they were hardly ever seen. If we compared the adverse events in exposure-adjusted incidence, literally all adverse events were two or three times higher in bendamustine-rituximab arm except for the bleeding tendency, which however was predominantly in CTCAE grade 1 and 2 with just 0.7% of grade 3 hemorrhage. Therefore, I think that we should actually put the best and the safest drugs upfront if we may, and pirtobrutinib is, or should be, the first choice if we choose monotherapy. Now, I understand that we are not presenting you the data of pirtobrutinib in combination with anti-CD20 or with BCL2 inhibitors, but that is to come. Dr. Jonathan Friedberg: Matt, how would you envision, were regulatory approval granted and this were an option, using this in the upfront patient population? Is there anybody who you would preferentially use this or start on this treatment? Or would this be something that you would tend to reserve for second line? Dr. Matthew Davids: So I would say that in general for most of my patients who would want to start with a continuous BTK inhibitor, I would still use a covalent BTK inhibitor, and I say that for a couple of reasons despite the very promising data from these studies. The first is that the follow-up for both of these phase 3 trials is still quite short, in the range of a median 18 to 24 months. And we know that CLL is a marathon, not a sprint, and these patients are going to probably be living for a very long time. And we do have much longer follow-up from the covalent BTK inhibitors, median of 10-year follow-up with ibrutinib and five to six years with zanubrutinib and acalabrutinib respectively. And you know, I do not think that the pirtobrutinib is going to fall off a cliff after two years, but on the other hand, I think there is a lot of value to long-term data in this disease, and that is why I think for most of my patients I would stick with covalent BTK inhibitors. But the other important factor that we need to consider is patients who are younger and may have many different CLL treatments over the years. We have to be very careful, I think, about how we sequence these drugs. We know right now that we can start with covalent BTK inhibitors and then subsequently patients will respond well to the non-covalent inhibitor pirtobrutinib in later lines of therapy. But right now we do not have prospective data the other way around. So how will the patients on these studies who progress on pirtobrutinib respond to covalent BTK inhibitors? We do not know yet. There have not been a lot of progression events, which is great, but we would like to see some data in that respect to feel more comfortable with that sequence. Now, I do think that particularly for older patients and those who have significant cardiovascular comorbidities, if they wanted to go on a continuous BTK inhibitor, I do think these data really strongly support using pirtobrutinib as the BTK inhibitor of choice in that population. In particular, the cardiovascular risks with pirtobrutinib seem to be quite low. I was very struck in the comparison with BR that the rate of AFib was equivalent between the two arms of the study. And that is really the first time we have seen that with any of these BTK inhibitors, no elevated risk of AFib in a randomized study. I think that is the population where it will get the most traction first, is the upfront, sort of older patient with significant cardiovascular comorbidities. And as the data from these studies mature, I think that we will start to see more widespread use of pirtobrutinib in the frontline setting. Dr. Jonathan Friedberg: Jennifer, I am just curious if you have any personal experience or heard anecdotally about after progression on pirtobrutinib the use of other BTK inhibitors and whether there is a growing experience there. Dr. Jennifer Woyach: I do not think that there is much clinical experience, you know, as Matt alluded to, it certainly has not been tested yet. There has been some data in relapsed CLL suggesting that in people who have resistance mutations to covalent BTK inhibitors after treatment with pirtobrutinib, sometimes those mutations go away. I think most of us are concerned that they are probably not actually gone but maybe in compartments that we just have not sampled, suggesting that sort of approach where you might sequence a covalent inhibitor after a non-covalent in somebody who had already been resistant probably would not work that well. But, you know, in this setting where people had never been exposed to a covalent BTK inhibitor before, we really have no idea what the resistance patterns are going to be like. We assume they will be the same as what we have seen in relapsed CLL, but I think we just need some longer follow-up to know for sure. Dr. Wojciech Jurczak: If I may confront Dr. Davids about the use of covalent BTK inhibitors upfront, well, I think that we should abandon the idea of using the first and the second and the third generation, at least if we don't have medical lines. If we endlessly block the same pathway, it is not going to be effective. So if pirtobrutinib gets approval in first, second line, we do not necessarily have to use it in the first line. I am not here in a position to defend that we should treat patients with pirtobrutinib upfront and not BCL2 time-limited regimen. However, the way I look at CLL patients when choosing therapy is not just how should I treat them now, but what would be the best regimen in 5, 10 years if I have to re-treat them. And in some instances, the idea may be that in this setting we would like to have a BTK inhibitor upfront to have a BCL2 inhibitor later to make it time-limited. Although I understand and I agree with Matthew that if we have an elderly, fragile population, then the charm of having a drug taken once a day in a tablet with literally few cardiovascular adverse events might be an option. Dr. Jonathan Friedberg: And I will give Matt the last word whether he wants to respond to that, and also just as a forward-looking issue, I know both investigators have implied that there will be future studies looking at combinations with pirtobrutinib, and if you have any sense as to what you would be looking for there. Dr. Matthew Davids: The field really is heading toward time-limited therapy for most patients, I would say. There is a bit of a discrepancy right now in the field between sort of what we are doing in academic practice and what is done sort of more widely in community practice. And so right now we are going to see evolving datasets comparing these approaches. We are already seeing data now from the CLL17 study with ibrutinib comparing continuous to time-limited venetoclax-based therapy, and we are seeing similar efficacy benefits from these time-limited therapies without the need for continuous treatment. And so that is where I think some of the future studies with pirtobrutinib combining it with venetoclax and other partners are so important. Fortunately, several of these studies are already ongoing, including a phase 3 trial called CLL18, which is looking at pirtobrutinib with venetoclax, comparing that to venetoclax and obinutuzumab. So I am optimistic that we are going to be developing these very robust datasets where we can actually use pirtobrutinib in the frontline setting as a time-limited therapy as a component of a multi-drug regimen. So far, those early data are very promising. Dr. Wojciech Jurczak: Perhaps last but not least, in a single center we have treated over 300 patients with pirtobrutinib. So eventually some of them relapsed. And I must say that our experience on BCL2 inhibitors, not just venetoclax but including sonrotoclax, are appealingly good. Therefore, by using pirtobrutinib even earlier, we do not block the efficacy of other compounds. Dr. Jonathan Friedberg: All right. Well, I want to thank all of our speakers. I also want to congratulate our two guests who presented these very influential papers at the ASH Annual Meeting, and chose to publish them in JCO, so we thank you for that, and Dr. Davids for your commentary - really appreciated. That is this episode of JCO After Hours. Thank you for your attention. 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.   Disclosures Dr. Wojciech Jurczak Consulting or Advisory Role: BeiGene, Lilly, Abbvie/Genentech, Takeda, Roche, AstraZeneca Research Funding: Roche, Takeda, Janssen-Cilag, BeiGene, AstraZeneca, Lilly, Abbvie/Genentech Dr. Jennifer Woyach Consulting or Advisory Role: Pharmacyclics, Janssen, AstraZeneca, Beigene, Loxo, Newave Pharmaceutical, Genentech, Abbvie, Merck Research Funding: Company name: Janssen, Schrodinger, beone, Abbvie, Merck, Loxo/Lilly Dr. Matthew Davids Honoraria: Curio Science, Aptitude Health, Bio Ascend, PlatformQ Health, Plexus Consulting or Advisory Role: Genentech, Janssen, Abbvie, AstraZeneca, Adaptive Biotechnologies, Ascentage Pharma, BeiGene, Lilly, Bristol-Myers Squibb, Genmab, Merck, MEI Pharma, Nuvalent, Inc., Galapagos NV, Schroedinger Research Funding: Ascentage Pharma, Novartis, MEI Pharma, AstraZeneca  

