Podcasts about idh

Brasil sobe cinco posições em ranking de IDH e supera patamar pré-pandemia pela primeira vez. E Conclave para escolher novo papa começa hoje no Vaticano.See omnystudio.com/listener for privacy information.

Economista diz que IDH brasileiro tem tudo para subir ainda mais.

Confira nesta edição do JR 24 Horas: O Brasil subiu cinco posições no ranking do Índice de Desenvolvimento Humano, o IDH. Os dados divulgados pelo Programa de Desenvolvimento das Nações Unidas são referentes a 2023. O Brasil aparece na 84ª posição da lista de 193 países. No ano anterior, o Brasil estava na 89ª posição. O documento leva em consideração os indicadores de expectativa de vida, escolaridade e produto interno bruto per capita, ou seja, por pessoa. E ainda: Diesel fica R$ 0,16 mais barato nas refinarias.

Confira nesta edição do JR 24 Horas: O chefe de uma quadrilha especializada em roubar motos de luxo foi preso, nesta terça-feira (6), na zona leste de São Paulo. Durante a operação, a polícia localizou também um desmanche clandestino de motos. A quadrilha tinha como alvo preferencial motocicletas de luxo, que custam mais de R$ 100 mil. A polícia chegou aos criminosos com a ajuda de um rastreador em uma das motos roubadas. E ainda: Brasil avança cinco posições e chega ao 84° lugar no ranking internacional de IDH das Nações Unidas.

No podcast ‘Notícia No Seu Tempo’, confira em áudio as principais notícias da edição impressa do jornal ‘O Estado de S.Paulo’ desta terça-feira (06/05/2025): Nomeado na sexta-feira em substituição a Carlos Lupi, o novo ministro da Previdência Social, Wolney Queiroz, assinou proposta quando era deputado federal, em 2021, que adiou o prazo de fiscalização do desconto de mensalidades feito por associações e sindicatos na folha de pagamento de aposentados e pensionistas do INSS. A medida foi levada à Câmara por duas associações agora suspeitas de efetuar as cobranças indevidamente. Procurado, Wolney Queiroz não comentou. Uma medida provisória assinada pelo então presidente Jair Bolsonaro (PL), em 2019, estabelecia que todos os descontos na folha de pagamento precisariam ser revalidados ano a ano. Após o lobby de associações que se beneficiaram com esses descontos, o prazo foi adiado duas vezes e a necessidade de revalidação foi extinta em 2022. Wolney Queiroz estava presente na reunião em que Lupi foi alertado sobre as fraudes no INSS, em junho de 2023. E mais: Política: Com baixa aprovação entre as mulheres, Lula confirma troca de ministra da pasta Metrópole: Cardeais discutem divisões da Igreja Internacional: Netanyahu aprova plano para ampliar campanha militar e ‘capturar’ GazaSee omnystudio.com/listener for privacy information.

O Brasil subiu cinco posições no relatório de Desenvolvimento Humano produzido pelo Programa de Desenvolvimento das Nações Unidas. O Brasil aparece na posição 84 de um total de 193 países. A colocação é baseada em informações referentes ao ano de 2023, como expectativa de vida, escolaridade e PIB per capita.O Giro de Notícias mantém você por dentro das principais informações do Brasil e do mundo. Confira mais atualizações na próxima edição.

Na terceira edição deste boletim você confere:- Wall Street Journal diz que China parou de divulgar índices econômicos nos últimos anos;- Índia e Reino Unido firmam acordo de livre comércio;- Brasil sobe 5 posições no ranking de IDH da ONU.O Boletim Rádio Gazeta Online é um conteúdo produzido diariamente com as principais notícias do Brasil e do mundo. Esta edição contou com a apresentação da monitora Maria Eduarda Palermo, do curso de Jornalismo.Escute agora!

Texcoco  estrena la Universidad para el Bienestar "Benito Juárez García  Abierta convocatoria para operadoras de TrolebúsIrreversible la victoria de Albanese en Australia  Más información en nuestro podcast

Dr. Nimish Mohile and Dr. Jaishri Blakeley share the new rapid recommendation update to the therapy for diffuse astrocytic and oligodendroglial tumors in adults guideline. They review the evidence from the INDIGO trial that prompted this update, and how to incorporate the use of vorasidenib into clinical practice. They discuss the importance of molecular testing, particularly for IDH1 or IDH2 mutations and outstanding questions for treatment of patients with oligodendrogliomas and astrocytomas. Read the latest update, “Therapy for Diffuse Astrocytic and Oligodendroglial Tumors in Adults: ASCO-SNO Guideline Rapid Recommendation Update.” Transcript This guideline, clinical tools, and resources are available at http://www.asco.org/neurooncology-guidelines. Read the full text of the guideline and review authors' disclosures of potential conflicts of interest in Journal of Clinical Oncology.   Brittany Harvey: Hello and welcome to the ASCO Guidelines podcast, one of ASCO's podcasts delivering timely information to keep you up to date on the latest changes, challenges and advances in oncology. You can find all the shows, including this one at asco.org/podcasts.   My name is Brittany Harvey and today I'm interviewing Dr. Jaishri Blakeley from Johns Hopkins University School of Medicine and Dr. Nimish Mohile from the Department of Neurology and Wilmot Cancer Institute at the University of Rochester Medical Center, co-chairs on “Therapy for Diffuse Astrocytic and Oligodendroglial Tumors in Adults: American Society of Clinical Oncology-Society for Neuro-Oncology Guideline Rapid Recommendation Update.”  Thank you for being here today, Dr. Blakeley and Dr. Mohile.  Dr. Jaishri Blakeley: Thank you.  Dr. Nimish Mohile: Thank you for having us.  Brittany Harvey: And then before we discuss this guideline, I'd like to note that ASCO takes great care in the development of its guidelines and ensuring that the ASCO Conflict of Interest Policy is followed for each guideline. The disclosures of potential conflicts of interest for the guideline panel, including Dr. Blakeley and Dr. Mohile who have joined us here today, are available online with the publication of the guideline in the Journal of Clinical Oncology, which is linked in the show notes.   So then, to jump into the content here, Dr. Mohile, could you start us off by describing what prompted this rapid update to the ASCO-SNO therapy for diffuse astrocytic and oligodendroglial tumors in adults guideline, which was previously published in 2021?  Dr. Nimish Mohile: Yeah. So the key reason for this update is the publication of a study in 2023. And this was a study called the INDIGO study that looked at a new class of therapies, something called IDH inhibitors. And in this study with a drug called vorasidenib, changed how we think about the treatment of oligodendrogliomas and astrocytomas, so particularly the grade 2 oligodendrogliomas and grade 2 astrocytomas. Because of the results of that study, we decided that we needed to do an update to inform clinicians about some of these changes and how we might approach these tumors differently today.  Brittany Harvey: Great. I appreciate that background. So then, based off the new data from the INDIGO study, what are the updated and new recommendations from the expert panel?  Dr. Nimish Mohile: So the key findings from the INDIGO study involved people who had grade 2 astrocytomas and grade 2 oligodendrogliomas. And in the setting after surgery, they were treated with vorasidenib, and what they found is that this delayed the time to next intervention. And the key aspect of that is that it delayed when we could start radiation and chemotherapy in these patients.   So what we did in the guidelines is that for both low grade oligodendrogliomas and low grade astrocytomas, we added one additional guideline statement. Our previous guideline in 2021 offered the options for observation or treatment with radiation and chemotherapy. And now in this guideline, we have options for observation, treatment with vorasidenib in those in whom we feel it is safe to defer radiation and chemotherapy, and then treatment with radiation and chemotherapy. So we've added in an additional option here. And the key message of the guideline is really on how, as clinicians, we think about using the vorasidenib and what the ideal setting for using the vorasidenib is.  Brittany Harvey: Excellent. It's great to hear about this new option for patients. So then you were just talking about how we think about who to offer this IDH inhibitor to. So, Dr. Blakeley, what should clinicians know as they implement these new recommendations into practice?  Dr. Jaishri Blakeley: Yes. So, first and foremost, let's go back to 2021, and a key note from those guidelines was the importance of molecular testing. And at that point, the importance of molecular testing, which in large part was focused on IDH1 or IDH2 mutations, was prognostic. We could say there's a difference in an IDH1 mutant astrocytoma and an IDH1 wild type astrocytoma, but we didn't have a specific therapeutic recommendation attached to that, like Dr. Mohile just said. And the big shift here is now we have a specific therapeutic for that population with IDH1 or IDH2 mutant glioma.   So for clinicians, we hope that they've been getting molecular testing on newly diagnosed glioma already, but now there's an additional motivation to do so because it may change your treatment plan in the right circumstance. So since the publication of the phase III INDIGO study that Dr. Mohile mentioned, and the FDA approval of vorasidenib, if you meet the specified criteria in the clinical trial - which the guidelines point out is a little different than what's on the FDA label, so clinicians might want to dig into that a little bit - then there is a treatment option that is new and different than combined chemoradiation or radiation alone or observation.  Brittany Harvey: I appreciate those clarifications there.   So then also, Dr. Blakeley, how does this update impact patients with astrocytic or oligodendroglial tumors?  Dr. Jaishri Blakeley: So first, patients also should know if they have IDH mutant gliomas. And this update only applies to people with IDH1/2 mutant glioma. Perhaps, we're not sure, it might only apply to people who are in the newly or newly-ish diagnosed category because the INDIGO study required that people were within the first five years of their surgical diagnosis and had not had other treatment. So there are a lot of people who have astrocytoma or oligodendroglioma who may or may not know their IDH1/2 status and may have already had another therapy - this update doesn't apply to them. We hope that future research will teach us about that. This update is for people who are newly diagnosed and just starting the journey to figure out the best therapy. It does say that if you do have that IDH1/2 alteration in your tumor, there is a drug therapy that is different from the drug therapies we would offer gliomas that do not have the IDH1/2 mutation.  Brittany Harvey: Absolutely. I think both that emphasis on molecular testing is very important and also thinking about that study inclusion criteria and how it impacts who's eligible for this treatment.   So then finally, Dr. Mohile, what are the outstanding questions about vorasidenib or other interventions for gliomas in adults?  Dr. Nimish Mohile: I think the key question for clinicians is exactly who we're going to use this in. The challenges with inclusion criteria in clinical trials is they don't actually always match what we're seeing in the clinic. And I think it brings up the question of, in low grade oligodendrogliomas which we think of as very slow growing tumors, do we have the option outside of the strict inclusion criteria to use that drug in other settings? I think it brings up the question for some clinicians in some of the higher grade tumors, in the grade 3 tumors, we don't yet have data in that area and our guideline doesn't address that. But I think some will be asking what the clinical activity of vorasidenib is in that setting. There are some suggestions that the IDH inhibitors may impact seizure control, and I think that that's data that we're continuing to wait on.   So I think that there's several outstanding questions there that we will have answers for hopefully in the next several years. I think the big question that we don't have an answer for and that will take a long time to know is whether the addition of vorasidenib in this setting actually improves how long people live. And given how long people with low grade oligodendrogliomas and low grade astrocytomas live today, we probably won't have an answer to that question for more than a decade.  Brittany Harvey: Definitely. We'll look forward to these ongoing developments and eventually longer term data on overall survival on these agents.   So, I want to thank you both so much for your work to rapidly include this information from this new trial. And thank you for your time today, Dr. Blakeley and Dr. Mohile.  Dr. Jaishri Blakeley: Thank you so much.  Dr. Nimish Mohile: Thank you Brittany.  Brittany Harvey: And thank you to all of our listeners for tuning in to the ASCO Guidelines podcast. To read the full guideline, go to www.asco.org/neurooncology-guidelines. You can also find many of our guidelines and interactive resources in the free ASCO Guidelines app, which is available in the Apple App Store or the Google Play Store. If you have enjoyed what you've heard today, please rate and review the podcast and be sure to subscribe so you never miss an episode.    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. 

