Podcasts about myeloid

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Best podcasts about myeloid

Latest podcast episodes about myeloid

Curiosity Daily
Healing Hearing Hairs, Sun Phones, Chicken Gods

Curiosity Daily

Play Episode Listen Later Aug 4, 2022 12:00


Hear about a new treatment that may be able to reverse hearing loss, how new solar energy storage technology could eventually power our phones, and the surprisingly grand history of chickens.Reversing hearing loss. “Reversing hearing loss with regenerative therapy” by Zach Winnhttps://news.mit.edu/2022/frequency-therapeutics-hearing-regeneration-0329“What are Progenitor Cells? Exploring Neural, Myeloid and Hematopoietic Progenitor Cells” by Nicole Gleichmannhttps://www.technologynetworks.com/cell-science/articles/what-are-progenitor-cells-exploring-neural-myeloid-and-hematopoietic-progenitor-cells-329519“Quick Statistics About Hearing” by the National Institute on Deafness and Other Communication Disordershttps://www.nidcd.nih.gov/health/statistics/quick-statistics-hearing“PCA Approach” and “About Hearing Loss” by Frequency Therapeuticshttps://www.frequencytx.com/science/pca-approach/https://www.frequencytx.com/hearing-loss/about-hearing-loss/“FX-322 in Adults With Acquired Sensorineural Hearing Loss” by Frequency Therapeutics Clinical Trialhttps://clinicaltrials.gov/ct2/show/NCT05086276Phone charger, but make it the sun.“Converting solar energy to electricity on demand” by Chalmers University of Technologyhttps://techxplore.com/news/2022-04-solar-energy-electricity-demand.html“For a Better Future” by The MOST Solar Projecthttps://mostsolarproject.eu/“Molecular solar thermal (MOST) energy storage and release system” by Kasper Moth-Poulsen, et al.https://pubs.rsc.org/en/content/articlelanding/2012/ee/c2ee22426g“Solar Energy: Benefits and Drawbacks” by Matthew Johnstonhttps://www.investopedia.com/articles/investing/053015/pros-and-cons-solar-energy.aspChicken breeding.“The biocultural origins and dispersal of domestic chickens” by Joris Peters, Ophélie Lebrasseur, Evan K. Irving-Pease, Ptolemaios Dimitrios Paxinos, Julia Best, Riley Smallman, Cécile Callou, Armelle Gardeisen, Simon Trixl, Laurent Frantz, Naomi Sykes, Dorian Q. Fuller, and Greger Larson.https://www.pnas.org/doi/full/10.1073/pnas.2121978119“A new origin story for domesticated chickens starts in rice fields 3,500 years ago” by Bruce Bower.https://www.sciencenews.org/article/chicken-domestication-bones-origin-asia-rice-fields-exotic-animals“Redefining the timing and circumstances of the chicken's introduction to Europe and north-west Africa” by Julia Best, Sean Doherty, Ian Armit, Zlatozar Boev, Lindsey Büster, Barry Cunliffe, Alison Foster, Ben Frimet, Sheila Hamilton-Dyer, Tom Higham, Ophélie Lebrasseur, Holly Miller, Joris Peters, Michaël Seigle, Caroline Skelton, Rob Symmons, Richard Thomas, Angela Trentacoste, Mark Maltby, Greger Larson, and Naomi Sykeshttps://www.cambridge.org/core/journals/antiquity/article/redefining-the-timing-and-circumstances-of-the-chickens-introduction-to-europe-and-northwest-africa/0797DAA570D51D988B0514C37C2EC534Follow Curiosity Daily on your favorite podcast app to get smarter with Calli and Nate — for free! Still curious? Get exclusive science shows, nature documentaries, and more real-life entertainment on discovery+! Go to https://discoveryplus.com/curiosity to start your 7-day free trial. discovery+ is currently only available for US subscribers.Find episode transcripts here: https://curiosity-daily-4e53644e.simplecast.com/episodes/healing-hearing-hairs-sun-phones-chicken-gods

Mornings with Jeff & Rebecca
Miracles Still Happen Every Day

Mornings with Jeff & Rebecca

Play Episode Listen Later Jun 30, 2022 1:47


A pastor named Dave had been fighting Acute Myeloid Leukemia for a while and all signs were pointing up that he was going to beat this but then something tragic happened. His appendix ended up rupturing and because of that, he was in some real trouble. The cancer had destroyed all of his white blood cells which prevented him from fighting off any sort of infection.But just as the doctors and members of his church were losing hope of him beating this, one lady at his church said something that stuck with him. 

ASCO Daily News
Advances in Hematologic Malignancies at ASCO22

ASCO Daily News

Play Episode Listen Later Jun 22, 2022 16:13


Dr. Stephen Ansell, of the Mayo Clinic in Minnesota, tells host Dr. John Sweetenham, of the UT Southwestern Harold C. Simmons Comprehensive Cancer Center, about ECHELON-1's compelling overall survival analysis in newly diagnosed Hodgkin lymphoma and key advances in the SHINE, MOMENTUM, and ASCEMBL trials that were featured at the 2022 ASCO Annual Meeting.   TRANSCRIPT Dr. John Sweetenham: Hello, I'm Dr. John Sweetenham, the associate director for Clinical Affairs at UT Southwestern's Harold C. Simmons Comprehensive Cancer Center, and host of the ASCO Daily News Podcast.  My guest today is Dr. Stephen Ansell, a professor and chair of medicine at the Department of Hematology at the Mayo Clinic in Minnesota. Dr. Ansell shares his insights on key advances in hematologic malignancies that were featured at the 2022 ASCO Annual Meeting.  Our full disclosures are available in the show notes and disclosures of all guests on podcasts can be found on our transcripts at asco.org/podcasts.   Stephen, it's great to have you on the podcast today.  Dr. Stephen Ansell: Thanks so much for having me, John.  Dr. John Sweetenham: So, Stephen, I'd like to start with your thoughts on Abstract 7503, which of course is one that you authored, and this is a 6-year follow-up study of the ECHELON-1 trial. This includes a positive overall survival analysis for brentuximab vedotin in newly diagnosed advanced Hodgkin lymphoma. Can you tell us more about this?  Dr. Stephen Ansell: Yeah, sure, John. And you know, as you point out, the thing that's really interesting and unique about this trial is we haven't had a lot of studies in Hodgkin lymphoma that show an overall survival advantage as you well know. Doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) chemotherapy has actually been quite difficult to beat when it's been an overall survival endpoint that one has been looking at.  There have been some other strategies in the past that have been looked at—the escalation of therapies such as escalator BEACOPP, and maybe modification of therapy to minimize toxicity, such as the RATHL trial where bleomycin is dropped out.  In all of these studies, there have been advantages for progression-free survival, but not clearly against ABVD as the standard and overall survival advantage. So, our listeners would probably know that ECHELON-1 was a comparison between brentuximab vedotin ABVD chemotherapy, and ABVD chemotherapy as the standard, showing an initially modified progression-free survival advantage and subsequently a progression-free survival advantage. But now with 6 years of follow-up, an overall survival advantage. And I think that's really what makes this quite unique.  Dr. John Sweetenham: One of the reasons I think many people, myself included, thought that it was going to be a very high bar to show an overall survival difference in this study was simply the fact that treatments to relapsed and refractory Hodgkin lymphoma, in general, have improved really quite substantially, both before and during the conduct of this trial.  Do you have any thoughts on that? Were you surprised? And any thoughts on why we're seeing this in the face of the rapidly evolving treatment landscape in the relapse setting?  Dr. Stephen Ansell: Yeah, I think that's an excellent point. And, John, I think there have been 2 schools of thought, as you know, those that have felt that the first shot was always the best one. And you should go hard right off the bat and others have said, you don't need to give everybody intensive treatment, because as you say, subsequent therapies can be very effective.  This would actually challenge that second position because when we looked at how patients were managed in both groups when they relapsed, the vast majority of relapsing patients in the group that got ABVD subsequently got brentuximab vedotin, as part of their regimen. Most patients—and it was balanced in both arms—got the standard kind of salvage treatment, autologous stem cell transplant approach, and some patients in both arms, got novel agents, including PD1 blockade, that was a minority, partly because of the timing of when the study was done.  But I think all of the things that we would normally do were done, and yet there's still a survival advantage. The one interesting thing I think that's worth taking away from this is when one looked at some of the influences on what might have made that overall survival difference, there were more patients progressing and dying from Hodgkin's in the ABVD arm suggesting that adding brentuximab vedotin does make a difference to the disease itself. But also interestingly, there were fewer patients in the brentuximab arm, who got a second lymphoma.  And interestingly, there were quite a substantial number of people in the ABVD arm when they relapsed to or subsequently got a different lymphoma, suggesting that the brentuximab vedotin, may actually target a precursor cell in a heme malignancies space and actually may have a benefit that way.  Dr. John Sweetenham: So, what's your overall conclusion from this study now that brentuximab vedotin plus ABVD is the standard of care for patients with newly diagnosed advanced Hodgkin lymphoma?  Dr. Stephen Ansell: I would say that if you have advanced-stage disease with classical Hodgkin lymphoma histology, it's very difficult not to say that this would be the standard of care to manage the patients.  I think we've learned that this study applied to older patients who are often difficult to treat. And so, hence, that's also a very valid treatment to give. And it's very difficult to argue against giving treatment that has an overall survival advantage for patients. So, in my practice, this has become the standard of care.  Dr. John Sweetenham: Okay, great. Thanks, Stephen. Let's move on and talk about LBA7502. This reported on the primary results of a double-blind placebo-controlled study known as SHINE, which looks at the use of ibrutinib in combination with bendamustine and rituximab followed by rituximab maintenance as a first-line treatment for older patients with mantle cell lymphoma. What are your thoughts and key takeaways from this study?  Dr. Stephen Ansell: Again, I think this is a very important study in older patients with mantle cell lymphoma. So, as you well know and many of our listening audience would know that we kind of has 2 strategies in mantle cell lymphoma. In younger patients, we may treat them with a more intense approach, sometimes with autologous stem cell transplant, often with a kind of alternating high-intensity therapies.  For patients who are older, bendamustine rituximab is really a standard therapy for patients with that demographic. And this now really pushes the field forward by showing that if you take bendamustine rituximab and add ibrutinib an effective therapy in the relapse setting, in the upfront setting, there is a substantial advantage for how patients do.  If one looks at the overall outcomes, it shows that progression-free survival is improved; we don't have overall survival benefit yet. But as we track these patients, it'll be interesting to see if that does transpire in time.  I will say again that I always like placebo-controlled arms because it helps us really get a handle on toxicities. And in general, in this population of patients, it was well tolerated. So, I think this, again, is a regimen that is going to be very useful in older patients.  Dr. John Sweetenham: I think that the lack of an overall survival benefit so far could of course be because there was a crossover in a study for those patients who progressed on the placebo-controlled arm.  But my other question about this, just to get your impression, is that there is a subgroup of elderly patients or older patients with a very slowly progressive disease where the management approach has been more of a watch-and-wait and observation-only approach until they become symptomatic. Do you think results like this, which start to show a progression-free survival benefit from upfront therapy, change that philosophy? Should we be thinking harder about whether anyone should be observed now?  Dr. Stephen Ansell: I think that's a good question. And to be frank, I will say that in my practice, I still have a spirit of, I'm happy to watch patients who have a very low burden of disease to just get a sense of the pace of the disease. Because as you say, you may be surprised by a subset of patients whom you may not need to treat for a year or even longer. And my view is that a year of no treatment is always better than a prolonged progression-free survival interval on treatment. So, I take the view that if you don't need to treat, that is still the best management.  Dr. John Sweetenham: Great, thank you! So, we're going to change gear for a moment and move out of lymphoid malignancy and talk a little about Myeloproliferative Syndrome. I'm interested to hear your thoughts on the MOMENTUM study. So, this was Abstract 7002, another phase 3 randomized study, in this case, looking at the use of momelotinib versus danazol in symptomatic and anemic patients with Myelofibrosis, who previously had a JAK inhibitor. What are your thoughts on this study?  Dr. Stephen Ansell: I think again, this is really good and very interesting data because those that treat Myelofibrosis will know these are challenging to treat. And many times, the symptoms they experience, the transfusion challenges they have, and the difficulty they have with very large spleens are all things that impact the quality of life quite profoundly. And therapies, in general, that would benefit those symptoms are always highly valuable.  So, I did find, again, I'm not as much of an expert in Myelofibrosis, but certainly, my colleagues who are were very satisfied with these results, basically showing improvement when compared to danazol, which again, I would anticipate as modest control with not particularly good efficacy, again, some of those symptoms I just spoke about, but momelotinib really showed a substantial benefit for the symptoms that this disease causes, and obviously transfusion requirements and improved spleen sizes and spleen symptoms.  So, I think in general, for managing patients for whom the quality of life is profoundly impacted, this is going to be a useful agent moving forward.  Dr. John Sweetenham: Okay, great. Thanks. And staying on the theme of Myeloid diseases, Abstract 7004 reported on the efficacy and safety, from the so-called ASCEMBL study, another phase 3 study, in this case, looking at the use of asciminib versus bosutinib in patients with Chronic Myeloid Leukemia (CML) who are in chronic phase, and who had already received 2 or more tyrosine kinase inhibitors. And this was an update at week 56 of the study. Why do you think this study should be on our radar?  Dr. Stephen Ansell: Well, I think again, we're always looking for agents that make a difference, particularly with subsequent lines of therapy in this disease. I think bosutinib is really regarded as a standard of care in this population of patients and an agent that comes along, ascitinib in this case, that shows a significant benefit, that really brings yet another tool for us to utilize in these patients.  I must say, again, as I looked at the results, comparing also looking for the major molecular responses, and the benefit and durability thereof, this was pretty impressive data. And so, I think it's very useful in this disease to have a plethora of tools that we can reach to be able to really impact the outcome of patients. So, I think, again, this is highly relevant data that we would use in the clinic in the not-distant future.  Dr. John Sweetenham: Do you think it's likely it'll move into frontline treatment over time?  Dr. Stephen Ansell: So, I think that is a good question. I don't know the answer to that, except to say that these results are pretty impressive. And so, I do believe that that's going to need to be tested, but as has been done in CML over the decades and which is really to be applauded, there have been randomized trials, comparing head-to-head agents showing which agent really has the greatest benefit and efficacy. So, I'll watch that space with a lot of interest.  Dr. John Sweetenham: Thanks! And finally, I'd like to return to lymphoid malignancy. In the 2020s, it would be almost impossible to review a meeting such as ASCO without saying something about CAR T-cell therapy, and this podcast is going to be no exception.  So, I wonder if I could get your thoughts on Abstract 7571. And this was an abstract, which reported real-world outcomes for axicabtagene ciloleucel, otherwise known as the Axi-Cel, for the treatment of large B-cell lymphoma. And it looked at the outcomes according to race and ethnicity. What are your thoughts on this study?  Dr. Stephen Ansell: Well, John, I smiled when you were said there's not a possible to really have a conversation without bringing in CAR T-cell somewhere along the way, but what I liked about this abstract, is it really was bringing in the real-world data, because many times and again, I have to stress that real-world data, when it comes to CAR T-cells is probably not the real world in the most real-world nature of things. And that is just you have to have access to certain centers to be able to get this therapy. And I think that's what this abstract actually points to.  It does look at almost 1,400 patients treated with Axi-Cel. And now that in large cell lymphoma, this is a standard of care where we either use a post-transplant and now even as a first relapse therapy, this is becoming highly relevant. And the question is just always seeing discrepancies between various population groups when we look at how outcomes transpire from this therapy.  And as it turns out, if one looks at Asian populations, those are really not adversely impacted, or Hispanic populations. But the African American population continues to have a less favorable outcome, even with this sophisticated therapy.  And that does suggest that possibly, when those patients, in general, can get access to this care, might actually be a little later in the disease, greater disease burden, possibly a little later line of therapy, resulting in not as favorable results.  I think this is whereas health care providers, we need to turn our attention in the future. And that is to say, how can we make care be equally good for all patients everywhere within our country, rather than there being nuggets where certain people benefit a lot and other areas where people benefit very little.  Dr. John Sweetenham: Yeah, thank you. There was good discussion after this study was presented and I think much of it focused around exactly what you've just said. Most of this difference is almost certainly not biological but it's really related to access to care and so on and that was an important take-home message. So, thanks for emphasizing that.  Stephen, thanks so much for sharing your insights with us today regarding the 2022 ASCO Annual Meeting on our podcast. I really appreciate your being willing to talk to us.  Dr. Stephen Ansell: John, thank you very much for having me.  Dr. John Sweetenham: And thank you to our listeners for joining us today. You'll find links to the abstract discussed today on the transcripts 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.    Disclosures:  Dr. John Sweetenham:  Consulting or Advisory Role: EMA Wellness  Dr. Stephen Ansell:  Honoraria: WebMD, Research to Practice  Research Funding (Inst.): Bristol-Myers Squibb, Seattle Genetics, Affimed Therapeutics, Regeneron, Trillium Therapeutics, AI Therapeutics, ADC Therapeutics  Disclaimer:  The purpose of this podcast is to educate and 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.       