Good morning from Pharma Daily: the podcast that brings you the most important developments in the pharmaceutical and biotech world. Today, the landscape of the pharmaceutical and biotech industries is marked by groundbreaking scientific advancements, regulatory shifts, and strategic collaborations that promise to reshape patient care and drug development significantly.A controversy has emerged in the wake of proposed changes to U.S. vaccine regulations by Dr. Vinay Prasad, a senior FDA official. This proposal has sparked considerable opposition from 12 former FDA commissioners who argue that these regulatory overhauls could potentially undermine public trust in vaccines. Former leaders from both the CDC and FDA have expressed concerns over these proposed vaccine policy changes during an ACIP meeting, discussions that could influence future public health strategies and vaccine trust. At a time when vaccine confidence is crucial, maintaining the integrity of regulatory processes is vital to public health efforts.Leadership changes are also afoot within the FDA, as Dr. Tracy Beth Hoeg steps into the role of acting director for the Center for Drug Evaluation and Research. Her appointment signals a shift towards leaders with direct experience in public health crises. This comes amidst further internal restructuring at the FDA, including the transfer of Theresa Michele, long-standing director of the Office of Nonprescription Drugs, indicating dynamic changes within the agency.In the realm of oncology, Eli Lilly's progress with its Bruton's tyrosine kinase inhibitor, Jaypirca, is noteworthy. The drug's expanded label now includes earlier treatment stages for chronic lymphocytic leukemia and small lymphocytic lymphoma. This expansion underscores the therapeutic potential of non-covalent BTK inhibitors and may significantly improve patient outcomes by offering earlier intervention options.Geopolitical challenges are impacting the industry as WuXi AppTec, a major China-based biopharmaceutical contractor, faces scrutiny from the Pentagon amid concerns about its potential ties with the Chinese military. This development highlights the complex interplay between global security concerns and international biotech collaborations. The intersection of global security concerns continues to impact biopharmaceutical supply chains as WuXi AppTec faces increased scrutiny from U.S. authorities.On the manufacturing front, Quvara Medical's emergence as a new contract development and manufacturing organization following Buckland Group's acquisition of a Becton Dickinson facility in the UK reflects industry trends toward consolidating manufacturing capabilities to meet growing biopharmaceutical demand efficiently.AstraZeneca is enhancing its pipeline through a renewed partnership with Neurimmune for an amyloidosis asset. This collaboration, potentially worth up to $780 million, highlights AstraZeneca's strategic focus on rare diseases and underscores their commitment to expanding their therapeutic portfolio through successful alliances.Regulatory updates from the FDA propose reductions in user fees for early-stage clinical trials conducted domestically while considering additional fees for overseas developments. This initiative aims to incentivize research activities within the U.S., potentially accelerating drug discovery timelines and fostering domestic innovation.In surgical technology advancements, Medtronic's Hugo surgical robot has secured FDA clearance for procedures involving prostate, kidney, and bladder removal. This marks a significant advancement in robotic-assisted surgeries and could enhance patient outcomes across approximately 230,000 surgeries annually in the U.S.As we explore more about financial maneuvers within this sector, Royalty Pharma's $275 million financing deal for Denali Therapeutics' Hunter syndrome drug reflects confidence in Denali's pipeline pendinSupport the show