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Dr. John Sweetenham and Dr. James Foran discuss the evolving treatment landscape in acute myeloid leukemia, including new targeted therapies, advances in immunotherapy, and the current role for allogeneic transplantation. TRANSCRIPT Dr. John Sweetenham: Hello, I'm Dr. John Sweetenham, the host of the ASCO Daily News Podcast. There has been steady progress in the therapies for acute myeloid leukemia (AML) in recent years, largely based on an increasing understanding of the molecular mechanisms which underlie the disease. On today's episode, we'll be discussing the evolving treatment landscape in AML. We'll explore risk group stratification, new targeted therapies, advances in immunotherapy for AML, and also a little about the current role for allogenic transplantation in this disease.  I'm delighted to welcome Dr. James Foran to this discussion. Dr. Foran is a professor of medicine and chair of the Myeloid Malignancies and Blood and Marrow Transplant Disease Group at the Mayo Clinic Comprehensive Cancer Center. He's based in Jacksonville, Florida.  Our full disclosures are available in the transcript of this episode.  James, it's great to have you join us on the podcast today, and thanks so much for being here. Dr. James Foran: I'm delighted and thank you for the invitation. Thank you very much. Dr. John Sweetenham: Sure, James, let's get right into it. So, our understanding of the molecular mechanisms underlying AML has resulted not only in new methods for risk stratification in this disease, which have added refinement to cytogenetics, but also has resulted in the development of many new targeted agents. Understanding that this is a complex area of investigation, and our time is somewhat limited, can you give us a high-level update on the current state of the art in terms of how risk factors are being used for treatment selection now? Dr. James Foran: Absolutely. I think in the past, you know, we had things broken down pretty simply into make a diagnosis based on morphology, do cytogenetics, break patients into the groups of those who were more likely to benefit from therapy – so-called favorable risk – those where the intensive therapies were less likely to work – so-called poor adverse risk, and then this large intermediate group that really had variable outcomes, some better, some worse. And for a long time, the progress was in just identifying new subtle cytogenetic risk groups. And then, late 1990s, we began to understand that FLT3 mutations or NRAS mutations may be more adverse than others that came along. In the first part of this millennium, in the, you know, 2000-2010 range, a lot of work was being done to understand better or worse risk factors with single genes. The ability to do multiplex PCR, and then more recently NGS platforms, have allowed us to really look at many genes and identify many mutations in patients. At the beginning that was used just to sort of refine – who did a little better, who did a little worse with intensive therapy – helped us decide who may benefit more from an allogeneic transplanter for whom that would not be necessary.  But the good news is that really, we're now starting to target those mutations. One of the first molecularly targeted treatments in leukemia was FLT3 mutations, where we knew they were adverse. Then along came targeted treatments. I was involved in some of those early studies looking at sunitinib, sorafenib, more recently midostaurin, now quizartinib, FDA approved, and gilteritinib in the relapse refractory setting.  So we're moving into a state where we're not just refining prognosis, we're identifying targets. You know, it's been slow progress, but definite incremental progress in terms of outcomes by looking for FLT3 mutations, then looking for IDH mutations, and more recently, mutations involving NPM1 or rearrangement of what we used to call the MLL gene, now the lysine methyltransferase 2A or KMT2A rearrangement, where we now have targets. And it's not just for refinement of prognosis, but now we're identifying therapeutic targets for patients and ways to even look for measurable residual disease which is impacting our care. Dr. John Sweetenham: That's great, James. And I'm going to expand on that theme just a little bit and perhaps ask you to elaborate a little bit more on how the introduction of these new therapies have specifically impacted frontline therapy. And a couple of ancillary questions maybe to go along with that: First of all, is ‘7+3' a standard therapy for anybody in 2025? And maybe secondly, you know, could you comment also maybe briefly on older patients with AML and how you think maybe the treatment landscape is changing for them compared with, say, 5 or 10 years ago? Dr. James Foran: I'll start with the therapy and then work my way back. So we've had ‘7+3' cytarabine daunorubicin or cytarabine anthracycline since 1976, and we're still using it as the backbone of our intensive therapy. There is still an important role for it, particularly in younger or fitter patients, and particularly for those with intermediate or favorable risk genetic groups or cytogenetic risk groups just because we achieve high rates of remission. Our 30-day induction mortality rates are lower now than they were 10 and 20 years ago. Our supportive care is better. And we still have a busy inpatient hospital service here at Mayo Florida and my colleagues in Rochester and Arizona as well giving intensive therapy. So that remains the backbone of curative therapy for younger adults. We are trying to be a little more discriminating about who we administer that to. We are trying to add targeted agents. We know from, now, two different randomized trials that the addition of a FLT3 inhibitor, either midostaurin or more recently quizartinib, has a survival advantage in patients with a FLT3 mutation, or for quizartinib, a FLT3/ITD mutation. And so yes, ‘7+3' remains important.  Off protocol for somebody who just comes in with acute leukemia in a 40-year-old or 30-year-old or even early 60s and fit, we would still be considering ‘7+3' therapy and then waiting for an expedited gene mutation panel and an expedited cytogenetics panel to come back to help us discriminate is that a patient for whom we should be giving a FLT3 inhibitor? I think there's a little more nuance about when we do a day 14 bone marrow, do they really matter as much anymore? I still do them. Some of my colleagues find them less important. But we're still giving intensive therapy. We're still giving high-dose ARA-C consolidation for younger patients who achieve complete remission.  In older adults, it's a different story. You know, it was only in the early part of the 2000s – 2004, 2007 range – where we really got buy-in from randomized studies that low-dose therapy was better than no therapy. There was a lot of nihilism before then about therapy for older adults, especially over age 75. We know that low-dose ARA-C is better than nothing. It looked like azacitidine was better than ARA-C or at least equivalent or slightly better. But with the advent of venetoclax it was a game changer. I ran a national randomized study of intensive therapy in AML. It was the last national randomized study of intensive therapy in older patients right before venetoclax got approved. And we were very excited about our results, and we thought we had some really interesting clinical results. And suddenly that's a little bit obsolete in patients over 70 and particularly over age 75 because of the high remission rates with azacytidine venetoclax or hypomethylating agents, so-called HMAs and venetoclax and the survival advantage. Now, it's not a home run for everybody. We quote 60% to 70% remission rates, but it's a little different based on your cytogenetics and your mutation profile. You have to continue on therapy so it's continuous treatment. It's not with curative intent, although there are some people with long-term remission in it. And the median survival went from 10 months to 15 months. So home run? No, but definitely improved remissions, meaningful for patients off transfusions and better survival. So right now it's hard to find an older adult who you wouldn't give azacitidine and venetoclax or something similar, decitabine, for instance, and venetoclax, unless somebody really was moribund or had very poor performance status or some reason not to. And so ‘7+3' is still relevant in younger adults. We're trying to get better results with ‘7+3' by adding targeted agents and azacitine and venetoclax in older adults.  I think the area of controversy, I guess there are two of them, is what to do in that overlap age between 60 and 75. Should people in that age still get intensive therapy, which we've used for years – the VIALE-A trial of aza-venetoclax was age 75 plus – or with cardiac comorbidities? And I think if you're 68 or 72, many of us are starting to bias towards aza-venetoclax as generally being better tolerated, generally being more outpatient, generally being slow and steady way to get a remission. And it doesn't stop you from going to transplant for somebody who might still be a candidate.  The other area of controversy is somebody under 60 who has adverse cytogenetics where we don't do very well with ‘7+3,' we still give it and we might do just as well with decitabine venetoclax. A lot of us feel that there's equipoise in the 60 to 75 group where we really can ask a question of a randomized study. Retrospective studies might suggest that intensive therapy is a little better, but there are now a couple of randomized studies happening saying, “Can we replace ‘7+3' in that intermediate age with aza-venetoclax?” And for younger adults similarly, we're looking to see how we apply that technology. Those are the areas where we're really trying to investigate what's optimal for patients and that's going to require randomized trials. Dr. John Sweetenham: Oh, that's great, thank you. And I'll just extend that question a little bit more, particularly with respect to the new targeted therapies. How much are they impacting the treatment of these patients in the relapse and refractory setting now? Dr. James Foran: Oh, they're definitely impacting it. When I trained and probably when you trained, AML was still a medical emergency. But that was the thing that you admitted to the hospital immediately, you started therapy immediately. The rule was always that's the one thing that brings the fellow and the consultant in at night to see that new patient on a Friday or Saturday. Now, we'll still admit a patient for monitoring, but we try not to start therapy for the first three or five or seven days if they're stable, until we get those genetics and those genomics back, because it helps us discriminate what therapy to pursue. And certainly, with FLT3 mutations, especially FLT3/ITD mutations, we're adding FLT3 inhibitors and we're seeing a survival advantage. Now, on the surface, that survival advantage is in the range of 7% or 10%. But if you then pursue an allogeneic transplant in first remission, you're taking disease where we used to see 30%, 40% long-term survival, maybe less, and you're pushing that to 60%, 70% in some studies. And so we're now taking a disease that– I don't want to get off topic and talk about Ph+ ALL. But that's a disease where we're actually a little excited. We have a target now, and it used to be something really adverse and now we can do a lot for it and a lot about it.  The other mutations, it's a little more subtle. Now, who knew until 2010 that a mutation in a sugar metabolism gene, in isocitrate dehydrogenase, or IDH was going to be so important, or even that it existed. We know that IDH1 and IDH2 mutations are still a minority of AML, certainly less than 10% to 15%, maybe overall. But we're able to target those with specific IDH1 and IDH2 inhibitors. We get single-agent responses. There are now two approved IDH1 inhibitors on the market. We don't yet have the randomized data that adding those to intensive therapy is better, but we're getting a very strong hint that it might be better in older adults who have an IDH mutation, maybe adding those is helpful and maybe adding those to low-intensity therapy is helpful. Those studies are ongoing, and we're also trying with low-intensity treatments to add these agents and get higher remission rates, deeper remissions, longer remissions. I think a lot of work has to be done to delineate the safety of that and the long-term efficacy. But we're getting hints it's better, so I think it is impacting.  The other area it's impacting is when you pick up adverse mutations and those have crept into our classification systems like an ASXL1 mutation or RUNX1 mutation for instance, or some of the secondary AML mutations like BCOR and others, where that's helping us discriminate intermediate-risk patients who we think aren't going to do as well and really helping us select a group who's more likely to get benefit from allogeneic transplant or for whom at least our cure rates without allo transplant are low. And so I think it's impacting a lot. Dr. John Sweetenham: Great. And I'm going to pick up now, if I may, on a couple of things that you've just mentioned and continue the theme of the relapsed and refractory setting. We've started to see some reports which have looked at the role of immune strategies for patients with AML, in particular CAR T or NK cells. Can you comment a little on this and let us know whether you think either these two strategies or other immune strategies are likely to have a significant role in AML in the future? Dr. James Foran: They are, but I think we're still a step behind finding the right target or the right way to do it. If you think of allogeneic transplantation as the definitive immune therapy, and we know for adverse AML we can improve survival rates and cure rates with an allotransplant, then we know inherently that immune therapy matters. And so how do we do what they've done in large cell lymphoma or in CD19 targeting for B cell malignancies? How do we bring that to acute myeloid leukemia? There have been a number of efforts. There have been at least 50 trials looking at different targets. CD33, CD123, CD7, others, CLL-1. So, there have been a number of different trials looking at how to bind a CAR T or a CAR T construct that can be active. And we have hints of efficacy. There was kind of a provocative paper in the New England Journal of Medicine a year ago in April of last year from a Chinese group that looked at a CD7-based CAR T and it was 10 patients, but they used CD7 positive acute leukemia, AML or ALL and had a CD7-targeted CAR T and they actually incorporated that with a haploidentical transplant and they had really high remission rates. People tolerated it quite well. It was provocative. It hasn't yet been reproduced on a larger scale, but the strong hints that the strategy is going to work.  Now, CD33 is a little tricky to have a CAR T when CD33 is expressed on normal hematopoietic cells. CD123 likewise. That's been something where there's, I think, still promise, but we've struggled to find the trials that make that work. Right now, there's a lot of interest in leveraging NK cells and looking, for a couple of reasons, but NK cells are attractive and NK cell markers might be attractive targets. NK cells might have similar degrees of immune efficacy. It's speculative, but they are likely to have less cytokine release syndrome and less neurotoxicity than you see with CAR T. And so it's kind of attractive to leverage that. We have had some ongoing trials looking at it with bispecifics and there certainly are trials looking at it with CAR NK-based strategies. One of the antigens that people looked at is the NK group 2D. NK group 2D or NKG2D is overexpressed in AML and its ligands overexpressed. And so that's a particular potential target. So, John, it's happening and we're looking for the hints of efficacy that could then drive a pivotal trial to get something approved.  One of the other areas is not restricting yourself just to a single antigen. For instance, there is a compound that's looking at a multi-tumor-associated antigen-specific T-cell therapy, looking at multiple antigens in AML that could be overexpressed. And there were some hints of activity and efficacy and actually a new trial looking at a so-called multi-tumor associated antigen-specific T cell therapy. So without getting into specific conflicts of interest or trials, I do think that's an exciting area and an evolving area, but still an investigational area. I'll stop there and say that we're excited about it. A lot of work's going there, but I'm not quite sure which direction the field's going to pivot to there. I think that's going to take us some time to sort out. Dr. John Sweetenham: Yeah, absolutely. But as you say, exciting area and I guess continue to watch this space for now.  So you've mentioned allogeneic stem cell transplants two or three times during this discussion. Recognizing that we don't have an imatinib for AML, which has kind of pushed transplant a long way further back in the treatment algorithm, can you comment a little on, you know, whether you think the role of stem cell transplantation is changing in AML or whether it remains pretty much as it was maybe 10 years ago? Dr. James Foran: By the way, I love that you use imatinib as an introduction because that was 6 TKIs ago, and it tells you the evolution in CML and you know, now we're looking at myristoyl pocket as a target, and so on. That's a great way to sort of show you the evolution of the field.  Allogeneic transplant, it remains a core treatment for AML, and I think we're getting much smarter and much better about learning how to use it. And I'm just going to introduce the topic of measurable residual disease to tell you about that. So I am a little bit of a believer. Part of my job is I support our allogeneic transplant program, although my focus is acute myeloid leukemia, and I've trained in transplant and done it for years and did a transplant fellowship and all that. I'm much more interested in finding people who don't need a transplant than people who do. So I'm sort of looking for where can we move away from it. But it still has a core role. I'll sidestep and tell you there was an MDS trial that looked at intermediate or high-risk MDS and the role of allogeneic transplant that shows that you about double your survival. It was a BMT CTN trial published several years ago that showed you about double your three-year survival if you can find a donor within three months and get to a transplant within six months. And so it just tells you the value of allotransplant and myeloid malignancy in general. In AML we continue to use it for adverse risk disease – TP53 is its own category, I can talk about that separately – but adverse risk AML otherwise, or for patients who don't achieve a really good remission. And I still teach our fellows that an allotransplant decreases your risk of relapse by about 50%. That's still true, but you have to have a group of patients who are at high enough risk of relapse to merit the non-relapse mortality and the chronic graft versus host disease that comes with it. Now, our outcomes with transplant are better because we're better at preventing graft versus host disease with the newer strategies such as post-transplant cyclophosphamide. There are now new FDA-approved drugs for acute and chronic graft versus host disease, ruxolitinib, belumosudil, axatilimab now. So we have better ways of treating it, but we still want to be discriminating about who should get it.  And it's not just a single-minded one-size-fits-all. We learned from the MORPHO study that was published in the JCO last year that if you have FLIT3-positive AML, FLIT3/IDT-positive AML, where we would have said from retrospective studies that your post-transplant survival is 60% give or take, as opposed to 15% or 20% without it, that we can discriminate who should or shouldn't get a transplant. Now that trial was a little bit nuanced because it did not meet its primary endpoint, but it had an embedded randomization based upon MRD status and they used a very sensitive test of measurable residual disease. They used a commercial assay by Invivoscribe that could look at the presence of a FLT3/ITD in the level of 10 to the minus 5th or 10 to the minus 6th. And if you were MRD-negative and you went through a transplant, you didn't seem to get an advantage versus not. That was of maintenance with gilteritinib, I'll just sort of put that on there. But it's telling us more about who should get a transplant and who shouldn't and who should get maintenance after transplant and who shouldn't.  A really compelling study a year ago from I don't know what to call the British group now, we used to call them the MRC and then the NCRI. I'm not quite sure what to call their studies at the moment. But Dr. Jad Othman did a retrospective study a year ago that looked at patients who had NPM1 mutation, the most common mutation AML, and looked to see if you were MRD positive or MRD negative, what the impact of a transplant was. And if you're MRD negative there was not an advantage of a transplant, whereas if you're MRD positive there was. And when they stratified that by having a FLT3 mutation that cracked. If you had a FLT3 mutation at diagnosis but your NPM1 was negative in remission, it was hard to show an advantage of a transplant. So I think we're getting much more discriminating about who should or should not get a transplant by MRD testing for NPM1 and that includes the patients who have a concomitant FLT3 mutation. And we're really trying to learn more and more. Do we really need to be doing transplants in those who are MRD-negative? If you have adverse risk genetics and you're MRD-negative, I'll really need good data to tell me not to do a transplant, but I suspect bit by bit, we'll get that data. And we're looking to see if that's really the case there, too. So measurable residual disease testing is helping us discriminate, but there is still a core role of allogeneic transplant. And to reassure you, compared to, I think your allotransplant days were some time ago if I'm right. Dr. John Sweetenham: Yes. Dr. James Foran: Yeah. Well, compared to when you were doing transplants, they're better now and better for patients now. And we get people through graft versus host disease better, and we prevent it better. Dr. John Sweetenham: That's a great answer, James. Thanks for that. It really does help to put it in context, and I think it also leads us on very nicely into what's going to be my final question for you today and perhaps the trickiest, in a way. I think that everything you've told us today really emphasizes the fact that the complexity of AML treatment has increased, primarily because of an improved understanding of the molecular landscape of the disease. And it's a complicated area now. So do you have any thoughts on what type of clinical environment patients with AML should be evaluated and treated in in 2025? Dr. James Foran: Yeah, I want to give you a kind of a cautious answer to that because, you know, I'm a leukemia doctor. I work at a leukemia center and it's what we focus on. And we really pride ourselves on our outcomes and our diagnostics and our clinical trials and so on. I am very aware that the very best oncologists in America work in private practice and work in community practice or in networks, not necessarily at an academic site. And I also know they have a much harder job than I have. They have to know lung cancer, which is molecularly as complicated now as leukemia, and they have to know about breast cancer and things that I don't even know how to spell anymore. So it's not a question of competence or knowledge. It's a question of infrastructure. I'll also put a little caveat saying that I have been taught by Rich Stone at Dana-Farber, where I did a fellowship a long time ago, and believe Rich is right, that I see different patients than the community oncologists see with AML, they're seeing different people. But with that caveat, I think the first thing is you really want to make sure you've got access to excellence, specialized hematopathology, that you can get expedited cytogenetics and NGS testing results back. There was a new drug, approved just a few months ago, actually, for relapsed AML with a KMT2A rearrangement, revumenib. We didn't talk about the menin inhibitors. I'll mention them in just a second. That's a huge area of expansion and growth for us. But they're not found on NGS platforms. And normal cytogenetics might miss a KMT2A-rearrangement. And we're actually going back to FISH panels, believe it or not, on AML, to try to identify who has a KMT2A-rearrangement. And so you really want to make sure you can access the diagnostic platforms for that.  I think the National Referral Labs do an excellent job. Not always a really fast job, but an excellent job. At my institution, I get NGS results back within three days or four days. We just have an expedited platform. Not everybody has that. So that's the key, is you have to be able to make the diagnosis, trust the pathologist, get expedited results. And then it's the question of trying to access the targeted medications because a lot of them are not carried in hospital on formulary or take time to go through an insurance approval process. So that's its own little headache, getting venetoclax, getting gilteritinib, getting an IDH1 inhibitor in first line, if that's what you're going for. And so I think that requires some infrastructure. We have case managers and nurses who really expedite that and help us with it, but that's a lot of work. The other piece of the puzzle is that we're still with AML in the first month and maybe even the second month. We make everybody worse before we make them better. And you have to have really good blood bank support. I can give an outpatient platelet transfusion or red cell transfusion seven days a week. We're just built for that. That's harder to do if you're in a community hospital and you have to be collaborating with a local blood bank. And that's not always dead easy for somebody in practice. So with those caveats, I do find that my colleagues in community practice do a really good job making the diagnosis, starting people on therapy, asking for help. I think the real thing is to be able to have a regional leukemia center that you can collaborate with, connect with, text, call to make sure that you're finding the right patients who need the next level of diagnostics, clinical trial, transplant consults, to really get the best results.  There was some data at ASH a couple of years ago that looked at – the American Society of Hematology and ASCOs had similar reports – that looked at how do we do in academic centers versus community practice for keeping people on therapy. And on average, people were more likely to get six cycles of therapy instead of three cycles of therapy with azacitidine venetoclax at an academic center. Now, maybe it's different patients and maybe they had different cytogenetics and so on, but I think you have to be patient, I think you have to collaborate. But you can treat those patients in the community as long as you've got the infrastructure in place. And we've learned with virtual medicine, with Zoom and other platforms that we can deliver virtual care more effectively with the pandemic and beyond. So I think we're trying to offer virtual consults or virtual support for patients so they can stay in their home, stay in their community, stay with their oncologists, but still get access to excellent diagnostics and supportive care and transplant consults, and so on. I hope that's a reasonable answer to that question. It's a bit of a nuanced answer, which is, I think there's an important role of a leukemia center, and I think there's a really fundamental role of keeping somebody in the community they live in, and how we collaborate is the key to that. And we've spent a lot of time and effort working with the oncologists in our community to try to accomplish that.  John, I want to say two other things. I didn't mention in the molecular platforms that NPM1 mutations, we can now target those on clinical trials with menin inhibitors. We know that NPM1 signals through the Hoxa9/Meis1 pathway. We know that similar pathways are important in KMT2A rearrangements. We know that there are some other rare leukemias like those with NUP98 rearrangement. We can target those with menin inhibitors. The first menin inhibitor, revuminib, was approved by the FDA for KMT2A. We have others going to the FDA later this year for NPM1. There are now pivotal trials and advanced expanded phase 1/2 studies that are showing 30% response rates. And we're looking to see can we add those into the first-line therapy. So, we're finding more targets.  I'll say one last thing about molecular medicine. I know I'm a little off topic here, but I always told patients that getting AML was kind of like being struck by lightning. It's not something you did. Now, obviously, there are risk factors for AML, smoking or obesity or certain farm environments, or radioactive exposures and so on. But bit by bit, we're starting to learn about who's predisposed to AML genetically. We've identified really just in the last five or eight years that DDX41 mutations can be germline half the time. And you always think germline mutations are going to cause AML in a younger patient, but the median age is 60 to 70 just like other AMLs. They actually might do pretty well once they get AML. We've reported that in several papers. And so we're trying to understand who that has a RUNX1 mutation needs germline testing, who with a DDX41 needs germline testing. And we're trying to actually come up with a cleaner pathway for germline testing in patients to really understand predisposition, to help with donor selection, to help with family counseling. So I think those are other areas where a leukemia center can contribute for somebody in who's community practice to understand genomic or genetic complexity in these patients. And we're starting to develop the databases that support that. Dr. John Sweetenham: Yeah, great. Thanks, James. I loved your answer about the clinical environment too. And I know from a patient-centric perspective that I know that patients would certainly appreciate the fact that we're in a situation now where the folks taking care of them will make every effort to keep them close to home if they possibly can.  I want to thank you, James, for an incredible review of a very complex subject and I think you did a great job. I think we all will have learned a lot. And thanks again for being willing to share your insights with us today on the ASCO Daily News Podcast. Dr. James Foran: John, it's my pleasure. And as you know, I'll do anything for a latte, so no problem at all. Dr. John Sweetenham: Okay. I owe you one, so thank you for that.  And thank you to our listeners for your time today. You'll find links to the studies we've discussed today in the transcript of this episode. And finally, if you value the insights that you hear on the ASCO Daily News Podcast, please take a moment to rate, review and subscribe wherever you get your podcasts. Disclaimer: The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity or therapy should not be construed as an ASCO endorsement. Find out more about today's speakers:  Dr. John Sweetenham  Dr. James Foran Follow ASCO on social media: @ASCO on Twitter ASCO on Bluesky ASCO on Facebook  ASCO on LinkedIn  Disclosures:    Dr. John Sweetenham:    No relationships to disclose Dr. James Foran: Stock and Other Ownership Interests: Aurinia Pharmaceuticals Consulting or Advisory Role: Peerview, CTI BioPharma Corp, Remix Therapeutics, Cardinal Health, Medscape, Syndax, Autolus Therapeutics Research Funding (Inst.): Chordia Therapeutics, Abbvie, Actinium Pharmaceuticals, Kura Oncology, Sellas Life Sciences, Novartis, Roivant, Celgene/Bristol-Myers Squibb, Astellas Pharma, SERVIER Travel, Accommodations, Expenses: Peerview