Blood Podcast
Germline predisposition mutations in AML, a new way to resolve NETs, and venetoclax and BAX mutations in normal myeloid cells of CLL patients

Blood Podcast

Play Episode Listen Later Feb 24, 2022 18:46


In this week's podcast, we'll look at work from researchers who found pathogenic or likely pathogenic variants of cancer predisposition genes in nearly 14% of adults with AML. Next, we'll review research demonstrating that a recently identified series of resolvins reduces neutrophil extracellular trap formation and enhances clearance of these NETs by macrophages, suggesting a new mechanism for the resolution of inflammation and coagulopathies associated with various infections. We'll conclude with research demonstrating that patients with CLL undergoing long-term venetoclax treatment exhibit a high incidence of cytopenias, clonal hematopoiesis, and myeloid neoplasms, and may acquire BAX mutations in normal myeloid cells.

Circulation on the Run
Circulation October 12, 2021 Issue

Circulation on the Run

Play Episode Listen Later Oct 11, 2021 27:23


Please join author Milton Packer and Associate Editor Justin Ezekowitz as they discuss the Perspective "Heart Failure and a Preserved Ejection Fraction: A Side-by-Side Examination of the PARAGON-HF and EMPEROR-Preserved Trials." Dr. Carolyn Lam: Welcome to Circulation on the Run, your weekly podcast summary and backstage pass to the Journal and its editors. We're your co-hosts. I'm Dr. Carolyn Lam, Associate Editor from the National Heart Center. Dr. Greg Hundley: And I'm Dr. Greg Hundley, associate editor, director of the Pauley Heart Center at VCU Health in Richmond, Virginia. Dr. Carolyn Lam: Greg, it really is so great to be back with you chatting about the papers here in the Journal. Thank you for going solo and for just being the greatest partner on earth. Thank you for that. For everyone listening in, we are back with some gusto and especially with this feature discussion today. You are not going to want to miss it. We are talking to Dr. Milton Packer as well as Dr. Justin Ezekowitz. We are going to compare PARAGON and EMPEROR-Preserved trials in heart failure with preserved ejection fraction. A really interesting discussion you're not going to want to miss, but now let's start with some papers in today's issue. I'd like to start, please. Dr. Greg Hundley: You bet. Dr. Carolyn Lam: Greg, you know the optimal duration of antiplatelet therapy in patients with high bleeding risk with or without oral anticoagulation after coronary stenting? Well, that still remains a question. Today's paper is a pre-specified subgroup analysis of the MASTER DAPT trial and reports on the outcomes of patients with or without an oral anticoagulation indication in this study. Dr. Greg Hundley: Right, Carolyn. Remind us. What was the MASTER DAPT trial? What did it test? Dr. Carolyn Lam: Ah. MASTER DAPT investigated an abbreviated or one-month versus a non-abbreviated or three to 12-month dual antiplatelet therapy and a stopping of antiplatelet therapy at six months strategy after coronary stenting in an all-comer population at high bleeding risk. Dr. Greg Hundley: Carolyn, what did this subgroup analysis of outcomes in patients with and without oral anticoagulation show? Dr. Carolyn Lam: At 12 months of follow-up, ischemic and net risk did not differ with abbreviated versus non-abbreviated anti-platelet regimens in both subgroups, although significantly fewer clinically relevant bleeding events occurred in the group without an oral anticoagulation indication. Whereas only numerically fewer bleeding events occurred in the group with an oral anticoagulation indication that did not reach statistical significance. This subgroup analysis from the MASTER DAPT trial really adds additional evidence that dual antiplatelet therapy beyond one month in patients with or without an indication for oral anticoagulation really has no benefit and only increases bleeding risk. Dr. Greg Hundley: Oh, very important finding, Carolyn. Great research. Well, Carolyn, how the extracellular matrix microenvironment modulates the contractile phenotype of vascular smooth muscle cells and confers vascular homeostasis really remains elusive. Thus, these investigators led by Professor Wei Kong at Peking University applied protein-protein interaction network analysis to explore novel extracellular matrix proteins associated with the vascular smooth muscle cell phenotype. Dr. Carolyn Lam: Huh. Interesting. What did they find, Greg? Dr. Greg Hundley: Right, Carolyn. By combining an in-vitro and an in-vivo genetic mice vascular injury model, they identified nidogen-2, a basement membrane glycoprotein, as a key extracellular matrix protein for maintenance of vascular smooth muscle cell identity. Nidogen-2 exerted its protective function via direct interaction and modulation of Jagged1-Notch3 signaling. Dr. Carolyn Lam: Wow! Nidogen-2 and Jagged1-Notch3. I always learn so much. What are the clinical implications, Greg? Dr. Greg Hundley: Right, Carolyn. Perhaps targeting nidogen-2 to precisely modulate Jagged1-Notch3 signaling, well, that may provide novel therapeutic strategy for atherosclerosis and post-injury restenosis. Dr. Carolyn Lam: Very nice. Well, in the next paper, we discuss inflammation in heart failure. We know that inflammation contributes to the pathogenesis of heart failure, but there is limited understanding of inflammation's potential benefits. Interesting, huh? Well, these authors, Dr. Wollert and colleagues from Hannover Medical School in Germany, identified an adaptive crosstalk between inflammatory cells and cardiomyocytes that protects against persistent afterload stress-induced heart failure in mice. Monocytes and macrophages produced myeloid-derived growth factor in the pressure overloaded myocardium to augment SERCA2a expression in cardiomyocyte's calcium cycling and contractility. Myeloid-derived growth factor plasma concentrations were also found to be elevated in patients with aortic stenosis and to decline after aortic valve implantation indicating that pressure overload also triggers myeloid-derived growth factor release in humans. Dr. Greg Hundley: Carolyn, really informative preclinical science, but what are the clinical implications? Dr. Carolyn Lam: Ah. These observations molecularly defined a feature of the inflammatory response to hemodynamic overload that protects against heart failure development. Inflammation's beneficial trade therefore need to be considered when developing inflammation as a therapeutic target in heart failure. All of this is really discussed in a lovely editorial entitled Inflammation and Heart Failure: Friend or Foe? That's by Drs. Hajjar and Leopold. Dr. Greg Hundley: Great job, Carolyn. Well, my next paper focuses on resistant hypertension. Carolyn, although lifestyle modifications generally are effective in lowering blood pressure among patients with unmedicated hypertension or those treated with one to two antihypertensive agents, the value of exercise and diet for lowering blood pressure in patients with resistant hypertension is unknown. To address this, Professor James Blumenthal and co-authors at Duke University Medical Center enrolled 140 patients with resistant hypertension with an average age of 63 years, 48% women, 59% black, 31% diabetes, and 21% with chronic kidney disease and randomly assigned them to A, a four-month cardiac rehab center-based program of lifestyle modification. We're going to call that C-LIFE, consisting of dietary counseling, behavior and weight management, and exercise. Or number 2 or the B, a single counseling session providing standardized education and physician advice. We'll call that SEPA. Dr. Greg Hundley: The primary endpoint was clinic measured systolic blood pressure. Secondary endpoints included 24-hour ambulatory blood pressure and selective cardiovascular disease biomarkers including baroreflex sensitivity to quantify the influence of baroreflex on heart rate; high-frequency heart rate variability to assess vagally-mediated modulation of heart rate; flow-mediated dilation to evaluate endothelial function; and pulse wave velocity to assess arterial stiffness; and then finally left ventricular mass to characterize left ventricular structure and remodeling. Dr. Carolyn Lam: Wow! That is a very, first of all, important clinical question. Then also, just very intricate methodology in assessing this. What did they find? Dr. Greg Hundley: Right, Carolyn. Between-group comparisons revealed that the reduction in clinic systolic blood pressure was greater in C-LIFE compared with SEPA. Next, 24-hour ambulatory systolic blood pressure also was reduced in C-LIFE with no change in SEPA. Then next, compared with SEPA, C-LIFE resulted in greater improvements in baroreflex sensitivity, high-frequency heart rate variability, and flow-mediated dilation. There was no between-group differences in pulse wave velocity or LV mass. Dr. Greg Hundley: Carolyn, diet and exercise can lower blood pressure in patients with resistant hypertension. When delivered in a cardiac rehabilitation setting, a four-month program of diet and exercise as adjunctive therapy, results in a significant reduction in clinic and ambulatory blood pressure, and improvement in selected cardiovascular disease biomarkers. Dr. Carolyn Lam: Wow! Really nice, Greg. Okay. Well, looks like we're all going to round up already with what else there is in today's issue. Let me start. There's an exchange of letters between Drs. Fang and Vinceti regarding the article Blood Pressure Effects on Sodium Reduction: Dose-Response Meta-analysis of Experimental Studies. Dr. Greg Hundley: Right, Carolyn. I've got a few things in the mail bag. First, Professor Anker has a Research Letter regarding the Kidney Function After Initiation and Discontinuation of Empagliflozin in Heart Failure Patients With and Without Type 2 Diabetes: Insights From the EMPERIAL Trials. Dr. Gerstenfeld has an ECG challenge entitled Atrioventricular Block with Narrow and Wide QRS: The Pause That Refreshes. Then lastly, Dr. Donald Lloyd-Jones has an AHA update regarding the American Heart Association's focus on primordial prevention. Well, Carolyn, I can't wait to hear this fantastic feature discussion with you and Dr. Packer. How about we jump to that? Dr. Carolyn Lam: Great. Let's go, Greg. Dr. Carolyn Lam: Because side-by-side exam of PARAGON and EMPEROR is like side-by-side of... Dr. Justin Ezekowitz: You can compare our new and our old prime minister much like your paper did. Dr. Milton Packer: Yeah, yeah. Dr. Justin Ezekowitz: There are [crosstalk] and it could be viewed until they perform in the broader world how it goes. You don't quite know. Dr. Milton Packer: The only problem is you can't do a head-to-head comparison of the old prime minister and the new prime minister. Dr. Justin Ezekowitz: That is true except that the head-to-head comparison includes excellent care by both the new and the old. I think that comparison's going to be pretty equal. I think we can case-control that one. Dr. Carolyn Lam: I really liked that that was politically correct because we are recording. Everybody, welcome to the feature discussion. I am here with Dr. Milton Packer from Baylor and he really needs no introduction. We're discussing heart failure with preserved ejection fraction. As well as our associate editor, Dr. Justin Ezekowitz from University of Alberta. Hence, in case anybody's wondering, we were talking about the Canadian elections. Let's just launch straight into it, a side-by-side comparison of PARAGON and EMPEROR-Preserved. Dr. Packer... Milton, if I may, what in the world drove you to do this? Dr. Milton Packer: My God. Oh, my God. Yes. Dr. Carolyn Lam: Tell us about what drove you to do this and please, if you could just summarize the results. Dr. Milton Packer: Well, let me just say from the outset that this was a commentary, not an original research article. Dr. Carolyn Lam: Yes. Dr. Milton Packer: The commentary was motivated by two very straightforward observations. We had two large scale outcome trials of two different drugs in heart failure with a preserved ejection fraction. I was privileged to serve as you were, Carolyn, on the leadership committees of both trials. It's not as if we have involvement in only one trial. We have involvement in both trials and we are very proud of that involvement. Dr. Milton Packer: One trial came in with a effect size of about 13% on its primary endpoint with a borderline P-value. A second trial, EMPEROR-Preserved, came in with a 21% reduction and its primary endpoint with a really small and persuasive P-value. The two patient populations in the two trials were really amazingly similar. We wanted to understand why it was 21% in one trial and persuasively so and why it appeared to be smaller in the PARAGON trial with sacubitril/valsartan. We thought, well, maybe that difference was related to how endpoints were defined or maybe that difference was related to the influence of ejection fraction. The reason we got excited about that was that as almost everyone knows, PARAGON found an influence of ejection fraction on the effect of sacubitril/valsartan in patients with HFpEF. We found an influence of ejection fraction on the effect of empagliflozin in HFpEF in EMPEROR-Preserved. We wanted to understand whether that influence was similar in the two trials. Dr. Milton Packer: Just to make life simple, PARAGON had created certain cut points for ejection fraction. They had presented and previously published in Circulation endpoints based on those cut points of ejection fraction. All we did was we used their endpoints and their cut points, and we put the two trials side by side. We did not do a statistical comparison of the effect size. There're actually no P-values in the whole commentary. But what we wanted to see was: Was the shape of the ejection fraction influence relationship similar or different in the two trials? Well, very simple. In PARAGON, as has been reported, there was a linear relationship: as ejection fraction increased, the effect of sacubitril/valsartan got smaller. In EMPEROR-Preserved, there was also an attenuation at a highest ejection fraction, but the relationship wasn't linear. It was like a hockey stick. It was flat and then went up at an ejection fraction over 62.5, which was the cut point that PARAGON used. Dr. Milton Packer: When we compared patients between the low 40s and the low 60s, the effect size in empagliflozin appeared to be larger than the effect size of sacubitril/valsartan in that ejection fraction group using the same endpoints. In fact, for hospitalizations for heart failure, which is really what SGLT2 inhibitors do, it was twice as great with empagliflozin in EMPEROR-Preserved than with sacubitril/valsartan in PARAGON-HF. We thought this was really interesting. We put the pictures up side by side. We wrote a commentary and Circulation was so kind to accept it. Dr. Carolyn Lam: Oh, but Milton, you were very, honestly as always, very clever to have done this analysis. But if I could reiterate a few things for the audience, which is very important. First of all, as you rightly first pointed out, it's a perspective piece. It is not a head-on comparison with P-values. It could not be. Let's just also give the audience a bit of background in that PARAGON included patients with an ejection fraction of 45% and above. EMPEROR-Preserved was above 40. PARAGON looked at total heart failure hospitalizations and cardiovascular death as a primary outcome. EMPEROR looked at first cardiovascular death or heart failure hospitalization. Dr. Carolyn Lam: Let's just remember the designs were different. Of course in the comparison, PARAGON compared sacubitril/valsartan versus valsartan. I like the way you very carefully wrote in your study that it was more a study of neprilysin inhibition since it's sacubitril/valsartan against valsartan and it was empagliflozin versus placebo. We know that it's important to state that as a basis. Then really important to say to everybody out there, pick up our journal. You must look at this bigger. I myself have already cited it at least twice already, Milton, because people will just naturally ask that. "Are the results different because of ejection fraction or different endpoints?" What you did there in that beautiful figure is that you tried as best as you can to match it up in terms of ejection fraction bins and match it up in terms of hospitalizations. There. I just wanted to state those few things, but I'm really- Dr. Milton Packer: Oh, no. No. Carolyn, you're 100% right. That's why there are couple of things. I just want to underscore what you said because I think your points were spot on. First of all, we really lined up the endpoints and the ejection fraction. We tried our best to compare apples and apples. It would not have been a useful exercise for us to compare different endpoints and different ejection fraction subgroups. But I just want to make sure that everyone understands: I'm a big fan of sacubitril/valsartan and I'm a big fan of neprilysin inhibition. As you know, both PARADIGM-HF and PARAGON-HF weren't really tests of sacubitril/valsartan; they were tests of neprilysin inhibition. They were great tests at that. PARAGON in particular was a great test of that. We're comparing neprilysin inhibition and SGLT2 inhibition. Dr. Milton Packer: But here's my most important point: we do not want people to choose one over the other. That was not the intent. We think that there are data in patients with certain ejection fractions, let's say between 40 and 60, I'm just creating a range, where both interventions are appropriate. Now I understand there are cost considerations and I don't want to minimize that, but we are not suggesting that anyone prefer one drug over the other. All we wanted to do was we wanted to ask the question: Since the effect size in one trial seemed to be different than the effect size in the other trial, what were the ejection fraction subgroups that represented that difference? We found that the patients with ejection fractions greater than 60, 65% did not contribute to that difference. It was the patients with lower ejection fractions that contributed to the difference. I hope that's helpful. Dr. Carolyn Lam: Ah. That's wonderful. Justin, have you recovered from the talk about the Canadian elections? Dr. Justin Ezekowitz: Oh. I have indeed. Dr. Carolyn Lam: I'm on swinging. Dr. Justin Ezekowitz: I have indeed. Thanks for recognizing that Canada just had a major election we carried out in six weeks. But, Milton, I really enjoyed reading this. Maybe I can just ask you about two elements within this perspective piece, which is number 1, what's incredibly concordant is a lack of difference across cardiovascular death for both agents in both trials regardless of the trial differences and the potential differences in patient populations recruited; that's number 1. It's incredibly flat for cardiovascular death. Dr. Justin Ezekowitz: But number 2 is there is a danger in comparing trials even non-statistically. That's often a pitfall we get into, but we have to put some frame of reference on that. What is the one or two key things you think differ between PARAGON and EMPEROR-Preserved that you say, "You really need to look at these trials differently"? Those two questions came to mind when looking at this great figure that you produced. Dr. Milton Packer: Okay. The first question is so much easier and that is that these drugs don't reduce cardiovascular deaths. Full stop. It's really interesting because sacubitril/valsartan reduces cardiovascular death in people with ejection fractions of 40% or less, but not in patients with ejection fraction greater than that. The primary effect is heart failure hospitalizations. Empagliflozin didn't reduce cardiovascular death even in patients with the ejection fraction less than 40% or greater than 40%. What we're really, really talking about two drugs where the major effect is a reduction in heart failure hospitalizations. That comes out whether you do the analysis as time-to-first-event or total heart failure hospitalizations. Dr. Milton Packer: Of course, we're looking forward to the DELIVER trial with dapagliflozin. My own personal expectation is they're going to come out with a very striking effect on heart failure hospitalizations and not on cardiovascular deaths. Cardiovascular deaths in patients with HFpEF is really... It's a hard goal because only half of the deaths are cardiovascular. These patients have so many comorbidities that influence prognosis. The other thing, which is really important, is that heart failure hospitalizations only represented 18% of all hospitalizations in these patients; it's really small. I think of empagliflozin as being a treatment of the heart failure of HFpEF, not a treatment for HFpEF. I hope that makes sense. Justin, what was your second question? Dr. Justin Ezekowitz: Absolutely. Dr. Milton Packer: Oh, the differences between- Dr. Justin Ezekowitz: Yeah. Thank you, Milton. Dr. Milton Packer: Okay. There's always differences between two trials. As I said before, Carol and I were involved in both trials. They were done slightly at different times. They didn't overlap. Remember that the cut points in the two trials, one was 40%, one was 45%, really didn't matter to our analysis because we corrected for that in our ejection fraction subgroups. I was actually really much more impressed by the similarities than by the differences, but here's the catch. HFpEF is an incredibly heterogeneous disease. When we look at baseline characteristics, we're looking at means, medians, percentages. We're not picking up on any heterogeneity and there's a lot of heterogeneity. I actually think that HFrEF is a reasonably homogeneous disease. I think HFpEF is an incredibly diverse disease with a whole host of different disorders. What I'm amazed by is that we actually got an effect size that was greater than 20% in an all-comers HFpEF analysis. Dr. Milton Packer: But in all honesty, Justin, it wasn't really all-comers. We excluded people with BMIs over 45. There are a lot of patients who are obese and had BMIs greater than 45 who have HFpEF. By the way, especially in Texas. I didn't say that. We didn't enroll those patients. In all honesty, if I had to do it all over again, I would have. By the way, PARAGON didn't enroll them either. Dr. Carolyn Lam: Well, this is an incredible conversation. I know that we could just do a whole hour of chatting about what this implies for the higher ejection fraction, what this implies for how we should be treating heart failure. I don't even dare to ask for some last words maybe from both Justin and Milton, but recognizing that the time is short, anything else to add? Dr. Milton Packer: I think Justin should do last words. Dr. Justin Ezekowitz: Well, let me summarize by saying there is a hockey stick. We love hockey sticks in Canada. A simple and an excellent comparison. I think people should really look at that figure to understand it, but do not undertreat your patients with HFpEF and look at these with a grain of salt. Thanks for joining us, Milton. Thanks, Carolyn. Dr. Milton Packer: Thank you so much. Dr. Carolyn Lam: On behalf of Greg and I, you've been listening to Circulation on the Run. Thank you so much for joining us today and don't forget to tune in again next week. Dr. Greg Hundley: This program is copyright of the American Heart Association 2021. The opinions expressed by speakers in this podcast are their own and not necessarily those of the editors, or of the American Heart Association. For more, visit ahajournals.org.