In this special Derms and Conditions episode recorded live at Fall Clinical 2025, host James Q. Del Rosso, DO, is joined by April Armstrong, MD, MPH, and David Cohen, MD, to share highlights and clinical takeaways from this year's meeting. Dr Armstrong kicks off with updates in hidradenitis suppurativa (HS), noting the field's rapid progress with 3 FDA-approved therapies (adalimumab, secukinumab, and bimekizumab), emerging 3-year data for bimekizumab, and exciting new agents such as oral povorcitinib and topical ruxolitinib. She shares learnings on the importance of proactive flare management plans and setting realistic patient expectations, particularly regarding scarring and lymphedema. Dr Cohen and Dr Del Rosso echo the importance of reengaging patients with longstanding HS and highlight the promise of JAK inhibition in this complex disease. The discussion shifts to chronic spontaneous urticaria (CSU), where Dr Cohen spotlights remibrutinib, a twice-daily oral Bruton kinase inhibitor delivering rapid results sometimes within 1 to 2 weeks and potentially enabling dermatologists to manage CSU more directly. Dr Armstrong adds that dupilumab now offers another trusted option for CSU, with a head-to-head trial versus remibrutinib on the horizon. For chronic hand eczema (CHE), they discuss the paradigm-shifting approval of delgocitinib cream, a topical pan-JAK inhibitor effective across CHE subtypes and free of boxed warnings. They note strong data for pain and itch reduction and its potential to mitigate chronic steroid reliance. The episode closes with emerging oral psoriasis therapies, including 5-year deucravacitinib safety data and radiographic progression inhibition shown with guselkumab. Looking ahead, they predict major advances by 2026 in TYK2 inhibitors, OX40-targeted therapies, and personalized molecular profiling for atopic dermatitis. Tune in to the full episode for expert perspectives straight from the Fall Clinical stage!

The Go To Food Podcast returns with a legend. Margot Henderson OBE joins us for a gloriously frank, funny, and deeply human conversation about the craft of hospitality. From the early days at The Eagle and The French House to the white heat of opening St. John with Fergus Henderson, Margot traces the rise of modern British cooking, the joy of whole-animal kitchens, and the art of building atmosphere without gimmicks. Expect big stories, bigger flavours, and the kind of kitchen wisdom only a lifetime in service can teach.We record at The Three Horseshoes in Batcombe, Somerset, where the tomatoes burst like fireworks and the faggots arrive wrapped in caul and pride. Margot lifts the lid on a life spent nurturing chefs who fly the nest, the realities of PR, and why a great waiter can save a meal. She celebrates the producers around Bruton, tips her hat to Wescombe's cheddar cave, and recalls the art world and Anthony Bourdain putting rocket fuel under St. John. This is a rolling feast of memories, mishaps, and moments that changed the way Britain eats.There are love stories too. Sweetings proposals, bar counters, the rhythm of service, and the calm conviction that simple food, cooked honestly, can move a room. -------Sponsor: This episode is brought to you by Blinq—POS made simple: £69/month, unlimited devices, 24/7 UK support, no contracts or hidden fees. Use code GOTOBLINQ for a free month. Got a true kitchen nightmare? Send it in—Ben's favourite wins a year of Blinq. Hosted on Acast. See acast.com/privacy for more information.

NBL NOW | Everything NBLCal Bruton & Joel Peterson* Perth get the 'W' against Tasmania* Why aren’t we talking about Casey Prather more? * How you seeing Brisbane at the moment? * Jack McVeigh likely return, gives Cairns some hope? * Kings and Goorj under pressure* Big round of hoops aheadSee omnystudio.com/listener for privacy information.

For decades, allergists have focused on blocking what happens outside the mast cell: histamine, IgE, and interleukins. But now, there's a new way to stop allergic inflammation before it even starts: by targeting what happens inside the cell with BTK Inhibitors. Dr. Payel Gupta and Kortney are joined by Dr. Matthew Giannetti to unpack what BTK actually does and why inhibiting it represents an exciting breakthrough in allergy and immunology. Together, they explore how BTK inhibitors work, why this inside-the-cell approach is different from anything before, and what it could mean for people living with chronic spontaneous urticaria (CSU). What the episode covers about BTK inhibitors: BTK explained: Bruton's tyrosine kinase is a pivotal “last step” before mast-cell degranulation. How BTK inhibitors work: Blocking BTK can stop histamine release downstream of many outside triggers. The science: Why BTK binding is irreversible for each molecule and how the body “re-makes” BTK over time. Safety in brief: A look at petechiae (small pinpoint spots), what to monitor, and how shared decision-making guides treatment choices. The future of BTK inhibitors: Exploring their potential role in other allergic conditions.    ____ Made in partnership with The Allergy & Asthma Network. Thanks to Novartis for sponsoring today's episode.  This podcast is for informational purposes only and does not substitute professional medical advice. Always consult with your healthcare provider for any medical concerns.

DeAnte Bruton is a former college athlete currently working in IT. He is a BFM listener and still early on his Bitcoin journey and research. I helped to answer his big Bitcoin questions!› https://x.com/Deanteb_3PARTNERS

Jim and Evelyn Bruton, courtesy of Elanie Bruton. This is an edited version of a conversation with a  lighthouse keeper's daughter in British Columbia, Canada, first heard in episode 104 of Light Hearted. Jim Bruton was born in Wales in 1926, but his family relocated to British Columbia in Canada when he was just one year old. He started working in the logging industry as a boy. In a light keeping career spanning several decades, he served at light stations around Vancouver Island: Lennard Island, Discovery Island, and Chrome Island. Sheringham Point Lighthouse, BC. Photo by Jeremy D'Entremont. iThe Brutons eventually had four children, three girls and a boy. The family moved to Sheringham Point, a mainland lightstation in Shirley on the southwest coast of Vancouver Island, in 1968. They lived there for nearly two decades, until 1986, when Jim Bruton retired. Our guest today, Elanie Bruton, lived at the light stations with her family until she was 18. She remains an active volunteer of the Sheringham Point Lighthouse Preservation Society, which now owns the lighthouse and surrounding land.