This week, Jonathan is joined by Eytan Stein, Chief of the Leukaemia Service and an Attending Physician at Memorial Sloan Kettering Cancer Center, New York, USA.  Timestamps:      (00:00)-Introduction  (01:05)-The current landscape of treatments  (02:26)-The promise and peril of differentiation therapy  (05:55)-Highlighting the most impactful clinical trials  (08:38)-Epigenetics and the future of targeted therapies  (10:40)-The BEAT AML master clinical trial  (12:57)-The latest research into IDH inhibitors  (16:10)-Therapies for splicing factor mutations  (19:29)-Reducing patient fear with education   (22:46)-Stein's three wishes for healthcare   

“I didn't set out to be an entrepreneur, but when I couldn't find a company doing what I believed in, I built my own.” In part two of our conversation with Kate Yen, Founder and CEO of Auron Therapeutics, we explore her journey from leading a novel cancer therapy program at Agios to founding her own biotech company. Kate shares insights into drug development, clinical trials, and the business of biotech, highlighting the importance of translational biology, strategic partnerships, and lean operations in building a successful biotech startup. Kate earned her Ph.D. in Biological Chemistry from UCLA, where she also completed her postdoc. Before Auron, she held roles at Merck and as a UCLA professor before joining Agios Pharmaceuticals, where she led the IDH translational research team behind two FDA-approved IDH mutant inhibitors and co-led the discovery of vorasidenib, a promising glioma therapy now in clinical development.

Part 1 of 2: Our guest today is Kate Yen, Founder and CEO of Auron Therapeutics. Auron Therapeutics leverages cutting-edge science and AI-powered analysis to develop next-generation cancer therapies by mapping key drivers of tumorigenesis. Kate earned her Ph.D. in Biological Chemistry from UCLA, where she also completed her postdoc. She held roles at Merck and as a UCLA professor before joining Agios Pharmaceuticals, where she led the IDH translational research team behind two FDA-approved IDH mutant inhibitors and co-led the discovery of vorasidenib, a promising glioma therapy now in clinical development. With deep expertise in preclinical and clinical research, a proven track record in advancing breakthrough therapies, and a passion for oncology, Kate's journey and insights are invaluable.

En este episodio, Cam habla sobre algunos de los libros de los que ha aprendido cosas importantes para la vida real, en 4 categorías diferentes. Es como un Wrapped, pero de cultura. Muy culto todo.Libros mencionados en este episodio:Brillo de Raven LeilaniBreasts and Eggs de Mieko KawakamiAlas de Sangre, Alas de Hierro y Alas de Ónix de Rebecca YarrosUna corte de llamas plateadas de Sarah J. MaasMemorias de Idhún de Laura Gallego GarcíaLa emperatriz de los etéreos de Laura Gallego GarcíaBogotá con mar y otras cosas de Manuel Kalmanovitz G.Modern Love de Daniel JonesThe year of magical thinking de Joan DidionEverything I know about love de Dolly AldertonUn día cualquiera en Nueva York de Fran LebowitzAce: What Asexuality Reveals About Desire, Society, and the Meaning of sex de Angela ChenMi vida querida de Alice MunroPercy Jackson de Rick Riordan

In a conversation with CancerNetwork®, Shewetal Mehta, PhD, spoke about her research team's focuses in moving novel brain cancer therapies down the pipeline as part of an early phase clinical trials program at the Ivy Brain Tumor Center. Mehta, the deputy director and pre-clinical core leader at the Ivy Brain Tumor Center of Barrow Neurological Institute in Phoenix, Arizona, underscored a scientifically rigorous, patient-driven philosophy that drives her team members to deliver timely answers to those with brain cancer via work in a clinical lab and a pre-clinical arm. This collaboration helps identify therapeutic agents that may demonstrate activity in the brain while determining patient populations who are suitable to enroll on clinical trials. As part of her institution's early phase trial program, Mehta specifically highlighted work associated with a phase 0/1 clinical trial (NCT06072586) evaluating BDTX-1535, a brain-penetrant fourth-generation EGFR inhibitor, for those with recurrent high-grade glioma harboring oncogenic EGFR alterations or fusions.1 Investigators are incorporating liquid biopsy, sampling cerebrospinal fluid from patients on treatment to monitor potential evolutions or changes in brain tumors. Regarding biomarker testing, Mehta described the roles that gene sequencing and immunohistochemistry can play in identifying targetable alterations in patients with brain cancer. She mentioned vorasidenib (Voranigo), which received approval from the FDA in August 2024, as an example of a targeted therapy that may be suitable for use in patients who are found to have actionable IDH mutations. “Over the last year, we've seen that we were capable of not just doing these early phase clinical trials [but of entering] this phase of moving drugs into phase 3 [studies]. That's exciting,” Mehta stated regarding her outlook on the current state of brain cancer treatment. “Right now, we are excited about these new classes of agents that are within the space, like the proteolysis targeting chimeras, protein degraders, and antibody-drug conjugates, which have shown amazing promise in the rest of the oncology space.” References 1.        Study of BDTX-1535 in recurrent high-grade glioma (HGG) participants with EGFR alterations or fusions. ClinicalTrials.gov. Updated January 15, 2025. Accessed January 15, 2025. https://tinyurl.com/m6kwr2b3 2.        FDA approves vorasidenib for grade 2 astrocytoma or oligodendroglioma with a susceptible IDH1 or IDH2 mutation. News release. FDA. August 6, 2024. Accessed January 20, 2025. https://tinyurl.com/25r9fkvy