PeerView Internal Medicine CME/CNE/CPE Video Podcast
Naval Daver, MD - Optimizing Care for High-Risk Myeloid Cancers: Interprofessional Team Insights From a Center of Excellence

PeerView Internal Medicine CME/CNE/CPE Video Podcast

Play Episode Listen Later May 28, 2021 54:08


Go online to PeerView.com/BFT860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this CME/MOC/CC/NCPD-accredited activity, a hematologist-oncologist, a pathologist, and a physician assistant team up to discuss a collaborative approach to managing their patients with high-risk myeloid cancers, such as acute myeloid leukemia and myelodysplastic syndrome. Hear how Naval Daver, MD, Sanam Loghavi, MD, and Megan Wiese, PA-C, from the MD Anderson Cancer Center, collaborate on diagnosis, treatment decision-making, safety management, and patient education, with the ultimate goal of providing the best care for their patients. Upon completion of this activity, participants will be able to: Discuss the clinical signs and diagnostic principles of high-risk myeloid cancers, including TP53-mutant disease, Summarize current evidence related to the efficacy and safety of novel strategies for the management of high-risk acute myeloid leukemia or myelodysplastic syndromes, Develop team-based diagnostic, treatment, and safety management plans for patients presenting with high-risk myeloid cancers, Apply team-based educational interventions detailing prognostic and therapeutic expectations for patients with high-risk acute myeloid leukemia or myelodysplastic syndromes.

PeerView Oncology & Hematology CME/CNE/CPE Audio Podcast
Naval Daver, MD - Optimizing Care for High-Risk Myeloid Cancers: Interprofessional Team Insights From a Center of Excellence

PeerView Oncology & Hematology CME/CNE/CPE Audio Podcast

Play Episode Listen Later May 28, 2021 54:05


Go online to PeerView.com/BFT860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this CME/MOC/CC/NCPD-accredited activity, a hematologist-oncologist, a pathologist, and a physician assistant team up to discuss a collaborative approach to managing their patients with high-risk myeloid cancers, such as acute myeloid leukemia and myelodysplastic syndrome. Hear how Naval Daver, MD, Sanam Loghavi, MD, and Megan Wiese, PA-C, from the MD Anderson Cancer Center, collaborate on diagnosis, treatment decision-making, safety management, and patient education, with the ultimate goal of providing the best care for their patients. Upon completion of this activity, participants will be able to: Discuss the clinical signs and diagnostic principles of high-risk myeloid cancers, including TP53-mutant disease, Summarize current evidence related to the efficacy and safety of novel strategies for the management of high-risk acute myeloid leukemia or myelodysplastic syndromes, Develop team-based diagnostic, treatment, and safety management plans for patients presenting with high-risk myeloid cancers, Apply team-based educational interventions detailing prognostic and therapeutic expectations for patients with high-risk acute myeloid leukemia or myelodysplastic syndromes.

PeerView Oncology & Hematology CME/CNE/CPE Video Podcast
Naval Daver, MD - Optimizing Care for High-Risk Myeloid Cancers: Interprofessional Team Insights From a Center of Excellence

PeerView Oncology & Hematology CME/CNE/CPE Video Podcast

Play Episode Listen Later May 28, 2021 54:08


Go online to PeerView.com/BFT860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this CME/MOC/CC/NCPD-accredited activity, a hematologist-oncologist, a pathologist, and a physician assistant team up to discuss a collaborative approach to managing their patients with high-risk myeloid cancers, such as acute myeloid leukemia and myelodysplastic syndrome. Hear how Naval Daver, MD, Sanam Loghavi, MD, and Megan Wiese, PA-C, from the MD Anderson Cancer Center, collaborate on diagnosis, treatment decision-making, safety management, and patient education, with the ultimate goal of providing the best care for their patients. Upon completion of this activity, participants will be able to: Discuss the clinical signs and diagnostic principles of high-risk myeloid cancers, including TP53-mutant disease, Summarize current evidence related to the efficacy and safety of novel strategies for the management of high-risk acute myeloid leukemia or myelodysplastic syndromes, Develop team-based diagnostic, treatment, and safety management plans for patients presenting with high-risk myeloid cancers, Apply team-based educational interventions detailing prognostic and therapeutic expectations for patients with high-risk acute myeloid leukemia or myelodysplastic syndromes.

PeerView Internal Medicine CME/CNE/CPE Audio Podcast
Naval Daver, MD - Optimizing Care for High-Risk Myeloid Cancers: Interprofessional Team Insights From a Center of Excellence

PeerView Internal Medicine CME/CNE/CPE Audio Podcast

Play Episode Listen Later May 28, 2021 54:05


Go online to PeerView.com/BFT860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this CME/MOC/CC/NCPD-accredited activity, a hematologist-oncologist, a pathologist, and a physician assistant team up to discuss a collaborative approach to managing their patients with high-risk myeloid cancers, such as acute myeloid leukemia and myelodysplastic syndrome. Hear how Naval Daver, MD, Sanam Loghavi, MD, and Megan Wiese, PA-C, from the MD Anderson Cancer Center, collaborate on diagnosis, treatment decision-making, safety management, and patient education, with the ultimate goal of providing the best care for their patients. Upon completion of this activity, participants will be able to: Discuss the clinical signs and diagnostic principles of high-risk myeloid cancers, including TP53-mutant disease, Summarize current evidence related to the efficacy and safety of novel strategies for the management of high-risk acute myeloid leukemia or myelodysplastic syndromes, Develop team-based diagnostic, treatment, and safety management plans for patients presenting with high-risk myeloid cancers, Apply team-based educational interventions detailing prognostic and therapeutic expectations for patients with high-risk acute myeloid leukemia or myelodysplastic syndromes.

PeerView Clinical Pharmacology CME/CNE/CPE Audio Podcast
Naval Daver, MD - Optimizing Care for High-Risk Myeloid Cancers: Interprofessional Team Insights From a Center of Excellence

PeerView Clinical Pharmacology CME/CNE/CPE Audio Podcast

Play Episode Listen Later May 28, 2021 54:05


Go online to PeerView.com/BFT860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this CME/MOC/CC/NCPD-accredited activity, a hematologist-oncologist, a pathologist, and a physician assistant team up to discuss a collaborative approach to managing their patients with high-risk myeloid cancers, such as acute myeloid leukemia and myelodysplastic syndrome. Hear how Naval Daver, MD, Sanam Loghavi, MD, and Megan Wiese, PA-C, from the MD Anderson Cancer Center, collaborate on diagnosis, treatment decision-making, safety management, and patient education, with the ultimate goal of providing the best care for their patients. Upon completion of this activity, participants will be able to: Discuss the clinical signs and diagnostic principles of high-risk myeloid cancers, including TP53-mutant disease, Summarize current evidence related to the efficacy and safety of novel strategies for the management of high-risk acute myeloid leukemia or myelodysplastic syndromes, Develop team-based diagnostic, treatment, and safety management plans for patients presenting with high-risk myeloid cancers, Apply team-based educational interventions detailing prognostic and therapeutic expectations for patients with high-risk acute myeloid leukemia or myelodysplastic syndromes.

PeerView Immunology & Transplantation CME/CNE/CPE Video Podcast
Naval Daver, MD - Optimizing Care for High-Risk Myeloid Cancers: Interprofessional Team Insights From a Center of Excellence

PeerView Immunology & Transplantation CME/CNE/CPE Video Podcast

Play Episode Listen Later May 28, 2021 54:08


Go online to PeerView.com/BFT860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this CME/MOC/CC/NCPD-accredited activity, a hematologist-oncologist, a pathologist, and a physician assistant team up to discuss a collaborative approach to managing their patients with high-risk myeloid cancers, such as acute myeloid leukemia and myelodysplastic syndrome. Hear how Naval Daver, MD, Sanam Loghavi, MD, and Megan Wiese, PA-C, from the MD Anderson Cancer Center, collaborate on diagnosis, treatment decision-making, safety management, and patient education, with the ultimate goal of providing the best care for their patients. Upon completion of this activity, participants will be able to: Discuss the clinical signs and diagnostic principles of high-risk myeloid cancers, including TP53-mutant disease, Summarize current evidence related to the efficacy and safety of novel strategies for the management of high-risk acute myeloid leukemia or myelodysplastic syndromes, Develop team-based diagnostic, treatment, and safety management plans for patients presenting with high-risk myeloid cancers, Apply team-based educational interventions detailing prognostic and therapeutic expectations for patients with high-risk acute myeloid leukemia or myelodysplastic syndromes.

PeerView Immunology & Transplantation CME/CNE/CPE Audio Podcast
Naval Daver, MD - Optimizing Care for High-Risk Myeloid Cancers: Interprofessional Team Insights From a Center of Excellence

PeerView Immunology & Transplantation CME/CNE/CPE Audio Podcast

Play Episode Listen Later May 28, 2021 54:05


Go online to PeerView.com/BFT860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this CME/MOC/CC/NCPD-accredited activity, a hematologist-oncologist, a pathologist, and a physician assistant team up to discuss a collaborative approach to managing their patients with high-risk myeloid cancers, such as acute myeloid leukemia and myelodysplastic syndrome. Hear how Naval Daver, MD, Sanam Loghavi, MD, and Megan Wiese, PA-C, from the MD Anderson Cancer Center, collaborate on diagnosis, treatment decision-making, safety management, and patient education, with the ultimate goal of providing the best care for their patients. Upon completion of this activity, participants will be able to: Discuss the clinical signs and diagnostic principles of high-risk myeloid cancers, including TP53-mutant disease, Summarize current evidence related to the efficacy and safety of novel strategies for the management of high-risk acute myeloid leukemia or myelodysplastic syndromes, Develop team-based diagnostic, treatment, and safety management plans for patients presenting with high-risk myeloid cancers, Apply team-based educational interventions detailing prognostic and therapeutic expectations for patients with high-risk acute myeloid leukemia or myelodysplastic syndromes.

PeerView Heart, Lung & Blood CME/CNE/CPE Video Podcast
Naval Daver, MD - Optimizing Care for High-Risk Myeloid Cancers: Interprofessional Team Insights From a Center of Excellence

PeerView Heart, Lung & Blood CME/CNE/CPE Video Podcast

Play Episode Listen Later May 28, 2021 54:08


Go online to PeerView.com/BFT860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this CME/MOC/CC/NCPD-accredited activity, a hematologist-oncologist, a pathologist, and a physician assistant team up to discuss a collaborative approach to managing their patients with high-risk myeloid cancers, such as acute myeloid leukemia and myelodysplastic syndrome. Hear how Naval Daver, MD, Sanam Loghavi, MD, and Megan Wiese, PA-C, from the MD Anderson Cancer Center, collaborate on diagnosis, treatment decision-making, safety management, and patient education, with the ultimate goal of providing the best care for their patients. Upon completion of this activity, participants will be able to: Discuss the clinical signs and diagnostic principles of high-risk myeloid cancers, including TP53-mutant disease, Summarize current evidence related to the efficacy and safety of novel strategies for the management of high-risk acute myeloid leukemia or myelodysplastic syndromes, Develop team-based diagnostic, treatment, and safety management plans for patients presenting with high-risk myeloid cancers, Apply team-based educational interventions detailing prognostic and therapeutic expectations for patients with high-risk acute myeloid leukemia or myelodysplastic syndromes.