We're discussing Relationships and Community: the Fabric of Rural Health! Faisel and Dan are joined by Dr. Sonya Bruton: CEO and President of CCI Health Services, Clinical Psychologist, and Author.Our conversation revolves around the inherent link between physical and behavioral health, the necessity of physicians staying engaged with their passion for care, and the hesitancy of patients around AI in healthcare.

In this Made in America podcast episode, Nelson Bruton, President of Manufacturing Chats, shares insights on how manufacturers can boost their sales and business growth through practical, effective communication tools like live chat. The discussion covers the evolution of Manufacturing Chats from a full-service digital marketing agency to a specialized provider of live chat solutions tailored for industrial manufacturers. Nelson emphasizes the importance of real-time customer engagement, drawing parallels between live chat and trade show interactions. He also explores the potential of AI in chat services while highlighting the continued need for human interaction in complex sales environments. This episode is a valuable resource for manufacturers looking to enhance their sales strategies and improve customer engagement.  Youtube: https://youtu.be/SIXhUjWBpA4 Podcast Website: https://madeinamerica.compassmsp.com/nelson-bruton-manufacturing-chats Nelson Bruton's LinkedIn Manufacturing Chats Website  Manufacturing Chats LinkedIn Ari Santiago's LinkedIn CompassMSP Website CompassMSP LinkedIn Made in America Podcast Facebook Made in America Podcast LinkedIn Made in America Podcast YouTube Podcast produced by Miceli Productions.  

Featuring an interview with Dr Lindsey Roeker, including the following topics: Clinical development of novel Bruton tyrosine kinase (BTK) degraders in therapy for chronic lymphocytic leukemia (CLL) (0:00) Safety of BTK inhibitors in older and frail patients with CLL (3:41) Utility of minimal residual disease-guided treatment with venetoclax/obinutuzumab (9:20) Impact of the AMPLIFY study of acalabrutinib with venetoclax with or without obinutuzumab in CLL (16:32) Utility of acalabrutinib, venetoclax and obinutuzumab for high-risk CLL (23:31) Emerging data with sonrotoclax and zanubrutinib in treatment-naïve CLL (25:16) Sequencing, tolerability and future development involving pirtobrutinib (25:57) Emerging data with the addition of a BTK inhibitor to chimeric antigen receptor T-cell therapy (32:28) Clinical considerations in the management of Richter's transformation (38:14) Survival outcomes and quality of life for patients with CLL (41:02) Ongoing and future efforts to improve CLL treatment outcomes (45:01) CME information and select publications  

Featuring a slide presentation and related discussion from Dr Lindsey Roeker, including the following topics: Recent clinical updates with standard regimens for chronic lymphocytic leukemia (CLL) (0:00) Utility of minimal residual disease-guided treatment intensification after ibrutinib with venetoclax  (7:03) Major long-term findings from the GLOW study of ibrutinib with venetoclax (10:35) Principal findings from the AMPLIFY study of acalabrutinib with venetoclax with or without obinutuzumab (12:28) Findings with combined acalabrutinib, venetoclax and obinutuzumab for patients with previously untreated high-risk disease  (15:52) Early clinical findings with sonrotoclax and zanubrutinib as front-line treatment for CLL (18:12) Principal findings from the BRUIN CLL-321 trial of pirtobrutinib for patients who previously received a covalent Bruton tyrosine kinase (BTK) inhibitor  (19:38) Emerging evidence with pirtobrutinib, venetoclax and obinutuzumab as front-line treatment  (22:15) Novel strategy combining lisocabtagene maraleucel with ibrutinib for relapsed/refractory (R/R) CLL (24:13) Available data with epcoritamab monotherapy for R/R CLL  (26:58) The emerging pharmacologic class of BTK degraders  (29:04) CME information and select publications

A host of exhibitions and events this month and next celebrate the 100th anniversary of the birth of the Swiss artist Jean Tinguely, one of the godfathers of kinetic and auto-destructive art. Ben Luke speaks to Roland Wetzel, the director of the Tinguely Museum in Basel about the artist's life and work, and the events marking the centenary. In Rotterdam in the Netherlands, Fenix, a museum about migration, has just opened, featuring a dramatic stainless steel tornado form on its roof. We discuss the museum with its director, Anne Kremers. And this episode's Work of the Week is by an immigrant artist, Ben Shahn, who was born in modern-day Lithuania but travelled as a child to the US, where he became a leading painter associated with Social Realism. Among his greatest achievements was the mural The Meaning of Social Security, painted between 1940 and 1942 in Washington D.C. to reflect the benefits of the then-recent Social Security Act. Shahn is the subject of a major show that opened this week at the Jewish Museum in New York. We speak to Laura Katzman, the co-curator of the exhibition with the Jewish Museum's Stephen Brown, about Harvesting Wheat (1941), Shahn's study for one of the figures in the mural.The Tinguely Museum in Basel, Switzerland, has a permanent display of his work; Scream Machines–Art Ghost Train, by Rebecca Moss and Augustin Rebetez, Tinguely Museum, until 30 August; Mechanics and Humanity: Eva Aeppli and Jean Tinguely, Lehmbruck Museum, Duisburg, Germany, until 24 August; Niki de Saint Phalle & Jean Tinguely: Myths & Machines, Hauser & Wirth Somerset, Bruton, UK, until 1 February 2026; Niki de Saint Phalle, Jean Tinguely, Pontus Hultén, Grand Palais, Paris, 20 June-4 January 2026.The Fenix museum is open now.Ben Shahn: On Nonconformity, Jewish Museum, New York, 23 May-12 October. The book accompanying it published on 3 June by Princeton University Press, priced $45.00/£38.00.The Meaning of Social Security murals:https://art.gsa.gov/artworks/637/the-meaning-of-social-security?ctx=3bc918796c456cc8fb8e3d3f033918d4249d0ce6&idx=6https://livingnewdeal.org/sites/wilbur-j-cohen-building-shahn-frescoes-washington-dc/#lg=1&slide=1 Hosted on Acast. See acast.com/privacy for more information.