- Ngày 05/12/2024, Bộ Công Thương phối hợp với Tổ chức sáng kiến thương mại bền vững (IDH) và các Hiệp hội Dệt may Việt Nam, Hiệp hội Bông sợi Việt Nam và Hiệp hội Da giày và Túi xách Việt Nam tổ chức Hội thảo quốc tế “Hợp tác phát triển bền vững ngành Dệt may và Da giày Việt Nam”. Hội thảo là hoạt động đầu tiên thuộc khuôn khổ hợp tác giữa Bộ Công Thương và IDH về hỗ trợ phát triển bền vững đối với các ngành Dệt may và Da giày - các ngành hàng xuất khẩu chủ lực của Việt Nam. Tác giả : Nguyên Long Chủ đề : Bộ Công Thương, Tổ chức sáng kiến thương mại bền vững (IDH), Hiệp hội Dệt may Việt Nam, Hiệp hội Bông sợi Việt Nam, Hiệp hội Da giày và Túi xách Việt Nam, Phát triển bền vững --- Support this podcast: https://podcasters.spotify.com/pod/show/vov1sukien/support

El Dr. Elias Ortega Chahla, oncólogo clínico del Instituto de Oncología Ángel H. Roffo en Buenos Aires, Argentina, presenta un resumen de los estudios que considera más relevantes en el ámbito de tumores del sistema nervioso central expuestos durante el Congreso de ESMO 2024. Abstract 440O: estudio en humanos de la vacuna contra el cáncer basada en ARNm CVGBM en pacientes con glioblastoma no metilado MGMT (O-6-metilguanina-ADN metiltransferasa) recién diagnosticado y resecado quirúrgicamente: primeros resultados de la fase de aumento de dosis. Abstract 443O: estudio perioperatorio, abierto de un solo brazo para evaluar la viabilidad, la farmacocinética y la farmacodinamia del tratamiento con safusidenib después de la biopsia y antes de la resección quirúrgica en pacientes con glioma con mutación IDH1 que no han recibido radioterapia ni quimioterapia. Abstract 444O: el objetivo de este estudio fue evaluar el impacto pronóstico de las deleciones heterocigóticas de CDKN2A/B en astrocitomas y oligodendrogliomas de bajo grado con mutación IDH. GLORIA: estudio fase I/II de un solo brazo con aumento de dosis de NOX-A12 en combinación con irradiación en pacientes con glioblastoma de primera línea inoperable o parcialmente resecado con promotor MGMT no metilado con un grupo de expansión de múltiples brazos. Abstract 451: estudio fase Ib/II el cual evalúa GLAS-DHIV, un inhibidor oral que está siendo investigado principalmente en combinación con otros tratamientos como temozolomida en el contexto de glioblastoma de recién diagnóstico. Fecha de grabación: 26 de septiembre de 2024.                      Todos los comentarios emitidos por los participantes son a título personal y no reflejan la opinión de ScienceLink u otros. Se deberá revisar las indicaciones aprobadas en el país para cada uno de los tratamientos y medicamentos comentados. Las opiniones vertidas en este programa son responsabilidad de los participantes o entrevistados, ScienceLink las ha incluido con fines educativos. Este material está dirigido a profesionales de la salud exclusivamente.

In today's episode, supported by Servier Pharmaceuticals, we had the pleasure of speaking with Jennie W. Taylor, MD, MPH, about the FDA approval of vorasidenib (Voranigo) for patients with IDH-positive grade 2 astrocytoma or oligodendroglioma. Dr Taylor is an associate professor of clinical neurology at the University of California, San Francisco (UCSF), as well as the community engagement liaison in the Neurologic Oncology Program at the UCSF Helen Diller Family Comprehensive Cancer Center. On August 6, 2024, the FDA approved vorasidenib for the treatment of adult and pediatric patients at least 12 years of age with grade 2 astrocytoma or oligodendroglioma harboring susceptible IDH1 or IDH2 mutations who have previously undergone surgery including biopsy, sub-total resection, or gross total resection. This regulatory decision was backed by findings from the phase 3 INDIGO trial (NCY04164901), in which, at a median follow-up of 14.0 months (interquartile range [IQR], 10.1-17.9), vorasidenib (n = 168) produced a median progression-free survival of 27.7 months (95% CI, 17.0-not estimated) vs 11.1 months (95% CI, 11.0-13.7) in the placebo arm (n = 163) at a median follow-up of 14.3 months (IQR, 10.0-18.1; HR, 0.39; 95% CI, 0.27-0.56; P < .001). In our exclusive interview, Dr Taylor discussed the significance of this approval, key data from INDIGO, and where vorasidenib fits into the astrocytoma or oligodendroglioma treatment paradigms.

- Dệt may, da giày là hai lĩnh vực được Bộ Công Thương Việt Nam và Tổ chức Sáng kiến và thương mại bền vững Hà Lan (IDH) lựa chọn để hỗ trợ phát triển bền vững. Tại buổi lễ ký kết “Bản ghi nhớ hỗ trợ phát triển bền vững ngành Dệt may và Da giày Việt Nam” diễn ra hôm nay (26/09/2024), có 4 nội dung chính sẽ được triển khai trong thời gian 6 năm (giai đoạn 2024-2030) nhằm giảm thiểu dấu ấn môi trường của các lĩnh vực xuất khẩu chủ lực của Việt Nam, biến đổi theo các tiêu chuẩn toàn cầu. Trong đó, giải pháp sử dụng năng lượng tiết kiệm và hiệu quả được xác định có vai trò hết sức quan trọng đối với sản xuất và tiêu dùng bền vững và tăng trưởng xanh. Tác giả : Nguyên Long Chủ đề : Sử dụng năng lượng hiệu quả góp phần phát triển bền vững các ngành dệt may, da giày Việt Nam, IDH, Bản ghi nhớ hỗ trợ phát triển bền vững ngành Dệt may và Da giày Việt Nam --- Support this podcast: https://podcasters.spotify.com/pod/show/vov1sukien/support

Dr. Maya Graham interviews Drs. Mary Jane Lim-Fat and Kee Kiat Yeo about their recent manuscript entitled "A comparative analysis of IDH-mutant glioma in pediatric, young adult, and older adult patients", published online in Neuro-Oncology in July 2024. Link: https://doi.org/10.1093/neuonc/noae142

Welcome to OncLive On Air®! I'm your host today, Ashling Wahner.  OncLive On Air is a podcast from OncLive®, which provides oncology professionals with the resources and information they need to provide the best patient care. In both digital and print formats, OncLive covers every angle of oncology practice, from new technology to treatment advances to important regulatory decisions.  In today's episode, we had the pleasure of speaking with Tarita Thomas, MD, PhD, MBA, and Rimas Lukas, MD, about abstracts presented during a brain cancer­–focused clinical science symposium at the 2024 ASCO Annual Meeting. Dr Thomas is an associate professor of radiation oncology and Dr Lukas is an associate professor of neurology (neuro-oncology; hospital neurology) at the Northwestern University Feinberg School of Medicine in Chicago, Illinois.  In our exclusive interview, Drs Thomas and Lukas discussed the results of 4 abstracts presented during the symposium. In particular, their discussion highlighted findings with ST101 in window-of-opportunity cohorts of patients with recurrent glioblastoma (GBM), the prognostic utility of cerebrospinal fluid circulating tumor DNA in recurrent high-grade glioma, the genomic drivers of GBM, and preclinical data with navtemadlin (KRT-232) in IDH wild-type GBM.  ___ That's all we have for today! Thank you for listening to this episode of OncLive On Air. Check back on Mondays and Thursdays for exclusive interviews with leading experts in the oncology field.  For more updates in oncology, be sure to visit www.OncLive.com and sign up for our e-newsletters.  OncLive is also on social media. On X, follow us at @OncLive. On Facebook, like us at OncLive, and follow our OncLive page on LinkedIn.  If you liked today's episode of OncLive On Air, please consider subscribing to our podcast on Apple Podcasts, Spotify, Amazon Music, and many of your other favorite podcast platforms,* so you get a notification every time a new episode is posted. While you are there, please take a moment to rate us!  Thanks again for listening to OncLive On Air. 

Matthew Spencer, global director of landscapes at IDH, talks with Innovation Forum's Toby Webb about implementing landscape and jurisdictional approaches for sustainable land management. They share practical insights on stakeholder engagement, overcoming political challenges and scaling successful landscape models, using real-world examples from Kenya, Brazil and more.

En resumen, adoro leer. Mis recomendaciones: - Cumbres Borrascosas - El Libro de las Ilusiones - Cualquiera de Charles Bukowski - La Plaça del Diamant - Tú y Yo - Los 7 Maridos de Evelyn Hugo - Las Memorias de Idhún - El Nombre del Viento - Cualquiera de Emily Henry - La Buena Suerte Y otros que no he mencionado: - El Verano en que Rompimos las Normas - Romper el círculo Sígueme en ⁠Good Reads⁠!!!

This week: IDH's global director of landscapes talks with Innovation Forum's Toby Webb about the practicalities and challenges of implementing a landscape or jurisdictional approach to commodity sourcing. They discuss insights into how business and stakeholders can align their efforts for long-term sustainability and environmental protection, emphasising the importance of collaboration at both local and governmental levels.   Plus: cocoa giants including Mars Wrigley, Ferrero and Tony's Chocoloney back EUDR amid calls for delay; Nestlé's cocoa plan expands to Ghana to boost yield and farmer incomes; Adidas, PVH, Zalando join Fashion for Good's circular footwear initiative; and, global wind targets fall short of tripling goal, according to an environmental group Ember, in the news digest.   Host: Ian Welsh    IDH will be at the upcoming sustainable commodities and land use forum in Amsterdam (22nd-23rdOctober). If you'd like to continue the conversation, click here for more information on how to get involved.

Dr Bill Nelson talks with Dr Matthias Holdhoff about the treatment of brain cancer and a significant FDA approval of a new drug treatment for a type of brain cancer, called low-grade glioma. The drug, called vorasidenib, is a targeted cancer therapy that works by inhibiting the activity of a mutated gene called IDH, slowing the growth of the cancer. Read more here 

Dr. Maya Graham interviews Dr. Martin van den Bent about his and his team's recent review article entitled "The biological significance of age, enhancement, extent of resection and tumor grade in IDH mutant gliomas: how should they inform treatment decision in the era of IDH inhibitors? Invited review", published online in Neuro-Oncology in

Some consider the number 13 unlucky; fear of the number has its own name, "triskaidekaphobia." So it is perhaps somewhat fitting that day 13 of our ASCO Odyssey is dedicated to the cancer type with which scientists and doctors have had arguably the least luck in treating: central nervous system cancers. We still await CNS oncology's immunotherapy or EGFR/ALK moment, and unfortunately, as of ASCO 2024, that has not come yet. However, that has not stopped legions of incredibly dedicated and intelligent people from trying. ASCO 2024 brought us several very interesting studies, both in form and function, that we hope will lay the groundwork for that magical breakthrough in this very difficult group of cancers.Links to studies discussed in this episode (subscription may be required)A phase II trial of olaparib and durvalumab in patients with recurrent IDH-mutated gliomas. LinkEvaluation of VAL-083 in GBM AGILE, a phase 3 registration platform trial for newly diagnosed and recurrent glioblastoma. LinkN2M2/NOA-20: Phase I/IIa umbrella trial of molecularly matched targeted therapies plus radiotherapy in patients with newly diagnosed glioblastoma without MGMT promoter hypermethylation. LinkAlliance A071401: Phase II trial of abemaciclib in patients with grade 2/3 meningiomas harboring somatic NF2 or CDK pathway alterations. LinkFor more episodes, resources and blog posts, visit www.inquisitiveonc.comPlease find us on Twitter @InquisitiveOnc!If you want us to look at a specific trial or subject, email us at inquisitiveonc@gmail.comOncology for the Inquisitive Mind is recorded with the support of education grants from Pfizer, Gilead Pharmaceuticals and Merck Pharmaceuticals. Our partners have no editorial rights or early previews, and they have access to the episode at the same time you do.Art courtesy of Taryn SilverMusic courtesy of AlisiaBeats: https://pixabay.com/users/alisiabeats-39461785/Disclaimer: This podcast is for educational purposes only. If you are unwell, seek medical advice. Hosted on Acast. See acast.com/privacy for more information.

Radiology read to you! Andrew reads the Radiopaedia article on glioblastoma to Frank. Definitions have changed in this area over the last decade with IDH-wildtype molecular status now forming the basis of diagnosis. Change can often cause confusion, but hopefully this episode helps keep everyone up to date and on the same page… for now at least. Radiopaedia's glioblastoma IDH-wildtype article  ► https://radiopaedia.org/articles/glioblastoma-idh-wildtype Radiopaedia 2024 Virtual Conference ► https://radiopaedia.org/courses/radiopaedia-2024-virtual-conference Become a supporter ► https://radiopaedia.org/supporters Get an All-Access Pass ► https://radiopaedia.org/courses/all-access-course-pass Andrew's X ► https://twitter.com/drandrewdixon Frank's X ► https://twitter.com/frankgaillard Ideas and Feedback ► podcast@radiopaedia.org   The Reading Room is a radiology podcast intended primarily for radiologists, radiology registrars and residents. 