PeerView Clinical Pharmacology CME/CNE/CPE Video
Naval Daver, MD - Optimizing Care for High-Risk Myeloid Cancers: Interprofessional Team Insights From a Center of Excellence

PeerView Clinical Pharmacology CME/CNE/CPE Video

Play Episode Listen Later May 28, 2021 54:08


Go online to PeerView.com/BFT860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this CME/MOC/CC/NCPD-accredited activity, a hematologist-oncologist, a pathologist, and a physician assistant team up to discuss a collaborative approach to managing their patients with high-risk myeloid cancers, such as acute myeloid leukemia and myelodysplastic syndrome. Hear how Naval Daver, MD, Sanam Loghavi, MD, and Megan Wiese, PA-C, from the MD Anderson Cancer Center, collaborate on diagnosis, treatment decision-making, safety management, and patient education, with the ultimate goal of providing the best care for their patients. Upon completion of this activity, participants will be able to: Discuss the clinical signs and diagnostic principles of high-risk myeloid cancers, including TP53-mutant disease, Summarize current evidence related to the efficacy and safety of novel strategies for the management of high-risk acute myeloid leukemia or myelodysplastic syndromes, Develop team-based diagnostic, treatment, and safety management plans for patients presenting with high-risk myeloid cancers, Apply team-based educational interventions detailing prognostic and therapeutic expectations for patients with high-risk acute myeloid leukemia or myelodysplastic syndromes.

PeerView Heart, Lung & Blood CME/CNE/CPE Audio Podcast
Naval Daver, MD - Optimizing Care for High-Risk Myeloid Cancers: Interprofessional Team Insights From a Center of Excellence

PeerView Heart, Lung & Blood CME/CNE/CPE Audio Podcast

Play Episode Listen Later May 28, 2021 54:05


Go online to PeerView.com/BFT860 to view the activity, download slides and practice aids, and complete the post-test to earn credit. In this CME/MOC/CC/NCPD-accredited activity, a hematologist-oncologist, a pathologist, and a physician assistant team up to discuss a collaborative approach to managing their patients with high-risk myeloid cancers, such as acute myeloid leukemia and myelodysplastic syndrome. Hear how Naval Daver, MD, Sanam Loghavi, MD, and Megan Wiese, PA-C, from the MD Anderson Cancer Center, collaborate on diagnosis, treatment decision-making, safety management, and patient education, with the ultimate goal of providing the best care for their patients. Upon completion of this activity, participants will be able to: Discuss the clinical signs and diagnostic principles of high-risk myeloid cancers, including TP53-mutant disease, Summarize current evidence related to the efficacy and safety of novel strategies for the management of high-risk acute myeloid leukemia or myelodysplastic syndromes, Develop team-based diagnostic, treatment, and safety management plans for patients presenting with high-risk myeloid cancers, Apply team-based educational interventions detailing prognostic and therapeutic expectations for patients with high-risk acute myeloid leukemia or myelodysplastic syndromes.

Oncology Knowledge into Practice Podcast
Haematology series | What is fitness in acute myeloid leukaemia?

Oncology Knowledge into Practice Podcast

Play Episode Listen Later Apr 13, 2021 17:55


Adult guidelines for acute myeloid leukaemia recommend determining a patient's fitness before treating with standard therapy, but what does this mean, what are the implications, and how does this work in practice for both adults and children? To answer our questions on this topic, we've invited the expertise of Dr Courtney DiNardo, Associate Professor in the Department of Leukemia at The University of Texas MD Anderson Cancer Center. References Heuser et al. Ann Oncol. 2020 Mar 17;S0923-7534(20)36079-8 PDQ Adult Treatment Editorial Board. Adult Acute Myeloid Leukemia Treatment (PDQ®): Health Professional Version. 2020 Aug 11 Krug U, et al. Lancet. 2010;376(9757):2000-8 Sorror, et al. 2017 Dec 1;3(12):1675-1682 PDQ Pediatric Treatment Editorial Board. Childhood Acute Myeloid Leukemia/Other Myeloid Malignancies Treatment (PDQ®): Health Professional Version. 2020 Aug 20 This series is supported by educational grants from Servier Pharmaceuticals LLC and Takeda, who have had no influence on the content or choice of faculty

Oncology Knowledge into Practice Podcast
Haematology series | Novel therapies for acute myeloid leukaemia

Oncology Knowledge into Practice Podcast

Play Episode Listen Later Mar 30, 2021 19:08


Despite available treatments, many patients with acute myeloid leukaemia, or AML, are in need of additional therapeutic options. Thankfully, there hundreds of clinical trials for new interventions that could rectify this, but which options can we start to consider, for which patients and when? To answer our questions on this topic, we've invited the expertise of Dr Navel Daver, Associate Professor in the Department of Leukemia at The University of Texas MD Anderson Cancer Center in Houston, Texas. References: Swords, et al. Blood. 2018;131(13):1415-1424 Stahl, et al. Curr Oncol Rep. 2019;21(4):37 Yee at al. Blood (2014) 124 (21): 116. Montesinos et al. Future Oncol. 2020 May;16(13):807-815. Ades, et al. ASCO 2020. Abstract 7506 DeAngelo, et al. Blood (2017) 130 (Supplement 1): 894. Ravandi, et al. Lancet Haematol. 2019 Sep; 6(9): e480-e488 Hofmann, et al. J Clin Med. 2019 Feb; 8(2): 200. This series is supported by educational grants from Servier Pharmaceuticals LLC and Takeda, who have had no influence on the content or choice of faculty

The BSH Guidelines Official Podcast
Guideline on the diagnosis and management of chronic myeloid leukaemia

The BSH Guidelines Official Podcast

Play Episode Listen Later Feb 19, 2021 14:25


Dr Graeme Smith presents a short podcast on the BSH Guideline for the management of mantle cell lymphoma The management of chronic myeloid leukaemia (CML) has seen considerable change in the last several years. The objective of this guideline is to provide healthcare professionals with clear guidance on the investigation and management of CML in adults and children. Dr Smith discusses the guideline in three parts: 1) Review of existing international guidelines on the investigation and management of myeloid leukaemia and why in his view there is a focus for U.K. guideline 2) Structure of the guideline 3) Discusses in detail four of the key areas that the guideline makes recommendations in terms of management of myeloid leukaemia in the U.K. Dr Graeme Smith at the time of recording is recently retired Haematologist and Clinical Director of the Leeds Oncology Centre; Leeds NHS Trust.

Oncology Today with Dr Neil Love
Acute Myeloid Leukemia with FLT3 Mutations

Oncology Today with Dr Neil Love

Play Episode Listen Later Oct 30, 2020 38:05


For this special edition of Oncology Today, I met with Dr Keith Pratz from the University of Pennsylvania in Philadelphia to discuss recently published and emerging research in the use of FLT3 inhibitors for patients with acute myeloid leukemia. CME information and select publications here (http://www.researchtopractice.com/OncologyTodayAMLFLT320).

PaperPlayer biorxiv neuroscience
Analysis of the Immune Response to Sciatic Nerve Injury Identifies Efferocytosis as a Key Mechanism of Nerve Debridement

PaperPlayer biorxiv neuroscience

Play Episode Listen Later Oct 24, 2020


Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.10.23.352872v1?rss=1 Authors: Kalinski, A. L., Yoon, C., Huffman, L. D., Duncker, P. C., Kohen, R., Passino, R., Hafner, H., Johnson, C., Kawaguchi, R., Carbajal, K. S., Jara, J. S., Hollis, E., Segal, B., Giger, R. J. Abstract: Sciatic nerve crush injury triggers sterile inflammation within the distal nerve and axotomized dorsal root ganglia (DRGs). Granulocytes and pro-inflammatory Ly6C high monocytes infiltrate the nerve first, and rapidly give way to Ly6C negative inflammation-resolving macrophages. In axotomized DRGs, few hematogenous leukocytes are detected and resident macrophages acquire a ramified morphology. Single-cell RNA-sequencing of injured sciatic nerve identifies five macrophage subpopulations, repair Schwann cells, and mesenchymal precursor cells. Macrophages at the nerve crush site are molecularly distinct from macrophages associated with Wallerian degeneration. In the injured nerve, macrophages "eat" apoptotic leukocytes, a process called efferocytosis, and thereby promote an anti-inflammatory milieu. Myeloid cells in the injured nerve, but not axotomized DRGs, strongly express receptors for the cytokine GM-CSF. In GM-CSF deficient (Csf2-/-) mice, inflammation resolution is delayed and conditioning-lesion induced regeneration of DRG neuron central axons is abolished. Thus, carefully orchestrated inflammation resolution in the nerve is required for conditioning-lesion induced neurorepair. Copy rights belong to original authors. Visit the link for more info

PaperPlayer biorxiv neuroscience
Time-resolved single-cell RNAseq profiling identifies a novel Fabp5-expressing subpopulation of inflammatory myeloid cells in chronic spinal cord injury

PaperPlayer biorxiv neuroscience

Play Episode Listen Later Oct 21, 2020


Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.10.21.346635v1?rss=1 Authors: Pluchino, S., Hamel, R., Peruzzotti-Jametti, L., Ridley, K., Testa, V., Yu, B., Rowitch, D., Marioni, J. Abstract: Innate immune responses following spinal cord injury (SCI) participate in early secondary pathogenesis and wound healing events. Here, we used time-resolved scRNAseq to map transcriptional profiles of SC tissue-resident and infiltrating myeloid cells post-SCI. Our work identifies a novel subpopulation of Fabp5+ inflammatory myeloid cells, comprising both resident and infiltrating cells and displaying a delayed cytotoxic profile at the lesion epicentre, which may serve as a target for future therapeutics. Copy rights belong to original authors. Visit the link for more info

Business Of Biotech
Summer Sessions 6: Alexis Peyroles On Myeloid Cells, Transplants, & Immuno-Oncology Inspiration

Business Of Biotech

Play Episode Listen Later Aug 17, 2020 34:15


OSE Immunotherapeutics CEO Alexis Peyroles joins The Business Of Biotech: Summer Executive Sessions to discuss myeloid cells' role in immunology, why a team of transplant specialists is key to his company's therapeutic development approach, and creating differentiation as a clinical-stage immunotherapy company in an ever-growing sea of competitors.

ReachMD CME
A Novel Therapeutic Approach in Myeloid Malignancies: Targeting the Neddylation Pathway

ReachMD CME

Play Episode Listen Later Jul 28, 2020


CME credits: 0.50 Valid until: 28-07-2021 Claim your CME credit at https://reachmd.com/programs/cme/a-novel-therapeutic-approach-in-myeloid-malignancies-targeting-the-neddylation-pathway/11694/ There is a lack of available therapeutic options for the management of patients with myeloid malignancies, including myelodysplastic syndromes (MDS), chronic myelomonocytic leukemia (CMML), and acute myeloid leukemia (AML). Novel therapeutic approaches are being evaluated, particularly those that target the NEDD8-activating enzyme (NAE). Evaluating the rationale for NAE inhibition, assessing emerging safety and efficacy data on use of NAE inhibitors in myeloid malignancies, and developing strategies based on the evolving implications of this research will allow for greater understanding of their potential impact on management and health outcomes of patients with MDS, CMML, and AML.