Las Vegas, Nevada is one of the most sought after tourist destinations in the world. For Mexico-born Willebaldo Dorantes Antonio, Las Vegas was booming with job opportunity and the chance to send money to his family back home. But in early May of 2007 an explosion would shock the city and leave Willebaldo's family to go on without him. Instagram: @CousinsonCrimePodcast Email: CousinsonCrime@gmail.com Theme Music by AleXZavesa Join our Patreon! https://www.patreon.com/CousinsOnCrime Check out our merch store! https://cousinsoncrime-shop.fourthwall.com/? Sources: https://www.rgj.com/story/news/crime/2022/09/29/las-vegas-police-arrest-fugitive-luxor-bomber-porfirio-duarte-herrera-after-prison-escape/10460956002/ https://www.nycourts.gov/JUDGES/evidence/4-RELEVANCE/4.20_Bruton.pdf https://www.rgj.com/story/news/2022/09/29/police-body-cam-video-luxor-bomber-porfirio-duarte-herrera-arrest/8129696001/ https://www.reviewjournal.com/news/2-avoid-death-penalty-get-life-in-prison-for-luxor-bombing/ https://case-law.vlex.com/vid/duarte-herrera-v-hutchings-934086256 https://apnews.com/article/crime-las-vegas-bombings-terrorist-attacks-de844f6f391f6472e23654573ffa921c https://apnews.com/article/las-vegas-immigration-bombings-96a60c9079984304b4bad2624d962c61

Featuring an interview with Dr John P Leonard, including the following topics: First-line therapy for diffuse large B-cell lymphoma (DLBCL) with polatuzumab vedotin and R-CHP; impact of DLBCL cell of origin (0:00) Epcoritamab, glofitamab and other bispecific antibodies as initial therapy for large B-cell lymphoma (9:27) Sequencing chimeric antigen receptor T-cell therapy and bispecific antibodies for patients with relapsed/refractory (R/R) DLBCL (12:30) Approved and investigational bispecific antibodies for the treatment of DLBCL (15:24) Practical considerations for the administration of mosunetuzumab (22:03) Tafasitamab combined with lenalidomide/rituximab as second-line treatment for follicular lymphoma (FL); third- and later-line therapy options (24:33) Activity of Bruton tyrosine kinase inhibitors in FL and other non-Hodgkin lymphomas (31:27) Risk of infection for patients receiving bispecific antibodies (33:23) Chemotherapy-free regimens for the treatment of mantle cell lymphoma (MCL) (36:21) Current role of transplant in the treatment algorithm for MCL; potential integration of bispecific antibodies into therapy for R/R disease (41:23) Myths and misperceptions about the management of DLBCL, FL and MCL (47:29) CME information and select publications

Featuring a slide presentation and related discussion from Dr John P Leonard, including the following topics: Five-year analysis of the POLARIX trial of polatuzumab vedotin with R-CHP for previously untreated diffuse large B-cell lymphoma (0:00) Epcoritamab, glofitamab and other bispecific antibodies for large B-cell lymphoma (5:33) Circulating tumor DNA as an early outcome predictor in patients with large B-cell lymphoma receiving second-line lisocabtagene maraleucel in the TRANSFORM study (16:44) The bispecific antibodies mosunetuzumab and odronextamab as initial therapy for follicular lymphoma (FL) (19:27) The Phase III inMIND trial of tafasitamab in combination with lenalidomide/rituximab for recurrent FL (22:58) Updated results from studies of bispecific antibodies and chimeric antigen receptor T-cell therapy for relapsed/refractory FL (24:58) Updates from the Phase III TRIANGLE and ECOG-ACRIN EA4151 trials on the role of autologous stem cell transplant in the treatment of previously untreated mantle cell lymphoma (MCL) (27:48) Novel treatment approaches with Bruton tyrosine kinase inhibitors for patients with newly diagnosed MCL (30:53) CME information and select publications

In this, the penultimate episode of Series 9, I talk to UKCP accredited psychotherapist Lisa Bruton who is also a guest tutor at the University of Oxford. We talk about the Parentified Child. Which is? A child who has been given too much responsibility - either physical or emotional - too young. The impact of this is interesting. Do you often find yourself being the most responsible person in the room? Do people look to you for advice (ahem) and guidance? It may be because you are used to performing this role, from way too young. Parentified children can grow up to be exhausted adults. Who looks after them? And why the phrase "my child is my best friend" gives Bruton and I pause.In this episode we look at what exactly being a parentified child looks and feels like, from both the child and adult's POV. What you can do if you recognise yourself as one and how to avoid doing that to your own children. More about Lisa here: https://www.lisabruton.comIf you'd like to support us you can leave a one off donation here: https://supporter.acast.com/conversations-with-annalisa-barbieriIf you'd like to listen to this episode, past or future ones, ad free then consider becoming a Substacker: https://pocketannalisa.substack.com/. From £5 a month or £50 a year you'll get access to all new podcasts as soon as they are available and before general release and ad-free. Plus subscriber exclusive newsletters.You can also support us by sharing this podcast far and wide, it's available wherever you listen to your podcasts. And leaving a review if you can. Thank you so much.Produced by Hester Cant. Art work by Lo Cole. Music by Toby Dunham.Support this show http://supporter.acast.com/conversations-with-annalisa-barbieri. Hosted on Acast. See acast.com/privacy for more information.