The May 2024 replay features four episodes on neuro-oncology for brain cancer awareness month. The episode begins with Dr. Philipp Karschnia discussing the assessment of whether MTHFR polymorphisms affect the risk for leukoencephalopathy. The episode continues with Dr. Ingo Mellinghoff discussing new treatment opinions for isocitrate dehydrogenase (IDH)–mutant grade 2 gliomas. The third interview leads into a conversation with Dr. Linda Liau on the study of vaccine-based therapy for GBM. The episode concludes with Dr. Teddy Totimeh talking about brain tumor programs in Asia and Africa. Podcast Links: MTHFR Polymorphisms and Leukoencephalopathy Risk in CNS Lymphoma Patients   New Treatment for IDH mt Gliomas  Study of Vaccine-Based Therapy for GBM Brain Tumor Programs in Asia and Africa  Article Links: https://doi.org/10.1212/WNL.0000000000207670  https://www.nejm.org/doi/full/10.1056/NEJMoa2304194 https://jamanetwork.com/journals/jamaoncology/fullarticle/2798847 https://doi.org/10.1016/j.wneu.2023.04.067 Disclosures can be found at Neurology.org.

In honor of Acute Myeloid Leukemia (AML) Awareness Day, Oncology Data Advisor Editorial Board and Fellows Forum members Tristan Knight, MD, FRCPC, Richa Thakur, MD, and Joseph Kalis, PharmD, BCOP, hosted a live panel discussion covering the evolving treatment landscape for AML, including: • Novel therapies and combinations such as chimeric antigen receptor (CAR) T-cell therapy and isocitrate dehydrogenase (IDH) inhibitors • The role of measurable residual disease (MRD) testing • Considerations for pediatric transplant and cellular therapy • Words of hope for patients undergoing treatment for AML Additionally, they answered live questions from the audience, including: • Do you have any first-line treatment recommendations for patients with a KMT2A mutation? • When do recommend that patients participate in a clinical trial? Take a listen to hear the panelists' answers to these questions and their perspectives on the ever-changing therapeutic landscape for AML!

Drs. Shaalan Beg and Aparna Parikh discuss the role of ctDNA as a powerful prognostic biomarker for GI cancers, along with its impact on risk stratification and the detection of recurrence. They highlight key studies in ctDNA that were featured at the 2024 ASCO GI Cancers Symposium, including COBRA, GALAXY, and BESPOKE in CRC, as well as the promise of ctDNA testing in the preoperative detection of iCCA. TRANSCRIPT Dr. Shaalan Beg: Hello, and welcome to the ASCO Daily News Podcast. I am Dr. Shaalan Beg, your guest host for the ASCO Daily News Podcast today. I am an adjunct associate professor at UT Southwestern's Harold Simmons Comprehensive Cancer Center in Dallas. On today's episode, we will be discussing the emergence of circulating tumor DNA (ctDNA) technology in GI cancers. I am delighted to be joined by Dr. Aparna Parikh, an assistant professor of medicine at Harvard University and the director for colorectal medical oncology at the Massachusetts General Hospital Cancer Center, where she also serves as the medical director of the Young Adult Colorectal Cancer Center. Dr. Parikh will share her insights on key research on this hot topic in GI oncology that was featured at the recent ASCO Gastrointestinal Cancers Symposium.  Our full disclosures are available in the transcripts of this episode, and disclosures related to all episodes of the podcast are available at asco.org/DNpod.  Dr. Parikh, it's great to have you on the podcast today. Dr. Aparna Parikh: Thanks so much, Dr. Beg.  Dr. Shaalan Beg: In recent years, it has become evident that liquid biopsy and other emerging ctDNA technologies are changing how we treat GI cancers, and colorectal cancer (CRC) is in the forefront of this space. Before we dive into key studies, can you briefly highlight for our listeners how ctDNA is advancing the field and how it can influence the care that we deliver to our patients in the future? Dr. Aparna Parikh: Absolutely, ctDNA is certainly a hot topic. What we have learned over the years is that ctDNA has emerged across many solid tumor types as one of the most powerful, if not the most powerful, prognostic biomarker we have to date. ctDNA has improved risk stratification. We have learned a lot about the role in what is called minimal or molecular residual disease in patients with early-stage disease, and ctDNA being a biomarker of recurrence for those patients, with ctDNA, we have a better understanding of tumoral heterogeneity, both spatially and temporally, getting a better glimpse of what is happening in a given patient with multiple metastases, as well as genomic evolution of tumors over time. So certainly many, many roles and areas where ctDNA is emerging. Dr. Shaalan Beg: This was a hot topic at the 2024 ASCO GI Cancers Symposium, and we're going to take a deep dive into some of the abstracts that were presented. Let's start with the COBRA study, which is the NRG-GI005. That was Abstract 5 at the ASCO GI Cancers Symposium, and the GALAXY study, which was Abstract 6 at the symposium. So, the COBRA study reported results of ctDNA as a predictive biomarker in adjuvant chemotherapy for people with colon cancer. At a high level, it was a negative study, but there are some important lessons for us to learn. Similarly, in the GALAXY study, investigators from Japan presented an updated analysis on the correlation of ctDNA dynamics with outcomes in colorectal cancer with minimal residual disease. How do you synthesize all this information and help the listeners understand our current state for ctDNA applications in colorectal cancer? Dr. Aparna Parikh: Yeah. Let's take the COBRA study first. Let's talk a little bit about the design of COBRA. COBRA was intended to look at patients that were resected, stage 2 colorectal cancer patients, or colon cancer patients who were 2A. These are patients where the treating physician would, at the outset, decide that there was no adjuvant chemotherapy indicated. These are patients where active surveillance would be entirely appropriate as the standard of care. Patients were randomized to arm 1, which was active surveillance, or randomized to arm 2, which was assay-directed therapy. If there were ctDNA positive in arm 2, then they were given chemotherapy, FOLFOX or CAPOX. And if they were “ctDNA not detected,” then they would also go on to active surveillance.   And so, the plan was that nearly 1,500 patients are to be recruited, and at the time of this data cut, they had around 630-some patients. The primary objective was to look at the clearance rates of ctDNA between the ctDNA-positive cohorts, remember, the chemotherapy and the active surveillance cohorts at 6 months. They had around a 5% detection rate of ctDNA patients. Ultimately, that was around 16 patients. The reason that the study shut down was that what they found was that in the surveillance arm, the arm that was not getting any treatment, they had a ctDNA clearance of 43% versus 11% in the chemotherapy arm. They had an interim analysis to look at the clearance rate between the 2 arms, and what was surprising to the investigators and the community was what was happening in terms of clearance. Why do we have a 43% clearance rate in patients that were not getting anything? And so, because of that, the study was shut down as it did not meet its prespecified interim look at clearance in those 2 arms.   Many things came up in terms of learnings from COBRA. Number one was the characteristics of the assay. And so, you take an assay in a low-risk patient population that has a fixed specificity, and when your baseline prevalence of recurrence is so low, for example, in low-risk stage 2 patients, your composite predictive value is very susceptible to small changes in that specificity. And so, your PPV is going to be a lot lower in a low-risk patient population than a higher-risk patient population. The COBRA study used an older version of a tumor-uninformed assay, so it definitely called into question some characteristics of the assay. Is one-time-point clearance sufficient, and is that the right endpoint? We have seen now, including the GALAXY study that we'll talk about here, previously reported just spontaneous clearance happening in 5%, 10% of patients. The question with that spontaneous clearance is: Was it actually clearance, or was chemotherapy just perhaps in a low ctDNA shedding state? Are you just suppressing the ctDNA below the level of limited detection?  And then in this study, the clearance draw was actually done in the chemotherapy arm right before the last cycle of chemotherapy, again to that point of, are you just suppressing the ctDNA with chemotherapy? There is also stochastic sampling error that can happen in patients with very low residual tumor volume. So, I think this is a disappointing study in the sense that it is still a really important question. There are still 2A patients that recur, but maybe [this was] not the right test, or maybe single-time-point testing wasn't enough. And so, lots of lessons to be learned from this study in terms of test and design, but hopefully more to come. I think certainly stage 2 patients remain an area where I think, hopefully, ctDNA still plays a factor for those patients.  Dr. Shaalan Beg: And how was the patient population for the GALAXY study? That was Abstract 6, compared to the COBRA study. Could you summarize those findings for us?  Dr. Aparna Parikh: Yeah, so GALAXY was part of a large study in Japan that includes an observational cohort plus therapeutic cohorts as well. And so, GALAXY was just further reporting of the observational cohort. So unlike COBRA, which is a low-risk, stage 2 study that was actually asking that interventional question: Can you use it to guide therapy? The GALAXY and the updated GALAXY just continues to show more clinical validity data rather than clinical utility data. And it was nearly 3,000 patients, pan stages. Again, the lion's share were stage 2 and 3 patients, but there were also stage 1 and stage 4 patients as well. And what they showed was that ctDNA is undoubtedly prognostic. They showed very consistent Kaplan-Meier curves, which we've seen time and time again, where if you're ctDNA-positive, you don't do as well.  What they showed was, not surprisingly, with longer-term follow-up – this is 24-month follow up, so longer-term follow up than was published in their paper last year – was that when you test at one time point, so landmark testing, the sensitivity of detecting recurrence was around 48%, and that fell from the publication last year which was around 58%, 59%, which is not surprising as you follow more people. I think single time point testing soon after surgery may miss those late recurrences, but it's still prognostic and showed a specificity of around 94%.   They also continued to show that if you continued to test with serial testing, your sensitivity improves, but what was really interesting and new, what they presented this time, was a clearance analysis. And showing, again, comparable to COBRA, in many ways, in the sense that clearance can be a little bit finicky, especially at one time point, is what they showed is that patients who had sustained clearance, and these are patients that had at least two time points with their ctDNA remained to be negative, they did very well. But if you had transient clearance, and again, the definition was a little bit broad, at least having one negative and then one positive, those patients ultimately, at 24 months, the curves came together with the no clearance curve. So initially, they did better than the people that didn't have any clearance. But if you transiently cleared at two years, the curves came back together.   And what was interesting is that in those patients that sort of transiently clear by 9 to 12 months, 80% of those are actually having a rapid return of ctDNA. And so this begs the question of was chemotherapy just suppressing that ctDNA or maybe if you have a better test you could have actually improved it.  These were some of the updated, interesting learnings from GALAXY, which remains incredibly prognostic. And then the concept of clearance, which I think we have to look into a little bit more as a field, and understanding that maybe just one time point clearance isn't sufficient.  Dr. Shaalan Beg: Yeah, and one of the most important applications for ctDNA can be its ability to inform adjuvant chemotherapy. Its ability to not only identify more people who may benefit from chemotherapy, but maybe even identify people who don't need chemotherapy. And along those lines, Abstract 9, the BESPOKE study, looked to understand the role of ctDNA-based detection of molecular residual disease to inform adjuvant therapy for stage 2 and 3 colorectal cancer. And they presented interim data at the GI ASCO this year. What were your takeaways from this study? Dr. Aparna Parikh: Exactly. Beyond the prognostic implications, I think what was really interesting was that there was the initial data looking at the benefit of adjuvant chemotherapy. So, what they did was they said, “Okay. We're going to take the MRD-positive patients and look at the benefit of adjuvant chemotherapy and then the benefit of adjuvant chemotherapy in the MRD-negative patients.” And again, remember, this is a prospective observational study, so it's not looking at negative and positive to guide therapy, but it's just looking prospectively and observationally at how those patients are doing. But what they showed again is that indeed, in the adjuvant chemotherapy group, the benefit of adjuvant chemotherapy again with the follow-up to date on the study was different in the MRD-positive patients.  First of all, I guess taking a step back, the DFS in the ctDNA-negative patients at 2 years was very good. So negative patients had over 98% 2-year DFS in both the adjuvant chemotherapy and observational group. And there was no real difference between adjuvant or not. But in the positive patients, not surprisingly, the DFS was worse. But what was reassuring to see is that you can make an impact with adjuvant chemotherapy in the positive patients. And the difference in DFS between the positive and negative patients, with adjuvant or not, was 42% versus 12.5%, in the observational patients. So, it is benefitting the patients who are positive so it does give us more data that, again, at least in the positive patients, you may be able to reverse the recurrences there with adjuvant chemotherapy. And maybe if you're negative, eventually, we'll get to a point of de-escalation of care. Again, keeping in mind the kinds of sensitivity limitations as well.  Dr. Shaalan Beg: Wonderful. And one of the other malignancies in the GI space where precision therapies and molecular biomarkers are making a huge difference are intrahepatic cholangiocarcinoma. Genomic profiling using ctDNA is increasingly being used in this population to inform precision oncology approaches and determine mechanisms of resistance to targeted therapies as well. In Abstract 528, investigators looked at the role of preoperative ctDNA testing for resectable intrahepatic cholangiocarcinoma. What are your thoughts on that study?  Dr. Aparna Parikh: Yeah, it's such an important area, as you mentioned, in the metastatic space – FGFR, IDH1, all these alterations that are emerging in intrahepatic cholangios. This was a very small study, it was preoperative, and so the tumor was intact, and around 14 patients. They used a tumor-informed approach just for detection and quantification of ctDNA. So this was not a study that was looking at a next-generation sequencing approach where you're going to actually be able to detect the alterations, but it's actually looking for the detection and quantification of ctDNA rather than genomic characterizations. And patients had about a month or so where they had their baseline blood detected. And I think what was reassuring to say was that ctDNA was actually detected in all the patients with the primary tumor intact, except for one patient who was a very low-risk stage 1A patient. There was some correlation, against a small number of patients, between the concentration of ctDNA in patients that had the lower stage and then the higher stage groups. Small numbers were actually hard to characterize and correlate with recurrence or mortality, but at least, some correlation with pathologic tumor size, they were able to because it was a bespoke panel and you're sampling the tissue and then looking in the blood, IDH1 and 2 were mutations that were tracked based on the genomic profiling and a couple of the patients were able to have their IDH mutations tracked.  So it gives us a sense, a little bit, that ctDNA, we know has a lot of variable shedding across disease states and tumor locations, but gives us some promise that it is reliably detected with the tumor-informed approach, at least preoperatively in cholangios. So may again open some more opportunities for MRD testing in cholangiocarcinoma as well.  Dr. Shaalan Beg: Thank you. That's a wonderful review of ctDNA applications in gastrointestinal cancers from the 2024 ASCO GI Cancers Symposium. Thank you, Dr. Parikh, for sharing your valuable insights with us on the podcast today. Dr. Aparna Parikh: Thank you so much for having me. Dr. Shaalan Beg: Thank you to our listeners for your time today. You'll find links to the abstracts discussed today in the transcript of this episode. Finally, if you value the insights that you hear on the ASCO Daily News Podcast, please take a moment to rate, review, and subscribe wherever you get your podcasts.   Disclaimer: The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement.   Find out more about today's speakers: Dr. Shaalan Beg @ShaalanBeg Dr. Aparna Parikh @aparna1024   Follow ASCO on social media:  @ASCO on Twitter  ASCO on Facebook  ASCO on LinkedIn    Disclosures: Dr. Shaalan Beg: Employment: Science 37 Consulting or Advisory Role: Ipsen, Array BioPharma, AstraZeneca/MedImmune, Cancer Commons, Legend Biotech, Foundation Medicine Research Funding (Inst.): Bristol-Myers Squibb, AstraZeneca/MedImmune, Merck Serono, Five Prime Therapeutics, MedImmune, Genentech, Immunesensor, Tolero Pharmaceuticals   Dr. Aparna Parikh: Consulting or Advisory Role (An Immediate Family Member): PMV Consulting or Advisory Role: Checkmate Pharmaceuticals, Guardant Health, Foundation Medicine, Abbvie, Value Analytics Labs, Bayer, Taiho Oncology, Delcath, Seagen, CVS, SAGA Diagnostics, Scarce, Illumina, UpToDate, Takeda, AstraZeneca, Takeda, Pfizer, Kahr, Xilio Therapeutics, Sirtex Research Funding: PMV Pharma, Erasca, Inc, Syndax Research Funding (Institution): Bristol-Myers Squibb, Genentech, Guardant Health, Array, Eli Lilly, Novartis Pharmaceuticals UK Ltd., PureTech, Mirati Therapeutics, Daiichi Sankyo, Karkinos Other Relationship: C2i Genomics, Xgenomes, Parithera, Cadex