ReachMD CME
A Novel Therapeutic Approach in Myeloid Malignancies: Targeting the Neddylation Pathway

ReachMD CME

Play Episode Listen Later Jul 28, 2020


CME credits: 0.50 Valid until: 28-07-2021 Claim your CME credit at https://reachmd.com/programs/cme/a-novel-therapeutic-approach-in-myeloid-malignancies-targeting-the-neddylation-pathway/11694/ There is a lack of available therapeutic options for the management of patients with myeloid malignancies, including myelodysplastic syndromes (MDS), chronic myelomonocytic leukemia (CMML), and acute myeloid leukemia (AML). Novel therapeutic approaches are being evaluated, particularly those that target the NEDD8-activating enzyme (NAE). Evaluating the rationale for NAE inhibition, assessing emerging safety and efficacy data on use of NAE inhibitors in myeloid malignancies, and developing strategies based on the evolving implications of this research will allow for greater understanding of their potential impact on management and health outcomes of patients with MDS, CMML, and AML.

PaperPlayer biorxiv neuroscience
Discordant transcriptional signatures of mitochondrial genes in Parkinson's disease human myeloid cells

PaperPlayer biorxiv neuroscience

Play Episode Listen Later Jul 22, 2020


Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.20.212407v1?rss=1 Authors: Navarro, E., Udine, E., de Paiva Lopes, K., Parks, M., Riboldi, G., Schilder, B. M., Humphrey, J., Snijders, G. J. L., Vialle, R. A., Zhuang, M., Sikder, T., Argyrou, C., Allan, A., Chao, M., Farrell, K., Henderson, B., Simon, S., Raymond, D., Elango, S., Ortega, R. A., Shanker, V., Swan, M., Zhu, C., Ramdhani, R., Walker, R. H., Tse, W., Sano, M., Pereira, A. C., Ahfeldt, T., Goate, A. M., Bressman, S., Crary, J. F., de Witte, L., Frucht, S., Saunders-Pullman, R., Raj, T. Abstract: An increasing number of identified Parkinson's disease (PD) risk loci contain genes highly expressed in innate immune cells, yet their potential role in pathological mechanisms is not obvious. We have generated transcriptomic profiles of CD14+ monocytes from 230 individuals with sporadic PD and age-matched healthy subjects. We identified dysregulation of genes involved in mitochondrial and proteasomal function. We also generated transcriptomic profiles of primary microglia from autopsied brains of 55 PD and control subjects and observed discordant transcriptomic signatures of mitochondrial genes in PD monocytes and microglia. We further identified PD susceptibility genes, whose expression, relative to each risk allele, is altered in monocytes. These findings reveal that transcriptomic mitochondrial alterations are detectable in PD monocytes and are distinct from brain microglia, and facilitates efforts to understand the roles of myeloid cells in PD. Copy rights belong to original authors. Visit the link for more info

Talk Psych to Me
Hold onto your peanuts

Talk Psych to Me

Play Episode Listen Later Mar 15, 2020 46:28


We are up again two infections right now: COVID-19 and panic. In this episode, Tania and Brian break down the psychology of mass panic (like panic shopping, dance plague, and penis panic), moral panic (like xenophobia), and individual panic. They explain why mental health = physical health and share their favorite ideas for how to keep your cool. Talk psych to us: Instagram: @talkpsychtomepodcastFacebook: @talkpsych2meTwitter: @talkpsych2meEmail: talkpsychpodcast@gmail.comFurther Reading:Collective Behavior by Turner, Ralph, and Killian (1993). Folk Devils and Moral Panics by Cohen (3rd edition - 2001).Medieval and Renaissance Medicine by Gordon (1959).Hoaxes, Myths, and Manias by Bartholomew and Radford (2003). Tarantella Dance video“Protean nature of mass sociogenic illness” by Bartholomew and Wessely (2002).“A brief history of hysteria: From the ancient to the modern” by Trimble and Reynolds (2016).“Spasms of the Soul: The Tanganyika Laughter Epidemic in the Age of Independence” by Nasser and Shiraz (2014). “Does stress alter everyday moral decision-making?” by Starcke et. al (2010).“Myeloid differentiation architecture of leukocyte transcriptome dynamics in perceived social isolation” by Steven Cole et. al. (2015) Lecture: The health and psychological effects of translating emotional experiences into words by Pennebaker (2017). Produced by Scarlet Moon ThingsMusic by Barrie Gledden, Kes Loy, and Richard Kimmings

Talk Psych to Me
Stop trying to make popular happen

Talk Psych to Me

Play Episode Listen Later Feb 24, 2020 44:47


What makes someone popular or unpopular? What are the pros and cons of popularity? And what was Brian's social status in high school?Talk psych to us: Instagram: @talkpsychtomepodcastFacebook: @talkpsych2meTwitter: @talkpsych2meEmail: talkpsychpodcast@gmail.comFurther Reading:“The neural bases of social pain: Evidence for shared representations with physical pain” by Naomi Eisenberger (2012) “Myeloid differentiation architecture of leukocyte transcriptome dynamics in perceived social isolation” by Steven Cole et. al. (2015) “Dimensions and types of social status: A cross-age perspective” by John Coie, Kenneth Dodge, & Heide Coppotelli (1982) Popular: Finding Happiness and Success in a World That Cares Too Much About the Wrong Kinds of Relationships by Mitch Prinstein (2018) “What Ever Happened to the ‘Cool’ Kids? Long‐Term Sequelae of Early Adolescent Pseudomature Behavior” by Joseph Allen (2014) Psychology of Popularity course on Coursera by Mitch Prinstein "Being a Celebrity: A Phenomenology of Fame" by Donna Rockwell & David Giles (2009)Produced by Scarlet Moon ThingsMusic by Barrie Gledden, Kes Loy, and Richard Kimmings

Belly of the Beast Life Stories
A Doctor Becomes the Cancer Patient with Dr. Julian Gold

Belly of the Beast Life Stories

Play Episode Listen Later Nov 25, 2019 57:54


A 30-year physician and two-time mayor of Beverly Hills, Dr. Julian Gold gained empathy and gratitude for community through his trial with cancer.   Dr. Julian Gold was 56-years-old when he was diagnosed with a deadly form of cancer, Acute Myeloid Leukemia. Then a 30-year physician, Dr. Gold was a member of the board of directors for Cedars-Sinai Hospital and one of the most respected medical professionals in Los Angeles. He had to learn quickly to ‘behave like a patient, not a doctor’ and focus on treatment. Dr. Gold established rules of recovery to stay positive and focused on getting better. A stem cell transplant procedure helped him survive -- but as you’ll learn being a ‘survivor’ is a tricky word when so many others don’t make it.   EPISODE SUMMARY - Dr. Julian Gold discusses how he discovered the pain which led to a diagnosis of Acute Myeloid Leukemia - Dr. Gold talks about efficacy of searching for answers on the internet and ultimately tells patients not to do it  - Discusses chemotherapy treatment, staying in hospital, good days and bad days - Stem Cell Transplant - urges everyone to get swabbed via ‘Be the Match’ program - Talks about important role of caregiver, family and community - Daily Rules of Recovery to stay positive and focused on getting better No matter how bad you feel, get up and out of bed  Take a shower and change clothes  Exercise as much as possible Stay engaged and relevant in your life outside hospital - routine is important - Life after - returning to normalcy, sweating the small stuff and loving it because the big stuff went away - Survivor is a ‘loaded word’    QUOTABLES - “Avoid the internet” if diagnosed. - “I had to behave like a patient, not a doctor.” - “This was like getting struck by lightning, I was fine one day and sick the next.” - “You have to take care of the caregiver.” - “Don’t sweat the small stuff unless it’s an indication of normalcy.” - “Recovery is not a straight line, expect good and bad days.” - “I got stronger for it.” Changed perspective on the world, greater appreciation for family and community, and greater sense of gratitude.    TRANSCRIPT AVAILABLE https://inourbelly.com/season-1/episode-2-dr-julian-gold/   RESOURCES Dr. Julian Gold on Instagram https://www.instagram.com/goldjmd/   Be the Match https://bethematch.org/   City of Hope Cancer Treatment and Research https://www.cityofhope.org/

blooducation's podcast
Management of acute myeloid leukaemia - Dr Manos Nikolousis

blooducation's podcast

Play Episode Listen Later Oct 21, 2019 43:45


Listen to Helen talk to Dr Manos Nikolousis about the recent changes in the management of acute myeloid leukaemia

CODEMOTION 2019
The Peter Moss Acute Myeloid/Lymphoblastic Leukemia AI Research Project - Estela Cabezas

CODEMOTION 2019

Play Episode Listen Later Oct 21, 2019 21:19


Otras charlas de Codemotion 2019 también en podcast: https://lk.autentia.com/Codemotion-Podcast The project is being coordinated by a group of volunteers with experience in computer vision / natural language processing, Leukemia research, Biochemistry, Molecular Biophysics, Immunology and Bioinformation. The purpose of the project is to share public information related to AML/ALL, as well as open source projects aimed at early dectection with convolutional neural networks, using natural language understanding for AML/ALL chatbots, and R&D for discovering potential candidates for drugs for AML/ALL.

Blood Advances Talks
Inherited predisposition to myeloid malignancies

Blood Advances Talks

Play Episode Listen Later Sep 10, 2019 18:39


Inherited predisposition to myeloid malignancies by Blood Advances Talks

CytoFluo@ICGEB 2019
J. Helft - Deciphering the myeloid cell infiltrate in breast tumors

CytoFluo@ICGEB 2019

Play Episode Listen Later Aug 26, 2019 42:52


Julie Helft, Institute Curie, Paris, France speaks on "Deciphering the myeloid cell infiltrate in breast tumors". This movie is part of "Flow cytometry: from basic principles to advanced application" Course, 8-10 May 2019, ICGEB Trieste, Italy.

Haematology Podcast
S01E04 Acute Myeloid Leukaemia with Andrew Wilson

Haematology Podcast

Play Episode Listen Later Apr 26, 2019 30:25


A discussion about Acute Myeloid Leukaemia, from diagnosing to devising a personalised treatment plan. We run through the challenges in the initial treatment of APML, namely differentiation syndrome and DIC, and delve briefly into functional neutropenia. Many thanks to Dr Andrew Wilson for his valuable insights. Andrew is a consultant haematologist at UCLH with a special interest in laboratory haematology and cancer education. Clinically he works in the MPN service and is one of the attending consultants for the leukaemia team. The rest of the time, he works in the UCLH Specialist Integrated Haematological Malignancy Diagnostic Service (SIHMDS) which reviews nearly 3,000 bone marrow samples every year. He is finishing his MA in clinical education and is keen to find ways to develop inter-professional learning. For more reading, take a look at the following articles. AML: https://www.nejm.org/doi/full/10.1056/NEJMra1406184 APML: http://www.bloodjournal.org/content/111/5/2505?sso-checked=true ALL: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5520400/pdf/bcj201753a.pd

CAPcast
Modern Genomic Profiling in Myeloid Disorders and Acute Leukemia

CAPcast

Play Episode Listen Later Nov 19, 2018 15:03


Morphologic examination by light microscopy remains an integral part of initial histopathologic assessment for hematolymphoid neoplasms; however, a variety of laboratory techniques are now being used to optimize diagnostic information in the appropriate clinical context. For diagnosing myeloid disorders and acute myeloid leukemia, one approach is to utilize an next gen sequencing panel and DNA-based cytogenomic microarray, according to Dr. Pranil Chandra, Chief Medical Officer of Genomic and Clinical Pathology with PathGroup. In this CAPcast, Dr. Chandra discusses why his laboratory, in conjunction with pathologist and oncologist colleagues, developed this technology and how they’ve implemented it into clinical practice. Dr. Chandra currently serves on the Personalized Healthcare Committee of the College of American Pathologists, and he’s written a short article now posted on CAP.org (https://capatholo.gy/2RO4h96) outlining the reasoning his team used to make this panel their standard of care.