Bryan Bruton shares his insane life story! Bryan's Links https://www.youtube.com/@UC_S8-o7r0W979pS8j_7snPw https://www.instagram.com/bryanbruton_/https://www.facebook.com/bryan.bruton.2025/Go to https://ground.news/Inside for abetter way to stay informed. Subscribe for 40% off unlimited access to world-wide coverage through my link.Do you want to be a guest? Fill out the form https://forms.gle/5H7FnhvMHKtUnq7k7Send me an email here: insidetruecrime@gmail.comDo you extra clips and behind the scenes content?Subscribe to my Patreon: https://patreon.com/InsideTrueCrime

On this episode of The Claw's Corner Rich "The Claw" Cyr has a great conversation with the Raizine Bruton of Best Video! They chat all things film and video and so much more! Visit Best Video! 1842 Whitney Avenue, Hamden, CT 06517 Find Best Video online: https://www.bestvideo.com/  / bestvideohamden   https://bestvideo.creator-spring.com/ Do not miss Rich's book, "Confessions of a Frenetic Mind" available now - https://www.amazon.com/Confessions-Fr... Copyright 2025 The Claw's Corner - Produced by Rich Cyr  / richtheclawcyr   Edited by Elmwood Productions - http://elmwoodproductions.com/index.html and subscribe to Elmwood Productions on YouTube:    / elmwoodproductions   Show some love for Elmwood! It's your support that keeps content like this coming! Join our Patreon now!  / elmwoodproductions  

For The Other Side NDE Videos Visit ▶️ youtube.com/@TheOtherSideNDEYT Today, a skilled pilot shares the gripping story of his near-death experience following a plane crash that should have claimed his life. In the moments beyond consciousness, he entered a space where time and reality blurred, encountering a presence that offered him a choice—to move on or return. Faced with this life-altering decision, he gained powerful insights into the interconnectedness of fate, free will, and the unseen guidance shaping our lives. ⭐ Check Out More Of Jim's Near Death Experience NDE On His Website

"In B cell malignancies, BTKi inhibits that BTK enzyme which is very upstream. It tells NF-κB to stop signaling into the nucleus and then inhibits proliferation and survival of B cells."  Puja Patel, PharmD, BCOP, Clinical Oncology Pharmacist at Northwestern Medicine Cancer Center at Delnor Hospital in Geneva, IL, told Jaime Weimer, MSN, RN, AGCNS-BS, AOCNS®, manager of oncology nursing practice at ONS, during a conversation about BTK inhibitors.  Music Credit: “Fireflies and Stardust” by Kevin MacLeod  Licensed under Creative Commons by Attribution 3.0   Earn 1.0 contact hours of nursing continuing professional development (NCPD) by listening to the full recording and completing an evaluation at courses.ons.org by January 17, 2027. The planners and faculty for this episode have no relevant financial relationships with ineligible companies to disclose. ONS is accredited as a provider of nursing continuing professional development by the American Nurses Credentialing Center's Commission on Accreditation.  Learning outcome: Learners will report an increase in knowledge related to the BTK inhibitor drug class.  Episode Notes   Complete this evaluation for free NCPD.  ONS Podcast™ Pharmacology 101 series  ONS Voice articles:  BTK Inhibitor Effective for Relapsed Hairy Cell Leukemia  FDA Grants Accelerated Approval to Pirtobrutinib for Chronic Lymphocytic Leukemia and Small Lymphocytic Lymphoma  Ibrutinib Is the First Anticancer Agent to Be Negotiated for Medicare Drug Pricing  Oncology Drug Reference Sheet: Pirtobrutinib  Oncology Drug Reference Sheet: Zanubrutinib  ONS books:  Clinical Guide to Antineoplastic Therapy: A Chemotherapy Handbook (fourth edition)  Chemotherapy and Immunotherapy Guidelines and Recommendations for Practice (second edition)  Clinical Journal of Oncology Nursing article: B-Cell Malignancies: The Use of Small Molecule Agents for Treatment and Management  ONS courses:   ONS Cancer Biology™  ONS/ONCC Chemotherapy Immunotherapy Certificate™   Safe Handling Basics   ONS Guidelines™ and Symptom Interventions:   Chemotherapy-Induced Diarrhea  Prevention of Bleeding  Prevention of Infection: General  ONS Learning Library: Oral Anticancer Medication  ONS/NCODA/HOPA/ACCC's Oral Chemotherapy Education Sheets  Other resources:  Advanced Practice Providers Oncology Summit  Ash Publications article: Managing Toxicities of Bruton Tyrosine Kinase Inhibitors  Blood Advances article: BTK Inhibitors in CLL: Second-Generation Drugs and Beyond  CLL Society Fact Sheets  International Journal of Molecular Sciences article: Bruton's Tyrosine Kinase Inhibitors: Recent Updates  National Cancer Institute article: Two Drugs Show Efficacy against Common Form of Leukemia  National Comprehensive Cancer Network Guidelines for Patients: Chronic Lymphocytic Leukemia  National Study of Lymphoma (University of Oxford network site-specific group— Hematology)  NCODA's Positive Quality Intervention resources  Pharmacy Times BTK Inhibitor Comparison Charts  ScienceDirect article: Treating CLL with Bruton Tyrosine Kinase Inhibitors: The Role of the Outpatient Oncology Nurse  The Video Journal of Hematology and Hematological Oncology  To discuss the information in this episode with other oncology nurses, visit the ONS Communities.   To find resources for creating an ONS Podcast Club in your chapter or nursing community, visit the ONS Podcast Library.  To provide feedback or otherwise reach ONS about the podcast, email pubONSVoice@ons.org.    Highlights From This Episode  “1952 we have the discovery by Colonel Ogden Bruton of that severe immunodeficiency due to lack of B-cell maturation, and next linked to e-gamma globular anemia. In 1993, we had Professor Vetrie and colleagues discover that this was actually due to mutation in a kinase, and they called that BTK. And then in 1993 was a discovery of our first BTKi inhibitor in the lab setting, and that's called LFM-A13. It wasn't until 2013, so that's 20 years after BTK kinase was discovered, where ibrutinib was our first-in-class BTK inhibitor, and the success of ibrutinib really promoted the exploration of second- and third-generation BTKis.” TS 6:24     “It's thought that BTK and other members in the pathway are constitutively phosphorylated, which just means they're spontaneously on. This leads to this uncontrolled activation of NF- κB signaling and thus uncontrolled proliferation and suppression of apoptosis. So, these B cells are rapidly dividing, but they're not functioning like they're supposed to be, meaning they won't differentiate, or, you know, they won't grow up to be either a plasma cell, like we talked about, or a memory B cell. They've been hacked.” TS 10:11     “This class is generally called—if you have to think of an umbrella term—it's just called targeted small molecule therapies. Now a subclass is BTKi or Bruton tyrosine kinase inhibitors. So, we're really shifting away from the use of cytotoxic chemotherapy, which is kind of designed to indiscriminately destroy rapidly dividing cells, to a more precise approach of targeting cells based on specific molecular changes in tumor DNA.” TS 13:47     “Cardiac toxicity can manifest as atrial fibrillation. And here I'll specifically talk about ibrutinib values because we have the most data with it, and the numbers actually get better with second- and third-generation BTKis. So frequency: Grade 1–2 atrial fibrillation was reported in 12%–15% of patients on Ibrutinib. And grade 3 AFib is 3%–5%. The onset, median onset is 8–13 months.” TS 20:23     “For nurses, they should really advise their patients that the caliber of headaches are easily managed and they will decrease over time over a period of four weeks. This is an upfront conversation reassuring the patient that this is not a long-term side effect.” TS 33:47     “One aspect that was being discussed at length was kind of identifying biases and then methods to neutralize those biases. So, I think first you have to identify what your bias could be toward BTK, maybe it's age or comorbidities or side-effect profile. And then, how can we mitigate our own biases is kind of the solution part to that.” TS 46:26 