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No episódio 182 do JKCast, José Kobori responde às dúvidas dos ouvintes sobre Gestão Ativa Renda Fixa, Mercado Futuro e Agronegócio, Cursos de Economia, PIB vs IDH, Comprar ou Alugar Imóvel, Opções, Indicadores para Pequenos Negócios. Envie sua pergunta em áudio ou texto para o JKCast: https://wa.me/5511955500005 ------------------------------------------------------------------------------------------------------

Last Thursday melanoma researcher Professor Georgina Long was announced as Australian of the Year, along with colleague and friend Professor Richard Scolyer. As co-medical directors of the Melanoma Institute Australia, the pair are credited with saving thousands of lives. Their pioneering immunotherapy treatments for advanced forms of the cancer have resulted in 5 year survival rates increasing from less than 5% to more than 50%. In June of last year Professor Scolyer was diagnosed with glioblastoma IDH wild-type, a cancer that is usually fatal within six to nine months. Rather than undergoing traditional treatment, Prof Scolyer decided to experiment on himself, with Professor Long designing world-first treatments based on their melanoma work.

This week, Ian Welsh and Bea Stevenson talk about the sustainable business issues likely to be on the agenda at the 2024 World Economic Forum annual meeting in Davos – in particular this year's focus on driving corporate transparency and accountability.    They also discuss this week's Innovation Forum European Union Deforestation Regulation webinar, at 1pm CET on Thursday 18th January, with panelists from the European Commission, Musim Mas and IDH who will debate potential consequences of the regulation's implementation and explore potential solutions to any challenges. Click here to join us. Plus, Innovation Forum's Hanna Halmari shares agenda updates and what to expect at the sustainable apparel and textiles conference, taking place in Amsterdam on 23rd-24th April. Register here to join us.

This week: another chance to hear our three most popular podcast interviews of 2023.   Innovation Forum's Ian Welsh talks with Rejane Souza, senior vice-president for global innovation at Norway-based fertiliser company Yara International, about the rise and rise of regenerative agriculture. They discuss the role of companies across the value chain in enabling technology and innovation, and the importance of taking a farmer-centric approach.   Ian also talks with Charlotte Bande, global food and beverage sector lead at Quantis, about how to improve the weak points in mainstream corporate sustainability decision making within the food and agriculture sector. They discuss the continued importance in peer-to-peer collaboration and share guidance on what a good just transition could look like.   And, IDH's regional director for Asia landscapes, Chi Tran, and senior programme manager for coffee, Tessa Meulensteen, discuss with Ian what the incoming EU's deforestation regulation will mean for the coffee sector. They discuss the opportunities and challenges to this regulation, including potential smallholder farmer exclusion and diversity loss in supply chains.

El podcast de Farid Kahhat para suscriptores analiza las noticias internacionales más importantes de los últimos días. Hoy Farid nos cuenta sobre la resolución del presidente de la corte IDH sobre el indulto a Fujimori, el plan de despliegue militar de Nicolás Maduro cerca a la región del Esquibo y la ofensiva de Israel en Gaza. Además, nos brinda un análisis sobre la transición de poder en la Argentina y lo que se viene con la presidencia de Javier Milei. También puedes ver este podcast en YouTube: https://youtu.be/rDuwS_xP1F8 Si quieres tener acceso a todos los episodios de este podcast exclusivo, puedes suscribirte a Comité de Lectura usando este link: https://comitedelectura.pe/pages/registrate

IDH's regional director for Asia landscapes, Chi Tran, and senior programme manager for coffee, Tessa Meulensteen, talk with Innovation Forum's Ian Welsh about what the incoming EU's deforestation regulation will mean for the coffee sector. They discuss the opportunities and challenges to this regulation, including potential smallholder farmer exclusion and diversity loss in supply chains.

This week: IDH's regional director for Asia landscapes, Chi Tran, and senior programme manager for coffee, Tessa Meulensteen, talk with Innovation Forum's Ian Welsh about the potential impact of the EU's deforestation regulation on the coffee sector and the unintended consequences that may arise. Plus: UBS and Santander's “green" bonds linked to Brazilian deforestation; Musim Mas to stop sourcing from smallholders for its EU supply chain in response to EUDR; and, European businesses excluding Scope 3 emissions from net zero planning, in the news digest by Innovation Forum's Bea Stevenson.   Host: Ian Welsh

Featuring articles on vorasidenib for IDH-mutant low-grade glioma; a trial of dietary intervention for cognitive decline; omitting radiotherapy after breast-conserving surgery in luminal A breast cancer; gene therapy for the Crigler–Najjar syndrome; and on abortion counseling, liability, and the First Amendment; a review article on community-acquired pneumonia; a case report of a man with fever and foot pain; and Perspective articles on prioritizing mental health in the HIV/ AIDS response in Africa, on reducing health care's climate impact, and on free and charitable clinics.