This Week in Virology
TWiV 511: Accessory found guilty in DC

This Week in Virology

Play Episode Listen Later Sep 16, 2018 108:55


Ned Landau joins the TWiV team to discuss restriction of HIV replication by SAMHD1, and a viral antagonist that can be used to produce a dendritic cell vaccine. Hosts: Vincent Racaniello, Dickson Despommier, Alan Dove, Rich Condit, and Brianne Barker Guest: Ned Landau Become a patron of TWiV! Links for this episode Support Viruses Gordon Conference TWiV #124 September 2008 SAMHD1 restricts HIV-1 replication (Nature) SAMHD1 restricts diverse retroviruses (Retrovirology) Vpx degradation of SAMHD1 independent of uncoating (J Virol) Transduction of myeloid cells with Vpx vector (Gene Ther) Letters read on TWiV 511 Timestamps by Jolene. Thanks! Weekly Science Picks Brianne- Online Immunology Course Alan- Bacteria Builder Rich- 2018 Ig Nobel Prizes Dickson- Between Fear and Hope Ned - HUSH silencing of transposons Vincent - Paywall publishing ban (Schlitz statement); Curry on DORA Listener Pick Steve- Paywall: Business of Scholarship and Biohazard Islam- Peer review Twitter post Intro music is by Ronald Jenkees. Send your virology questions and comments to twiv@microbe.tv

Circulation on the Run
Circulation July 10, 2018 Issue

Circulation on the Run

Play Episode Listen Later Jul 10, 2018 19:16


Dr Carolyn Lam:                Welcome to Circulation on the Run, your weekly podcast summary and backstage pass to the journal and its editors. I'm Dr Carolyn Lam, associate editor for the National Heart Center, and Duke National University of Singapore.                                                 How do resuscitation teams at top-performing hospitals for in-hospital cardiac arrest actually succeed? Well, to learn how, you have to keep listening to the podcast, because we will be discussing this right after these summaries.                                                 The first original paper this week tells us that recent developments in RNA amplification strategies may provide a unique opportunity to use small amounts of input RNA for genome wide-sequencing of single cells. Co-first authors, Dr Gladka and Molenaar, corresponding author, Dr van Rooij, and colleagues from Hubrecht Institute in Utrecht, the Netherlands, present a method to obtain high-quality RNA from digested cardiac tissue, from adult mice, for automated single-cell sequencing of both healthy and diseased hearts.                                                 Based on differential gene expression, the authors were also able to identify multiple subpopulations within a certain cell type. Furthermore, applying single-cell sequencing on both the healthy and injured heart indicated the presence of disease-specific cells subpopulations.                                                 For example, they identified cytoskeleton-associated protein 4 as a novel marker for activated fibroblasts that positively correlated with known myofibroblast markers, in both mouse and human cardiac tissue. This paper raises the exciting possibility for new biology discovery using single-cell sequencing that can ultimately lead to the development of novel therapeutic strategies.                                                 Myeloid-derived suppressor cells are a heterogeneous population of cells that expand in cancer, inflammation, and infection, and negatively regulate inflammation. However, their role in heart failure was unclear, at least until today's paper in this week's journal. Co-first authors Dr Zhou, Miao, and Yin, and co-corresponding authors, Dr Wang and Li, from Huazhong University of Science and Technology, measured the myeloid-derived suppressor cells by flow cytometry in heart failure patients and in mice with pressure overload–induced heart failure, using isoproterenol infusion or transverse aortic constriction.                                                 They found that the proportion of myeloid-derived suppressor cells was linked to heart failure severity. Cardiac hypertrophy, dysfunction, and inflammation were exacerbated by depletion of myeloid-derived suppressor cells but alleviated by cell transfer. Monocytic myeloid-derived suppressor cells exerted an antihypertrophic effect on cardiomyocyte nitric oxide, but monocytic and granulocytic myeloid-derived suppressor cells displayed antihypertrophic and anti-inflammatory properties through interleukin 10.                                                 Rapamycin increased accumulation of myeloid-derived suppressor cells by suppressing their differentiation, which in part mediated its cardioprotective mechanisms. Thus, these findings revealed a cardioprotective role from myeloid-derived suppressor cells in heart failure by their antihypertrophic effects on cardiomyocytes and anti-inflammatory effects through interleukin 10 and nitric oxide. Pharmacological targeting of myeloid-derived suppressor cells by rapamycin constitutes a promising therapeutic strategy for heart failure.                                                 In the FOURIER trial, the PCSK9 inhibitor evolocumab reduced LDL cholesterol and cardiovascular risk in patients with stable atherosclerotic disease. However, was the efficacy of evolocumab modified by baseline inflammatory risk?                                                 While Dr Bohula from the TIMI Study Group and colleagues explored this question by examining the efficacy of evolocumab stratified by baseline high sensitivity CRP. They also assessed the importance of inflammatory and residual cholesterol risk across the range of on-treatment LDL concentrations. They found that the relative benefit of evolocumab for the prevention of adverse cardiovascular events was consistent, irrespective of baseline high sensitivity CRP. However, because patients with higher high sensitivity CRP levels had higher rates of adverse cardiovascular events, they also tended to experience greater absolute benefit with evolocumab.                                                 In an analysis of baseline high sensitivity CRP in achieved LDL cholesterol, the authors found that at first cardiovascular event rates were independently associated with both LDL cholesterol and high sensitive CRP. Event rates were lowest in patients with the lowest hsCRP and LDL cholesterol, supporting the relevance of both inflammatory and residual cholesterol risk.                                                 The next paper provides further evidence that residual inflammatory risk, as measured by on-treatment high sensitivity CRP, remains an important clinical issue in patients on combination statin and PCSK9 inhibitor therapy. Dr Pradhan, from Brigham and Women's Hospital and colleagues, evaluated the residual inflammatory risk among patients participating in the SPIRE-1 and -2 cardiovascular outcome trials, who are receiving both statin therapy and the PCSK9 inhibitor bococizumab, according to on-treatment levels of high sensitivity CRP and LDL cholesterol measured 14 weeks after drug initiation.                                                 They found that among high-risk stable outpatients treated with moderate or high-intensity statins and PCSK9 inhibition, roughly one in two had residual inflammatory risk defined by an on-treatment high sensitivity CRP level of 2 or more mg per liters, and roughly one in three had values above 3 mg per liter.                                                 PCSK9 inhibition was associated with a 60% mean reduction in LDL cholesterol but little change in high sensitivity CRP. Levels of high sensitivity CRP above 3 mg per liter were associated with a 60% greater risk of future cardiovascular events, corresponding to a 3.6% annual event rate, even after accounting for on-treatment LDL cholesterol.                                                 Thus, PCSK9 inhibition, added to statin therapy in stable outpatients, does not lower high sensitivity CRP. Persistent elevations of CRP is associated with future cardiovascular risk in these patients, even after low levels of LDL cholesterol are achieved. If corroborated, these data suggests that inflammation modulation may yet have a role in the primary and secondary prevention of cardiovascular disease when LDL cholesterol is already controlled. Well, that wraps it up for our summaries. Now, for our future discussion.                                                 In-hospital cardiac arrests are common worldwide and they're so important because they represent opportunities for us to improve survival. Now, yet, overall rates of hospital survival after in-hospital cardiac arrests remain poor and there is substantial variation across facilities. This may be surprising because we all seem to follow or should follow the same ACLS algorithms across the world and yet, there are different outcomes.                                                 How do resuscitation teams, at top performing hospitals, for in-hospital cardiac arrest, how do they succeed? Pleased to be discussing this with a real star team in today's podcast. We have first and corresponding author of our feature paper, Dr Brahmajee Nallamothu. We also have Dr Steven Kronick, who is the chair of the CPR committee and both are from University of Michigan Medical School. We also have Dr Sana Al-Khatib, who is a senior associate editor of Circ, from Duke University. So, welcome everyone! Let’s go straight into it. Maybe starting with you Brahmajee, could you tell us what inspired you to perform this study? Dr Brahmajee Nallamothu            Thank you, Carolyn, for giving us the opportunity to talk about this study. I'm an interventional cardiologist here at the University of Michigan and typically, this isn't an area that interventional cardiologists are really greatly involved with. I became interested because I also, at times, I round in the cardiac intensive care unit, and that's a place where a lot of patients often times end up after they've had an in-hospital cardiac arrest at our institution and what I've noticed over the years, is the variability in care that would be occurring out there, and then also lots of gaps in the literature.                                                 Over a decade or so ago, I started partnering with a close friend and colleague, Paul Chan, from the Mid America Heart Institute and we started to do a series of studies on how in-hospital cardiac arrest care varies across institutions in the United States and we published a number of articles that have been in really high-profile journals over the last 10 years, but the problem has always been that even though we could describe really well what was happening, we had very little understanding of why it was happening or how certain hospitals were seeming to outperform others in this really challenging situation.                                                 We wanted to dive a bit deeper into the questions and reasons behind top performers doing so well and that's what brought us on to doing this study. Dr Carolyn Lam:                Great. You want to tell us a little bit about it? It's really very different from the other CPR studies I've seen. Could you tell us about it and what you've found? Dr Brahmajee Nallamothu:          Sure, so in the broader framework, it's a qualitative study and what I mean by qualitative is, we didn't really collect data either through surveys or through outcome assessments. What we did was, we actually went out and talked to people.                                                 The study though was really focused on what people call a mixed methods approach. We didn't just randomly talk to different hospitals, we actually focused on hospitals that were at the top-performing levels. We also focused on some hospitals that were non-top-performing as well, to get some contrast between the two and when I said we talked, we did this in a very systematic and pretty rigid way.                                                 We always had four interviewers go out to nine hospitals. We split them up, so we had two content experts and then two methodologic experts in qualitive studies, and we started to interview a bunch of people. In fact, we interviewed almost 160 people across these nine hospitals.                                                 We interviewed everyone from CEOs and hospital leadership, down to boots on the ground, including both clinical providers and even non-clinical providers, such as spiritual care, security. We tried to get this comprehensive view of what was actually happening during an in-hospital cardiac arrest across these nine hospitals, and really the results were quite fascinating to us.                                                 For someone, like myself, that's been in this space for ten years, I tell people I learn more talking to these nine hospitals than I have in the last ten years of looking at numbers on a spreadsheet. I really started to understand, for the first time, what was really going on, how these hospitals were dealing with these challenging situations because there's no bigger emergency in a hospital, and Steve, who we're going to hear from, we talk about this, but Steve has a great line about how when an in-hospital cardiac arrest occurs, that patient automatically becomes the sickest person in an institution and yet, we haven't set up systems that really build on how to handle that in the most consistent and positive way. Dr Carolyn Lam:                Oh, my goodness, I just love that line! Now, you have to tell us, so what's the secret? What's the secret of the succeeding hospitals? Dr Brahmajee Nallamothu:          What we found in general was, that resuscitation teams at top-performing hospitals really demonstrated the following features. They had dedicated or designated resuscitation teams. They really included the participation of diverse disciplines as team members during the in-hospital cardiac arrest. There were really clear roles and responsibilities of the team members that were set up right from the front.                                                 There was better communication and leadership, actually, during these events and finally, in the training aspect, one of the unique things we found was, the top-performing hospitals seem to have a high rate of in-depth mock codes, that they used as strategies for getting their clinicians ready for these events. Dr Carolyn Lam:                As you were speaking I was just thinking through the experiences of in-hospital cardiac arrests that I've encountered, and you're right. These elements, though we don't talk about them much, make a huge difference. Steve, I am so curious about your outlook. I mean you must have attended a kajillion CPRs as chair of the CPR committee. Tell us, what do you think is the take home message for clinicians and hospitals? Dr Steven Kronick:           My field is in emergency medicine and as chair of the CPR committee, I have responsibility of overseeing how we respond to cardiac arrests in our hospitals. I think that many institutions spend a lot of time and effort looking at in-hospital cardiac arrests are managed, and how to improve on it. We're able to use data to help compare ourselves to similar institutions, but beyond the bottom line of either ROSC or survival to discharge, we've most relied on process measures to figure out what we're doing.                                                 We're essentially flying blind, or at least not flying in any sort of formation when we do that. I think that this study validates some of the operational aspects of the arrest response, for those centers who use those and can help other decide where they want to direct their efforts. I think a good example that Brahmajee brought up, is this distinction we found between the use of dedicated teams, designated teams, or not having any organized team, and the impact that has on survival.                                                 The use of these teams can mean significant use of resources but showing that it's associated with better outcomes help provide support for that concept and for those centers who might already use one of those models, it helps them to steer their efforts to improving the delivery or the efficiency of that model. Dr Carolyn Lam:                Yeah, and indeed. Congratulations to both of you, Steve and Brahmajee. I do think that these are novel contemporary data, at least the first that I know of. Sana, you handle the paper and recognize this. Could you tell us a little about what you think are the novel and important aspects? Dr Sana Al-Khatib:            I really have been a fan of this paper from the get go and yes, it doesn't have the quantitative analysis that the statistical modeling, most of us are used to. It is a qualitative study, but I think that gives it strength. It makes it unique. This type of research, it can really only be effectively done through a qualitative study that really has all the important aspects of a good qualitative study, so I do want to congratulate them. Clearly, a lot of work went into this, and I appreciate all their efforts.                                                 In terms of the main findings, some of us might look at this data and say, well it's not surprising that those are the characteristics, or the features, of the top performing hospitals, but I felt like it was great, in terms of how the data were presented. Encouraging hospitals to adopt this. Giving them almost like a checklist of what they need to be doing to improve the outcomes of their in-hospital cardiac arrests, in terms of ensuring that they have designated resuscitation teams.                                                 The whole idea about diversity of participants in these arrests, and making sure everyone has a clear role and responsibility. The whole idea of making sure that somebody takes leadership and you have clear and very good communication among the different people who are doing this and great training. In fact, these people were doing in-depth mock codes. I think that spells it out very nicely and gives a lot of the hospitals, hopefully, action items that they can implement to improve the outcomes these patients. I love this paper. Dr Carolyn Lam:                Sana, I love the way you put that. Checklist, and you know what I was thinking as Brahmajee and Steve were talking earlier? I was thinking blueprint, almost, of the things that we should have. So Steve, could I ask your thoughts. I mean, are you going to put some of these things into practice in your own committee and how? Dr Steven Kronick:           There are a variety of things we can do. Some of these things are a pretty high-functioning place, but still looking at recommendations that have been laid out and how we help modify those things. Though the example is the roles that people play at an arrest. We can certainly improve on assigning those roles, how people work together as a team, and then also, getting to work more as a team, so that when they are called upon to perform those duties, they can do it in a more coordinated way. Dr Carolyn Lam:                How beautifully put. I'm going to steal a couple of minutes at the end of this podcast. I really have to because it's so rare to have Brahmajee on the line today and he's the Editor-in-Chief of Circ: Cardiovascular Quality and Outcomes. Brahmajee, could I ask you to say a few words to our worldwide audience about your journal? Dr Brahmajee Nallamothu:          We are a kind of daughter journal to Circulation. We are a bit more unique than the others, in the sense that we aren't disease or subspecialty focused. We deal with, broadly, the issues around outcomes research, health services research, quality of care research, and really health policy. We publish an issue once a month. We have a broad interest in things that are really relevant to the community around outcomes research and health services research.                                                 I will say that I really appreciate this because of the worldwide audience and reach, one of the big issues we've been very interested in is expanding our reach, from the United States to other parts of the world, and in fact, last fall, we had a global health issue, which was well received, and we received papers from across the world.                                                 In fact, every paper in that issue was a non-US-based paper, and it touched on a number of things from issues around healthcare utilization in Asia to demographics and disease registries in Africa, and it was a wonderful experience, so I think it's a journal that we're excited about.                                                 It was first launched by Harlan Krumholz, who has set a high bar and standard for us, and I think that my editorial team, which has been fantastic, has continued with that work. We would love to see papers from your readers and your listeners from across the world and excited about what that journal is going to be doing in the next five years. Dr Carolyn Lam:                Oh wow! That's so cool! Well listeners, you heard it right here, first time on Circulation on the Run. Thank you so much for joining us today. Don't forget to tune in again next week.  