Built airplane. Flew airplane. Crashed airplane. Met God. all set.Jim Bruton knows life. His past is marked by relentless curiosity and remarkable achievement. He was an African wilderness guide, Emmy Award-winning wildlife film director, aviator, adventurer, inventor of the satellite videophone, NBC News Middle East war correspondent, a husband, and a father.His passion - building and flying WWI-era aircraft - led him where he never imagined he'd go: a horrific crash that left him for dead. For one week, Jim Bruton hovered in the place that is not life and not death, a place he came to know as the In Between. He came back, and this is his report of what he has seen.Bruton takes us along for a by turns hair-raising and ultimately triumphant story of his coming to grips with what has happened to him. As he heals, his experiences in the In Between become more and more pressing. They download into his mind like rushing movie stills. His life of action turns internal. He uses all he knows - from quantum physics and battlefield memories to scenes of childhood and familial love - for a new deeper understanding of what it means to live.Jim Bruton, the man who fell from the sky, is not the same man who flew into it. And if you walk some of his journey with him, neither are you.About the author: Jim Bruton has lived a life many people dream of but few experience. As a little boy, he lived within an active imagination, including a love for wildlife filming, international travel, science fiction, and vintage aviation. In adulthood, he checked every one of those off his list with internationally recognized achievements, an Emmy for a National Geographic wildlife film, traveling to all seven continents, the Titanic, the North Pole, and Mt. Everest, shrinking a satellite TV truck into a backpack, and transmitting live video from places before impossible and building and flying historical reproduction aircraft from World War I and the early 1930s.For many, any one of these adventures resulted in a single lifetime achievement. For Jim, it was just the beginning, climaxing with the crash of his last aircraft and the near-death experience that followed.Jim is an Emmy award winning journalist and in this episode we talk about his about his Near Death Experience.From Jim's website;Generally, people who have had NDEs aren't trying to “sell” anything, other than perhaps a seminar, book or DVD.  We don't try to sell a new religion, because we left all that behind.  However, spirituality plays a pretty strong role in the experiences we share.  One of the strangest things I've noticed is that for those of us who had our NDEs as a result of some horrific accident, while in most cases the accident and its crazy circumstances would be the focus of any compelling story, an NDE negates that.Once an NDE enters the picture, you almost forget about the accident- it becomes the least important part of the story, next to the NDE.  My accident was amazing as accidents go, and I have an NDE friend who is only one of a handful in the world that she knows of who suffered and survived an internal decapitation.  But to NDE'ers, the circumstances that nearly, or do, kill us are just a footnote.  I'm sure that must be surprising, in some way.https://www.inbetweenproductions.com/https://www.amzn.com/dp/B098KQHX57 https://www.pastliveshypnosis.co.uk/https://www.patreon.com/ourparanormalafterlife

Join host Dan Dworkis on The Emergency Mind Podcast as he interviews Vinton Bruton, Director of the Wilson Center for Leadership in the Public Interest at Hampden-Sydney College. Drawing on his diverse background as a Marine infantry officer, educator, and volunteer firefighter, Vinton shares insights on leadership development, character education, and the importance of experiential learning. Discover how principles from the military and outdoor adventure can be applied to teaching the next generation of leaders in various high-pressure environments, including emergency medicine. Don't miss this engaging discussion on developing effective, resilient leaders for tomorrow's challenges.