ASCO: You're listening to a podcast from Cancer.Net. This cancer information website is produced by the American Society of Clinical Oncology, known as ASCO, the voice of the world's oncology professionals. 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. Guests' statements on this 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. Cancer research discussed in this podcast is ongoing, so data described here may change as research progresses. The theme of the 2023 American Society of Clinical Oncology (ASCO) Annual Meeting was “Partnering With Patients: The Cornerstone of Cancer Care and Research.” From June 2 to 6 in Chicago, Illinois, and online, cancer researchers and clinicians from around the world gathered to discuss the latest cancer research and how to ensure that all people receive the cancer care they need. In the Research Round Up series, members of the Cancer.Net Editorial Board discuss the most exciting and practice-changing research in their field presented at the meeting, and explain what it means for people with cancer. In today's episode, our guests will discuss new research in breast cancer, lymphoma, multiple myeloma, and brain tumors. First, Dr. Norah Lynn Henry discusses new research in early stage and metastatic breast cancer. Dr. Henry is Professor and Interim Chief of the University of Michigan's Division of Hematology/Oncology in the Department of Internal Medicine and the Breast Oncology Disease Lead at the Rogel Cancer Center. She is also the 2023 Cancer.Net Associate Editor for Breast Cancer. You can view Dr. Henry's disclosures at Cancer.Net. Dr. Henry: Hi, I'm Dr. Lynn Henry, a breast cancer oncologist from the University of Michigan Rogel Cancer Center. Welcome to this quick summary of the most exciting new research in breast cancer that was presented at the 2023 ASCO Annual Meeting. I have no conflicts of interest for any of the trials that I will talk about. First, I'm going to give a very brief overview of the types of breast cancer, then talk about some research that was presented on both early-stage and metastatic breast cancer. As a reminder, there are multiple kinds of breast cancer. Some breast cancers are called hormone receptor-positive or estrogen receptor-positive and are stimulated to grow by the hormone estrogen. We treat those cancers with anti-estrogen or anti-endocrine treatments, which block estrogen or lower estrogen levels. Other breast cancers are called HER2-positive. These are often more aggressive cancers. But because they have extra copies of HER2, they often respond to treatments that block HER2. Finally, there are breast cancers that don't have hormone receptors or HER2. These are called triple-negative breast cancer and are also often aggressive cancers. Most of the results I'm going to highlight today are treatments for estrogen receptor-positive and HER2-negative breast cancer. One of the main stories from the ASCO Annual Meeting was the result of the NATALEE trial. At the present time, for patients with estrogen receptor-positive, HER2-negative early-stage breast cancer who were at high risk of having their breast cancer come back, the currently recommended treatment is anti-endocrine therapy. Based on the results of a prior trial called monarchE, we also consider adding a medicine called abemaciclib, which turns off some enzymes in the cell that are called CDK4 and CDK6, which are known to make estrogen receptor-positive breast cancer cells grow. Abemaciclib can further reduce the risk of cancer recurrence compared to endocrine therapy alone, but it does have some side effects, most commonly, diarrhea. In the NATALEE trial, which was presented for the first time at this ASCO meeting, researchers studied a similar type of medication called ribociclib. It acts similarly to abemaciclib, although it is more likely to cause low blood counts and less likely to cause diarrhea. Ribociclib is currently routinely used in combination with anti-endocrine therapy to treat patients with metastatic estrogen receptor-positive breast cancer but is not yet routinely used in the early-stage setting. In the NATALEE trial, patients with estrogen receptor-positive, HER2-negative early-stage breast cancer who are at high risk of breast cancer recurrence were enrolled. Half the patients were treated with just standard anti-endocrine therapy and half also received ribociclib for 3 years. After the 3-year treatment period, those who received both ribociclib and anti-endocrine therapy were about 25% less likely to have their cancer come back compared to those who received only anti-endocrine therapy. Overall, the medication was quite well tolerated. It is important to note that this drug is not yet FDA-approved in the setting. The remaining trials I will highlight are for treatment of metastatic breast cancer. There were many trials examining how best to use drugs that we are actually already using in the clinic. For example, many presentations were about the CDK4/6 inhibitors that I just mentioned. Typically, patients who have just been diagnosed with estrogen receptor-positive, HER2-negative metastatic breast cancer get treated with anti-endocrine therapy plus a CDK4/6 inhibitor. One trial called SONIA examined whether this is the right approach, or whether patients should just get the anti-endocrine therapy up front and hold off on starting the CDK4/6 inhibitor medication until a later time. It appears that this delayed approach would reduce symptoms as well as cost of the medication, while not reducing benefit from the treatment. Therefore, it appears it is likely fine for some patients to get just anti-endocrine therapy alone initially. However, we don't know how to identify those patients. Researchers are still figuring out which patients should follow this new treatment plan and which should keep getting the double therapy at the beginning. Some more to come in the future. There was a different trial called PADA-1 that included patients taking anti-endocrine therapy and the CDK4/6 inhibitor, palbociclib, upfront. Those patients were monitored using a blood test, looking for a mutation or a change in the estrogen receptor in the cancer. Patients who had that mutation either remained on the same treatment that they'd been on or switched to the next line of therapy, even though their scans didn't show any progression of their cancer. Overall, this switching strategy looks like a very promising approach for managing patients since it may help patients' cancer respond to treatment for a longer period of time. Although this approach is not yet officially recommended according to our guidelines. In another example, many patients with all types of metastatic breast cancer are treated with a drug called capecitabine, also known as Xeloda. Although this drug is effective for many cancers, many patients experience hand-foot syndrome, nausea, diarrhea, and mouth sores. In the X7-7 clinical trial, the researchers compared the official standard FDA-approved dose based on a patient's height and weight and given for 14 days followed by 7 days off. That was compared to a fixed dose of treatment given 7 days on and 7 days off. The trial found that the fixed-dose regimen was easier to tolerate, but importantly, the benefit from the 2 doses and schedules of treatment appears to be similar. Therefore, we will likely be using this lower dose, 7 days on and 7 days off, for most of our patients who receive treatment with capecitabine for metastatic breast cancer, since it is likely to improve their quality of life while not negatively impacting the potential benefit they receive from the therapy. There were a lot of other research findings presented that are related to treatment for both early-stage and metastatic breast cancer at the meeting. Importantly, we got glimpses of the many new drugs on the horizon for treatment of breast cancer, including a new antibody-drug conjugate against HER2, as well as other new anti-endocrine and targeted treatments. We eagerly await the results of large, randomized trials so the drugs that work can be used to treat patients with breast cancer. But for now, that's it for this quick summary of important research from the 2023 ASCO Annual Meeting. Stay tuned to Cancer.Net for future updates from upcoming breast cancer conferences. Thank you. ASCO: Thank you, Dr. Henry. Next, Dr. Christopher Flowers discusses new research in lymphomas and multiple myeloma. Dr. Flowers is the Chair of the Department of Lymphoma/Myeloma at The University of Texas MD Anderson Cancer Center and Division Head ad interim of Cancer Medicine. He is also the 2023 Cancer.Net Associate Editor for Lymphoma. You can view Dr. Flowers' disclosures at Cancer.Net. Dr. Flowers: Hello. I'm Dr. Christopher Flowers, professor and chair of the Department of Lymphoma and Myeloma and interim division head for cancer medicine at the University of Texas MD Anderson. And it's my pleasure to talk to you today in this Cancer.Net podcast about latest updates in the hematological malignancies focused on lymphoid cancers from the American Society of Clinical Oncology Annual Meeting. The ASCO Annual Meeting every year is an exciting time for latest updates in the care of patients with cancer. And in particular this year, there were 3 abstracts that I'd like to highlight that were presentations at this meeting about lymphoid malignancies that have potential significant impact for patients over time. The first 2 come from a special session that was on late-breaking abstracts that were latest advances from clinical trials. The first is from the ZUMA-7 trial. This is a trial looking at axicabtagene ciloleucel, a chimeric antigen receptor T-cell therapy, or CAR T-cell therapy. The CAR T-cell trial in question here was led by Jason Westin, who's a colleague of mine at MD Anderson. And MD Anderson is a partner with Kite pharmaceutical company that is a manufacturer of this and has a research alliance with that group. In the ZUMA-7 trial, this was a trial that involved the use of CAR T-cell therapy in comparison to standard-of-care therapy, which typically would be aggressive chemoimmunotherapy followed by autologous stem cell transplantation for patients with relapse of large B-cell lymphoma. As many of you may know, large B-cell lymphoma is a kind of lymphoma that is potentially curable with standard frontline therapy. And when patients relapse, the standard of care historically had been for patients to receive autologous stem cell transplantation, which is also potentially a curative therapy. This trial to do a ZUMA-7 trial compared patients who received the typical standard of care, the autologous stem cell transplant following the aggressive chemoimmunotherapy regimen for patients who had relapsed early after their initial therapy, so within 12 months, or were refractory, meaning that they did not respond to their initial therapy. And this was compared to the axicabtagene ciloleucel or axi-cel CAR T-cell therapy. The initial publication of the trial came out in the New England Journal of Medicine in 2022 and showed that the event-free survival for patients who receive CAR T-cell therapy was superior. This update of the ZUMA-7 trial at the ASCO Annual Meeting that was presented by my colleague, Jason Westin, discussed the overall survival of the study, and in this update, it showed that overall survival was also improved for patients who received axi-cel as opposed to standard-of-care therapy. And now with a median follow-up of a little bit more than 47 months, axi-cel demonstrated superiority that was statistically significant and clinically meaningful over the traditional standard of care. In that same session, there was another trial looking at CAR T-cell therapy for patients with multiple myeloma. This was a BCMA-targeted CAR T-cell therapy that was presented by Dr. Dhakal in that session providing results from the CARTITUDE-4 global randomized phase 3 clinical trial. That was a trial that involved 419 patients where patients were randomized to cilta-cel CAR T-cell therapy for myeloma or standard-of-care therapy, which in this case included combination therapy. And in this trial, this showed that single agent with a single cell-to-cell infusion significantly improved progression-free survival versus standard of care for patients with multiple myeloma who had 1 to 3 prior lines of therapy and were refractory to lenalidomide. This is also a meaningful advance for patients with this disease. And the final abstract that I'll mention is an abstract that was presented by Dr. Alex Herrera from City of Hope and was presented in the Plenary session. And it was really exciting to see a Plenary session presentation focusing on lymphomas. So this trial presented by Dr. Herrera was led by the Southwest Oncology Group. Dr. Sara Ahmed from MD Anderson, from my institution, was a participant and actively engaged in this clinical trial. This trial was a success in a number of ways. First, it involved both pediatric and adult patients and is one of the first trials of its kind to involve both large populations of patients with pediatric lymphomas as well as adults with lymphomas. It helps to consolidate the approaches that we use for Hodgkin lymphoma, both in the pediatric population and the adult population. It also represents a major advance in the ways that we conduct clinical trials in the United States in that this clinical trial finished ahead of schedule in terms of completion of the trial with collaboration from the adult and pediatric groups across the National Clinical Trials Network. As I mentioned, this was presented by Dr. Alex Herrera in the Plenary session and involved patients with stage 3, 4 Hodgkin lymphoma, where patients were randomized 1 to 1 either to receive an anti-PD-1 therapy, nivolumab, with chemotherapy, the AVD chemotherapy regimen, or the antibody-drug conjugate, brentuximab vendotin, combined with that same AVD chemotherapy. And what this showed in 994 patients who were enrolled from 2019 to 2022 was that there was a benefit for patients who received the combination of nivolumab AVD or NAVD versus the group that received brentuximab and AVD. It improved the progression-free survival in patients with advanced-stage Hodgkin lymphoma. In this trial, few immune-related adverse events were observed and a lesser number of patients went on to receive radiation therapy, which is also a benefit for patients with Hodgkin lymphoma. And this concludes my presentation of abstracts at the ASCO Annual Meeting and really exciting advances for patients with lymphoma that were presented this year. ASCO: Thank you, Dr. Flowers. Finally, Dr. Roy Strowd discusses new research in treating brain tumors, including those in people with von Hippel Lindau syndrome. Dr. Strowd is a neurologist and neuro-oncologist at Atrium Health Wake Forest Baptist Comprehensive Cancer Center. He is also the 2023 Cancer.Net Associate Editor for Central Nervous System Tumors. You can view Dr. Strowd's disclosures at Cancer.Net. Dr. Strowd: Hello, everyone. This is Roy Strowd. I'm a physician neuro-oncologist at Wake Forest University School of Medicine in our comprehensive cancer center. And I'm really excited to be with you for this podcast on important CNS or brain tumor updates from the 2023 ASCO Annual Meeting. I don't have any relevant disclosures for the research that we'll discuss today. It was a really exciting meeting. It was actually a really fun meeting to be a brain tumor doctor at ASCO this year. So I'm really excited to talk with you about some important updates. And I think it's actually a really important time to be a patient and a caregiver and know some of the things going on in brain tumor care. So I'm going to dive into 3 studies. And one that we just have to talk about, and this was a really exciting study called the INDIGO study. At ASCO, if you present a study, you want to have a Plenary presentation, you want to be up on the big stage presenting your work. And brain tumor studies aren't always on the big stage. We just haven't had enough really good treatments out there for brain tumor patients over the years. And this year, we had a Plenary presentation, a really big study, making a big splash. And that was this INDIGO study. So I'm going to spend a few minutes talking about that study. I want brain tumor patients and caregivers to know about this and know about some of the important updates from the Annual Meeting. The study was called the INDIGO study, and it's a phase 3 study. So when you think about clinical trials, there's a phase 1, phase 2, phase 3. That phase 3 is that last step, that last hurdle that a drug needs to overcome to move towards approval. And a positive phase 3 study is really exciting for the field and means that we may have a new treatment that will change how we take care of brain tumor patients. And that's what this study was. It was also a really unique study. So it's looking at a different group of brain tumor patients, patients that have an IDH mutant glioma. Most common brain tumors that we see are the glioblastomas. And those are often and really, by rule, IDH wild-type. IDH is a gene. It's called the isocitrate dehydrogenase gene. And it's one of these really important genes for us to understand how brain tumors are going to work and how they act and it turns out, with this study, how they may respond to treatment. So this study looked at enrolling patients that had an IDH-mutant low-grade glioma, or a grade 2 glioma. Those are those often slower-growing, but they continuously grow tumors that occur early in life, typically in the 30s or 40s for young people. And we haven't really had a lot of good treatments for these patients. And so this study looked at giving a new drug that's called vorasidenib. It's hard to say vorasidenib. And it's an IDH mutant inhibitor. So it attacks that IDH mutant gene that makes these tumors what they are. And it's been undergoing development for many years. It's an exciting treatment because it's what we call a molecularly targeted treatment. It specifically targets that IDH gene that makes the low-grade tumors low-grade tumors. This study enrolled 331 patients, so a large group of patients. Half of those patients received the drug, the vorasidenib, and half received placebo. And that's pretty uncommon in cancer. We don't often do studies that are placebo-controlled studies. But for these patients, there's often not a good treatment early in the course, they get surgery. And for patients that don't need an additional treatment, we do surgery and then we wait and watch and see what happens. And that gives us an opportunity as a brain tumor community to figure out whether this type of treatment will help prevent the need for a next treatment, prevent the need for radiation and chemotherapy. And so that's what was looked at in this study. And there was some really exciting data. So I'm going to go through a few numbers, but we just got to talk about these numbers because they're really important. So at 14 months, 28% of the patients receiving the drug vorasidenib had progressions. That's about a quarter of patients compared to half that received placebo. So that's a big improvement in the number of patients whose tumor grew. So this drug prevented tumor growth in these patients. And that's exactly what we want. That's why we develop drugs, is to prevent tumor growth. When we look at the time that those patients had until they needed a next treatment or until their tumor grew, it was over 2 years of time patients receiving the drug when their tumor grew versus less than a year, 11 months for those receiving placebo. So it's adding a lot of time for brain tumor patients without tumor growth or without needing another treatment. And typically, these patients with low-grade gliomas would need something like radiation therapy or chemotherapy. And those are good treatments, and we need those treatments. But they can have toxicity. And so this is the type of drug that could prevent that toxicity, cognitive decline, other problems that can happen with chemotherapy that those patients didn't potentially suffer. So there are some important things that we learned from the INDIGO study that I would want you to take away, kind of what do these data mean? The first is that we can target this IDH gene. And that's really important for our field. And it means if you're a brain tumor patient, knowing whether your tumor is IDH mutant or IDH wild-type is important, and that's something I want brain tumor patients to ask me as a neuro-oncologist and ask their cancer doctor because that's important in deciding treatment for them. The second is this medicine vorasidenib, it gets into the brain. And that's one of the big challenges that we have in brain tumor care in developing drugs is we need things that get into the brain. And this study really shows that this is a good medicine. There's a number of IDH inhibitors, but this medicine vorasidenib is one that we want to specifically think about for our patients. And this is a practice-changing study. So for the first time, we now have a treatment that works for grade 2 gliomas and really prevents the need for radiation therapy and chemotherapy. So those are 3 important things to take away from this. There's a number of things that we don't yet know. This medicine is not available. So patients coming in and emailing me and calling me, we don't have it yet. And after a big phase 3 study like this, this is announced. There's still a number of steps that need to happen to make sure that this can be delivered to patients safely and we can get it out there. And that's in partnership with groups like the FDA, the Food and Drug Administration, and others. So this is an important conversation to have with patients, neuro-oncologists, and to know that this is something that's on the horizon. Two other things is we don't know if this is going to work for all brain tumors. In particular, for these IDH wild-type glioblastomas, the most common brain tumor, this probably is not a good therapy that we don't have any data to suggest that it would work. They don't have that IDH mutation. And so this is important for some brain tumor patients but not for everybody. And that needs to prompt a conversation with the cancer doctor. And it may not work at all times. So there's some data to suggest that this is really a drug that's best given early in the course of treatment and not later on. And so it is something that I want my patients to be aware of at the first time that I see them so we can be deciding what kind of the right time is. So I want to give folks 2 take-homes from this study and summarize a few of these things that we heard about because it's such an important study. So what are the 2 take-homes from the INDIGO Study? The first that I wrote down is targeting IDH mutation in glioma works. And that's a groundbreaking discovery from this. This is really important for our field. IDH mutations have been important to diagnose brain tumors but have never been really a therapeutic target. And this changes the landscape, and we can now target IDH mutations in gliomas. And that's really important. The second thing, the second real take-home message, is we can safely delay radiation therapy and chemotherapy in some patients with these lower-grade gliomas, potentially with IDH mutation and IDH inhibition. And that's really important. Chemotherapy and radiation therapy are important, but if we can delay those treatments and prevent side effects, that could be helpful for some of our patients. So really important update from ASCO and what I want to spend most of the time on our podcast focusing on this INDIGO study. But there were a bunch of other things going on in brain tumors at ASCO, as there always are. And I want to highlight 2 studies about some things that the groups of patients may be interested in knowing that happened at the meeting. The first is a study called the INB-200 study. And this is a phase 1 study, so it's earlier in development. But it's an immunotherapy study. And brain tumor patients and caregivers will know that we've really wanted to find an immunotherapy that works for brain tumors. And we haven't yet. And we're still not there, but this study is an important step in that direction. So this study from a group at the University of Alabama looked at something called gamma delta T cells. And T cells are really important. They're part of the anti-tumor response. They're what the body uses to attack the tumor. So we like those T cells. And particularly, these gamma delta T cells are important in targeting tumor cells in glioblastoma cells. They're also unique. They can avoid the toxicity of chemotherapy. Radiation therapy and chemotherapy suppresses the T cells. They make some go down, or decreased in number, which is not what we want. And these gamma delta T cells were genetically created so that they were resistant to chemotherapy. And that's really, really important. We want an immunotherapy that works and one that isn't suppressed by our other treatments. And that's been a real barrier for glioma patients. So in this phase 1 study, they found the right dose of these gamma delta T cells, and that's the goal of a phase 1 study. But there were some early signs that this may be changing the tumor. One of the patients underwent surgery before and after they got this infusion. And we were able to see this. Investigators were able to see the gamma delta T cells up in the tumor. So this doesn't change practice. Patients don't need to go out and seek out the gamma delta T cells yet. But it's one of those early findings that says that we need to keep looking at immunotherapy. And as a community, this is something we need to keep focusing on. And then the last abstract and study I wanted to focus on is for a rare disease. This would not be something that would be relevant for all of our listeners and the brain tumor patients but for a subgroup of patients that have a condition called VHL, or von Hippel-Lindau. And von Hippel-Lindau is a genetic condition. So, most brain tumors are not inherited. You don't get it from a mom or a dad or pass it on, except for these patients, you do. And it comes from a gene that's inherited in families called the VHL or the von Hippel-Lindau gene. And these patients are predisposed to get tumors all throughout the body and the kidneys and the brain and the eye. And this is a lifelong disease where these tumors can really grow slowly over time and cause significant problems. And in the past few years, there's been a new treatment called belzutifan. Belzutifan is the name of this drug that has been shown to be effective in the kidney tumors for patients with VHL. And at ASCO this year, there was a new study showing that it's also effective in treating the brain tumors for these patients. And that's really important. We just haven't had a treatment other than surgery or radiation therapy for these tumors. And oftentimes, they grow after surgery and radiation therapy and we need an additional treatment. So in this study, the investigators looked at, "Does this drug belzutifan work for treating the CNS tumors, hemangioblastoma?" And found that around 50% of patients had a response, so a shrinkage in the size of the tumor. 90% of patients had control of their brain tumor disease, which is really important. And it worked really quickly, so it worked in about 3 to 5 months, which is shorter than what we would see for the kidney tumors. So that's exciting news for VHL patients, patients with von Hippel-Lindau, and another important update from the 2023 ASCO. So thanks for listening to this update of CNS brain tumors at the 2023 ASCO Annual Meeting. Again, I'm Roy Strowd, a neuro-oncologist at Wake Forest University School of Medicine. Delighted to bring you this brief summary of new research in the field. ASCO: Thank you, Dr. Strowd. You can find more research from recent scientific meetings at www.cancer.net. Cancer.Net Podcasts feature trusted, timely, and compassionate information for people with cancer, survivors, and their families and loved ones. Subscribe wherever you listen to podcasts for expert information and tips on coping with cancer, recaps of the latest research advances, and thoughtful discussions on cancer care. And check out other ASCO Podcasts to hear the latest interviews and insights from thought leaders, innovators, experts, and pioneers in oncology. Cancer.Net is supported by Conquer Cancer, the ASCO Foundation, which funds lifesaving research for every type of cancer, helping people with cancer everywhere. To help fund Cancer.Net and programs like it, donate at CONQUER.ORG/Donate.

Dr. Kathryn Nevel talks with Dr. Ingo Mellinghoff about how vorasidenib improved progression-free survival in patients with Isocitrate dehydrogenase (IDH)–mutant grade 2 gliomas. Read the related article in The New England Journal of Medicine. Visit NPUb.org/Podcast for associated article links.

Go online to PeerView.com/PYA860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Newer treatment modalities for acute myeloid leukemia (AML) have rapidly eclipsed the decades-long cytarabine-based standard of care and helped clinicians adopt more personalized management using innovative cytotoxic platforms, targeted agents (including FLT3, BCL2, and IDH inhibitors), and other unique management strategies. Clinicians can now improve patient outcomes across all AML treatment settings, while at the same time selecting the most potent, personalized option that can be designed to address a given patient's needs. This “Seminars and Tumor Board” activity, adapted from our recent live event held at the 2023 ASCO Annual Meeting and developed in collaboration with the HealthTree Foundation for Acute Myeloid Leukemia, reveals how modern baseline assessment paired with cutting-edge prognostication has pushed patient management to new heights of innovation and changed the management of patients with AML with therapeutically relevant features (such as FLT3 or IDH mutations), patients presenting without driver mutations, or individuals with comorbid illnesses or higher-risk features. Join the AML experts for a real-world “Tumor Board”–style discussion of how the latest evidence can inform your practice. Upon completion of this activity, participants should be better able to: Summarize baseline patient-related and disease-related factors, including age, comorbidities, functional status, and cytogenetic/mutational findings, that can influence prognostication and treatment selection in AML; Cite current evidence supporting the personalized use of novel treatment modalities, including new cytotoxic platforms, targeted agents, immunotherapy, and epigenetic strategies, for the management of newly diagnosed or relapsed/refractory AML; Integrate novel therapeutics into the personalized team-based management of AML according to the results of baseline assessment, presence or absence of targetable mutations, functional status, or AML subtype; and Address care delivery considerations, including optimized dosing and safety management, when caring for patients with AML

Go online to PeerView.com/PYA860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Newer treatment modalities for acute myeloid leukemia (AML) have rapidly eclipsed the decades-long cytarabine-based standard of care and helped clinicians adopt more personalized management using innovative cytotoxic platforms, targeted agents (including FLT3, BCL2, and IDH inhibitors), and other unique management strategies. Clinicians can now improve patient outcomes across all AML treatment settings, while at the same time selecting the most potent, personalized option that can be designed to address a given patient's needs. This “Seminars and Tumor Board” activity, adapted from our recent live event held at the 2023 ASCO Annual Meeting and developed in collaboration with the HealthTree Foundation for Acute Myeloid Leukemia, reveals how modern baseline assessment paired with cutting-edge prognostication has pushed patient management to new heights of innovation and changed the management of patients with AML with therapeutically relevant features (such as FLT3 or IDH mutations), patients presenting without driver mutations, or individuals with comorbid illnesses or higher-risk features. Join the AML experts for a real-world “Tumor Board”–style discussion of how the latest evidence can inform your practice. Upon completion of this activity, participants should be better able to: Summarize baseline patient-related and disease-related factors, including age, comorbidities, functional status, and cytogenetic/mutational findings, that can influence prognostication and treatment selection in AML; Cite current evidence supporting the personalized use of novel treatment modalities, including new cytotoxic platforms, targeted agents, immunotherapy, and epigenetic strategies, for the management of newly diagnosed or relapsed/refractory AML; Integrate novel therapeutics into the personalized team-based management of AML according to the results of baseline assessment, presence or absence of targetable mutations, functional status, or AML subtype; and Address care delivery considerations, including optimized dosing and safety management, when caring for patients with AML

Go online to PeerView.com/PYA860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Newer treatment modalities for acute myeloid leukemia (AML) have rapidly eclipsed the decades-long cytarabine-based standard of care and helped clinicians adopt more personalized management using innovative cytotoxic platforms, targeted agents (including FLT3, BCL2, and IDH inhibitors), and other unique management strategies. Clinicians can now improve patient outcomes across all AML treatment settings, while at the same time selecting the most potent, personalized option that can be designed to address a given patient's needs. This “Seminars and Tumor Board” activity, adapted from our recent live event held at the 2023 ASCO Annual Meeting and developed in collaboration with the HealthTree Foundation for Acute Myeloid Leukemia, reveals how modern baseline assessment paired with cutting-edge prognostication has pushed patient management to new heights of innovation and changed the management of patients with AML with therapeutically relevant features (such as FLT3 or IDH mutations), patients presenting without driver mutations, or individuals with comorbid illnesses or higher-risk features. Join the AML experts for a real-world “Tumor Board”–style discussion of how the latest evidence can inform your practice. Upon completion of this activity, participants should be better able to: Summarize baseline patient-related and disease-related factors, including age, comorbidities, functional status, and cytogenetic/mutational findings, that can influence prognostication and treatment selection in AML; Cite current evidence supporting the personalized use of novel treatment modalities, including new cytotoxic platforms, targeted agents, immunotherapy, and epigenetic strategies, for the management of newly diagnosed or relapsed/refractory AML; Integrate novel therapeutics into the personalized team-based management of AML according to the results of baseline assessment, presence or absence of targetable mutations, functional status, or AML subtype; and Address care delivery considerations, including optimized dosing and safety management, when caring for patients with AML

Go online to PeerView.com/PYA860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. Newer treatment modalities for acute myeloid leukemia (AML) have rapidly eclipsed the decades-long cytarabine-based standard of care and helped clinicians adopt more personalized management using innovative cytotoxic platforms, targeted agents (including FLT3, BCL2, and IDH inhibitors), and other unique management strategies. Clinicians can now improve patient outcomes across all AML treatment settings, while at the same time selecting the most potent, personalized option that can be designed to address a given patient's needs. This “Seminars and Tumor Board” activity, adapted from our recent live event held at the 2023 ASCO Annual Meeting and developed in collaboration with the HealthTree Foundation for Acute Myeloid Leukemia, reveals how modern baseline assessment paired with cutting-edge prognostication has pushed patient management to new heights of innovation and changed the management of patients with AML with therapeutically relevant features (such as FLT3 or IDH mutations), patients presenting without driver mutations, or individuals with comorbid illnesses or higher-risk features. Join the AML experts for a real-world “Tumor Board”–style discussion of how the latest evidence can inform your practice. Upon completion of this activity, participants should be better able to: Summarize baseline patient-related and disease-related factors, including age, comorbidities, functional status, and cytogenetic/mutational findings, that can influence prognostication and treatment selection in AML; Cite current evidence supporting the personalized use of novel treatment modalities, including new cytotoxic platforms, targeted agents, immunotherapy, and epigenetic strategies, for the management of newly diagnosed or relapsed/refractory AML; Integrate novel therapeutics into the personalized team-based management of AML according to the results of baseline assessment, presence or absence of targetable mutations, functional status, or AML subtype; and Address care delivery considerations, including optimized dosing and safety management, when caring for patients with AML

Check out this week's QuadCast as we summarize the most important results from ASCO 2023. This includes the PROSPECT trial for rectal cancer, final reporting of the ADAURA trial for NSCLC, a targeted therapeutic for IDH mutated gliomas, and much more. Quadshotnews@gmail.com

Featuring perspectives from Drs Courtney DiNardo and Mark Levis, including the following topics: Introduction (0:00) Case: A man in his early 80s with newly diagnosed acute myeloid leukemia (AML) with significant comorbidities receives decitabine/venetoclax — Rebecca L Olin, MD, MSCE (7:36) Cases: A man in his mid 50s after 7 + 3 and allogeneic stem cell transplantation (SCT) presents with myeloid sarcoma; a man in his late 70s after 7 + 3 and allogeneic SCT presents with myeloid sarcoma — Spencer H Bachow, MD and Ranju Gupta, MD (12:16) Case: A man in his late 30s with core binding factor AML after induction CLAG-M with gemtuzumab ozogamicin followed by high-dose cytarabine x 4 — Anna Halpern, MD (18:10) Case: A woman in her mid 60s with newly diagnosed del(5q) AML with monocytic differentiation and multiple mutations (GATA2, BCOR, NF1 and RUNX1) receives azacitidine and venetoclax — Bhavana (Tina) Bhatnagar, DO (31:05) Selection of Therapy for Patients with AML (35:20) Cases: A man in his early 50s with therapy-related AML with an MLL mutation who receives CPX-351; a man in his early 70s with secondary AML with an IDH mutation — Amany R Keruakous, MD, MS and Priya Rudolph, MD, PhD (41:42) Case: A man in his early 70s with recurrent AML with an IDH2 mutation receives enasidenib and develops differentiation syndrome/disease progression — Dr Halpern (50:00) CME information and select publications

Andrew Scarborough was first diagnosed with an aggressive form of Glioblastoma brain cancer (GBM), which is already very aggressive. Seeing that his form of GBM did not respond well to traditional chemo and radiation treatments, he stopped these and looked at alternative approaches. This led him to discovering the decades of work published in the metabolic mitochondrial theory of cancer and how a ketogenic diet could help the body fight off this deadly disease. From keto he found the carnivore way of eating, and has since stopped all medications, stopped his seizures without meds, and his most recent MRI of his brain shows that there has been no progression in a decade, where the average life expectancy for the average GBM without treatment is 3 months, and those getting full treatment have an average life expectancy of 15 to 18 months. And for his specific type of GBM (Unmethylated, IDH-wild type) it's even less. So, this is an exceptional case indeed. He has since moved to advance the medical literature by performing his own human trials with other GBM patients in the UK with a ketogenic/carnivore diet at Charring Cross Hospital, and is joined today with his research partner in this project, Isabella Cooper, to discuss his personal journey, their research, and a new hope for cancer victims. I hope you all enjoy this episode as much I had making it, and if you would like to learn more about Andrew and Isabella's work, you can find out more on the links below. Enjoy! Website www.beatbraincancer.co.uk The Human Guinea Pig Project podcast https://podcasts.apple.com/us/podcast/the-human-guinea-pig-project/id1488201848 Twitter (@ascarbs) https://mobile.twitter.com/ascarbs   And special thank you to the sponsor of this episode, The Carnivore Bar! Use discount Code "Anthony" for 10% off all orders! https://the-carnivore-bar.myshopify.com/?sca_ref=1743809.v3IrTuyDIi   Contact and Follow Dr Chaffee: ✅PATREON for early releases, bonus content, and weekly Zoom meetings https://www.patreon.com/AnthonyChaffeeMD ✅Sign up for our 30-day carnivore challenge and group here! https://www.howtocarnivore.com/ ✅INSTAGRAM: @anthonychaffeemd www.instagram.com/anthonychaffeemd/ ✅TWITTER: @Anthony_Chaffee ✅TIKTOK: @AnthonyChaffeeMD ✅Apple Podcast: The Plant Free MD https://podcasts.apple.com/au/podcast/the-plant-free-md-podcast/id1614546790 ✅Spotify: The Plant Free MD https://open.spotify.com/show/0WQtoPLuPMWWm3ZT3DYXzp?si=PPc2rXZzQXuzjIRK__SEZQ ✅To Sign up for a personal consultation with me, you can use my Calendly link below to schedule an appointment: ✅60 minute consultation https://calendly.com/anthonychaffeemd/60-minute-consultation ✅For collaborations, please email me at the below address. Please understand that I cannot give advice over email, but only in a consultation setting: AnthonyChaffee@gmail.com For more of my interviews and discussions, as well as other resources, go to my Linktree at: ✅ https://linktr.ee/DrChaffeeMD OR my website at: ✅ www.TheCarnivoreLife.com   Affiliate Links: ✅X3 bar system with discount code "DRCHAFFEE" https://www.kqzyfj.com/click-100676052-13511487 ✅THE CARNIVORE BAR: Discount Code "Anthony" for 10% off all orders! https://the-carnivore-bar.myshopify.com/?sca_ref=1743809.v3IrTuyDIi ✅CARNIVORE CRISPS: Discount Code "DRCHAFFEEMD" for 10% off all orders! www.carnivorecrisps.com ✅Shop Amazon https://www.amazon.com/shop/anthonychaffeemd?ref=ac_inf_hm_vp   And please like and subscribe to my podcast here and Apple/Google podcasts, as well as my YouTube Channel to get updates on all new content, and please consider giving a 5-star rating as it really helps! Music track: Acoustic Breeze from Bensound.com #nutrition #keto #bodybuilding #carnivore #fyp #motivation #carnivore #carnivorediet #weightloss #thecarnivorelife #weightsandsteaks #teamcarnivore #meatheals #yestomeat #nutrition #diet #autoimmune #rugby #rugbyunion #rugbyplayer #weightlossjourney #weightlifting #steak #bodybuilding #strength #strengthtraining #weighttraining #zerocarb #keto #ketovore #ribeye #liondiet #ketodiet #carnivoreketo #ketotransformation #carnivore75hard #vegan #sowell #thomassowell #dairy #milk #cheese #nsng #lchf #lcif