Built airplane. Flew airplane. Crashed airplane. Met God. all set.Jim Bruton knows life. His past is marked by relentless curiosity and remarkable achievement. He was an African wilderness guide, Emmy Award-winning wildlife film director, aviator, adventurer, inventor of the satellite videophone, NBC News Middle East war correspondent, a husband, and a father.His passion - building and flying WWI-era aircraft - led him where he never imagined he'd go: a horrific crash that left him for dead. For one week, Jim Bruton hovered in the place that is not life and not death, a place he came to know as the In Between. He came back, and this is his report of what he has seen.Bruton takes us along for a by turns hair-raising and ultimately triumphant story of his coming to grips with what has happened to him. As he heals, his experiences in the In Between become more and more pressing. They download into his mind like rushing movie stills. His life of action turns internal. He uses all he knows - from quantum physics and battlefield memories to scenes of childhood and familial love - for a new deeper understanding of what it means to live.Jim Bruton, the man who fell from the sky, is not the same man who flew into it. And if you walk some of his journey with him, neither are you.About the author: Jim Bruton has lived a life many people dream of but few experience. As a little boy, he lived within an active imagination, including a love for wildlife filming, international travel, science fiction, and vintage aviation. In adulthood, he checked every one of those off his list with internationally recognized achievements, an Emmy for a National Geographic wildlife film, traveling to all seven continents, the Titanic, the North Pole, and Mt. Everest, shrinking a satellite TV truck into a backpack, and transmitting live video from places before impossible and building and flying historical reproduction aircraft from World War I and the early 1930s.For many, any one of these adventures resulted in a single lifetime achievement. For Jim, it was just the beginning, climaxing with the crash of his last aircraft and the near-death experience that followed.Jim is an Emmy award winning journalist and in this episode we talk about his about his Near Death Experience.From Jim's website;Generally, people who have had NDEs aren't trying to “sell” anything, other than perhaps a seminar, book or DVD.  We don't try to sell a new religion, because we left all that behind.  However, spirituality plays a pretty strong role in the experiences we share.  One of the strangest things I've noticed is that for those of us who had our NDEs as a result of some horrific accident, while in most cases the accident and its crazy circumstances would be the focus of any compelling story, an NDE negates that.Once an NDE enters the picture, you almost forget about the accident- it becomes the least important part of the story, next to the NDE.  My accident was amazing as accidents go, and I have an NDE friend who is only one of a handful in the world that she knows of who suffered and survived an internal decapitation.  But to NDE'ers, the circumstances that nearly, or do, kill us are just a footnote.  I'm sure that must be surprising, in some way.https://www.inbetweenproductions.com/https://www.amzn.com/dp/B098KQHX57/ https://www.pastliveshypnosis.co.uk/https://www.patreon.com/ourparanormalafterlife

The coelacanth was believed to have gone extinct about 66 million years ago, until one was spotted in South Africa in 1938. Naturalist and museum curator Marjorie Courtenay-Latimer played a key part in that event. Research: Ashworth, Willam B. Jr. “Scientist of the Day – Marjorie Courtenay-Latimer.” Linda Hall Library. 2/24/2020. https://www.lindahall.org/about/news/scientist-of-the-day/marjorie-courtenay-latimer/ Bruton, Mike. “Curator and Crusader: The Life and Work of Marjorie Courtenay-Latimer.” Pinetown Printers, 2019. Courtenay-Latimer, M. “My Story of the First Coelacanth.” Occasional Papers of the California Academy of Sciences. No. 134. 12/22/1979. https://www.biodiversitylibrary.org/page/15956893#page/18/mode/1up Courtenay-Latimer, Marjorie. “Reminiscences of the Discovery of the Coelacanth, Latimeria chalumnae.” Interdisciplinary Journal of the International Society of Cryptozoology. Vol. 8. 1989. Hatchuel, Martin. “The Coelacanth.” Knysna Museums. https://www.knysnamuseums.co.za/pages/the-coelacanth/ Jewett, Susan L. “Marjorie Courtenay-Latimer: More than the Coelacanth!” Division of Fishes, Smithsonian Institution. Schramm, Sally. “Marjorie Eileen Doris Courtenay-Latimer: Beyond the Coelacanth.” Biodiversity Heritage Library Blog. https://blog.biodiversitylibrary.org/2019/03/marjorie-eileen-doris-courtenay-latimer.html Smith, Anthony. “Marjorie Courtenay-Latimer.” The Guardian. 5/20/2004. https://www.theguardian.com/news/2004/may/21/guardianobituaries Smith, J.L.B. “The Living Cœlacanthid Fish from South Africa.” Nature 143, 748–750 (1939). https://doi.org/10.1038/143748a0 Smith, J.L.B. “The Search Beneath the Sea: The Story of the Coelacanth.” New York. Holt. 1956. Smith, J.L.B. Living Fish of Mesozoic Type.” Nature 143, 455–456 (1939). https://doi.org/10.1038/143455a0 The Coelacanth : the Journal of the Border Historical Society. Vol. 42 No. 1 (2004). https://journal.ru.ac.za/index.php/Coelacanth/issue/view/143 Tyson, Peter. “Moment of Discovery.” PBS Nova. https://www.pbs.org/wgbh/nova/fish/letters.html Weinberg, Samantha. “A Fish Caught in Time: the Search for the Coelacanth.” New York : HarperCollins Publishers. 2001. Yanes, Javier. “The Woman Who Brought a Fish Back From the Dead.” BBVA Open Mind. 2/17/2023. https://www.bbvaopenmind.com/en/science/leading-figures/marjorie-courtenay-latimer-fossil-fish-coelacanth/ See omnystudio.com/listener for privacy information.