Oncotarget
Effective control of acute myeloid leukaemia and acute lymphoblastic leukaemia progression

Oncotarget

Play Episode Listen Later Jan 19, 2018 35:54


Effective control of acute myeloid leukaemia and acute lymphoblastic leukaemia progression by telomerase specific adoptive T-cell therapy Full Text- https://tinyurl.com/yb3gjwqs Telomerase (TERT) is a ribonucleoprotein enzyme that preserves the molecular organization at the ends of eukaryotic chromosomes. Since TERT deregulation is a common step in leukaemia, treatments targeting telomerase might be useful for the therapy of hematologic malignancies. Despite a large spectrum of potential drugs, their bench-to-bedside translation is quite limited, with only a therapeutic vaccine in the clinic and a telomerase inhibitor at late stage of preclinical validation. We recently demonstrated that the adoptive transfer of T cell transduced with an HLA-A2-restricted T-cell receptor (TCR), which recognize human TERT with high avidity, controls human B-cell chronic lymphocytic leukaemia (B-CLL) progression without severe side-effects in humanized mice. In the present report, we show the ability of our approach to limit the progression of more aggressive leukemic pathologies, such as acute myeloid leukaemia (AML) and B-cell acute lymphoblastic leukaemia (B-ALL). Together, our findings demonstrate that TERT-based adoptive cell therapy is a concrete platform of T cell-mediated immunotherapy for leukaemia treatment. Facebook - bit.ly/2xznxjV Twitter - bit.ly/2xzWvsu LinkedIn - bit.ly/2xzJ6kc Pintrest - bit.ly/2xzX8SS Reddit - bit.ly/2hoxI0N www.Oncotarget.com

Ringler Radio - Structured Settlements and Legal Topics

Benzene is a chemical widely used in a number of industries and products. Exposure to the chemical has been linked to Acute Myeloid Leukemia (AML), Myelodysplastic Syndrome (MDS), lymphomas and aplastic anemia. Many of these cases involving benzene exposure link back to the workplace. Ringler Radio host Larry Cohen and co-host, Keith Christie talk with attorney John Tomlinson, from the Beasley Allen law firm, about benzene exposure, litigation, and how exposure to benzene can be controlled, reduced or prevented.

Ringler Radio - Structured Settlements and Legal Topics

Benzene is a chemical widely used in a number of industries and products. Exposure to the chemical has been linked to Acute Myeloid Leukemia (AML), Myelodysplastic Syndrome (MDS), lymphomas and aplastic anemia. Many of these cases involving benzene exposure link back to the workplace. Ringler Radio host Larry Cohen and co-host, Keith Christie talk with attorney John Tomlinson, from the Beasley Allen law firm, about benzene exposure, litigation, and how exposure to benzene can be controlled, reduced or prevented.

AACR 2016
Identifying myeloid-driven biologies

AACR 2016

Play Episode Listen Later Aug 11, 2017 4:51


Dr Brian Ruffell speaks with ecancertv at AACR 2016 about his work with mouse models of myeloid cells. Focussing on the macrophage receptor to CSF1, he discusses cell plasticity between patients, sites and stress conditions.

ASH 2015
Tosedostat for elderly acute myeloid leukaemia

ASH 2015

Play Episode Listen Later Aug 8, 2017 6:30


Dr Visani talks to ecancertv at ASH 2015 about the use of the investigational drug tosedostat in the setting of elderly acute myeloid leukaemia (AML). Patients with AML aged 60 years and older can be a difficult population to treat as they are often resistant to or cannot tolerate intensive chemotherapy. As a result they generally have poorer outcomes than their younger counterparts with shorter overall survival. Tosedostat is a new, orally bioavailable inhibitor of members of the M1 and M17 classes of aminopeptidases that has shown efficacy in both de novo and relapsed AML. In the interview, Dr Visani talks about the results of a prospective phase II multicenter study that looked at combining tosedostat with low-dose cytarabine versus the chemotherapy alone in 33 elderly patients with AML. Dr Visani highlights that 45% of patients achieved complete remission with the combination versus 25% of those who had the chemotherapy alone. The duration of remission was also lengthened by the addition of tosedostat.

ASH 2015
First targeted therapy for genetically defined subset with acute myeloid leukaemia significantly improves survival

ASH 2015

Play Episode Listen Later Aug 8, 2017 5:20


Dr Stone talks to ecancertv at ASH 2015 about a multinational, randomised, phase III trial that evaluated the benefit of the multi-kinase drug midostaurin in adult patients with acute myeloid leukaemia (AML). The aim of the study was to see if adding midostaurin to induction and consolidation therapy followed by 1 year of maintenance would improve overall survival (OS) compared to standard chemotherapy in younger adults with activating FLT3 mutations. Around 700 patients were randomized and results showed there was a 23% lower risk of dying if patients had been randomised to receive the additional targeted treatment.

ASH 2015
First targeted therapy for genetically defined subset of patients with acute myeloid leukaemia significantly improves survival

ASH 2015

Play Episode Listen Later Aug 8, 2017 3:31


Dr Stone presents, at a press conference at ASH 2015, results from an international prospective randomised P-controlled double-blind trial. The findings shows the multi-kinase inhibitor midostaurin prolongs survival, compared with placebo in combination with daunorubicin/cytarabine induction, high-dose C consolidation, and as maintenance therapy in newly diagnosed acute myeloid leukaemia patients with FLT3 Mutations.

ASH 2016
Highlights in myeloid leukaemia research from ASH 2016

ASH 2016

Play Episode Listen Later Aug 2, 2017 7:04


Dr Mazzarella meets with ecancer at ASH 2016 to discuss his personal highlights from the conference, with special focus on improved understanding of the biologic factors and diagnostic utility in treating myeloid leukaemias. Next-generation sequencing in clinical analysis of blood cancers was reported by the group led by Dr Torsten Haferlach in the most recent issue of Blood. Dr Mazzerella considers how persistence of mutated cells might lead to relapse, to resistance and how randomised trials will shore up these initial investigations into disease clonotypes.

ASH 2016
Azacitidine plus nivolumab against acute myeloid leukaemia

ASH 2016

Play Episode Listen Later Aug 2, 2017 8:21


Prof Daver joins ecancertv at ASH 2016 to discuss preliminary outcomes of immunochemotherapy targeting the PD-1 checkpoint in the treatment of AML. He describes the therapy, combining standard doses of azacitadine and nivolumab, as having the potential to deliver durable complete remissions, even in relapsed patients, though does note immune toxicity in some organs. Overall, there is a significant improvement in overall survival for salvage patients, with greatest response from patients with high CD8 T cell presence. Prof Daver considers how the use of PD-1 therapies in haematological malignancies differs from solid tumours, and future avenues for immunotherapy in leukaemia treatments.

EHA 2017
Metabolic adaptations to targeted therapy in FLT3 mutated acute myeloid leukaemia

EHA 2017

Play Episode Listen Later Jul 28, 2017 4:37


Dr Gallipoli talks with ecancer at EHA 2017 about his work on FLT3 mutated acute myeloid leukaemia. He discusses how, without sugar, AML relies on glutamine metabolism, mostly channelled towards glutathione production, while also supporting the citric acid cycle, and both these fates contribute to its protective effects following FLT3 TK inhibition by counteracting oxidative damage and sustaining cellular metabolism. Dr Gallipoli highlights how unveiling this pathway may be lead to targets for future therapies

EHA 2016
Risk adapted therapy for acute myeloid leukaemia - Prof Jorge Sierra

EHA 2016

Play Episode Listen Later Jul 30, 2016 4:51


Prof Sierra talks to ecancertv at EHA 2016 about how patients therapy selection to treat acute myeloid leukaemia (AML) can be guided through risk factors determined through genetic analysis. He describes how informing patients and care providers of their risk stratification can craft personalised therapy and minimise the chances of failed treatment.

Brain Matters – Johns Hopkins Medicine Podcasts

This month Michael Lim, MD, talks about using viruses and other aspects of immunotherapy for brain tumors. Program notes: 0:22 Polio virus and brain tumor treatment 1:21 Genetically modify viruses to attack tumors 2:21 Implanted melanoma tumors 3:22 Myeloid cells play an important role 4:23 May not need a neurotropic virus 5:25 Timeline relative to […]

Understanding Childhood Cancer With Dr Geoff
Acute Myeloid Leukamia 2: Treatment of AML

Understanding Childhood Cancer With Dr Geoff

Play Episode Listen Later Aug 13, 2015 23:51


AML requires chemotherapy treatment, and sometimes bone marrow transplantation.

EHA 2015
Exploring "bad luck" - why do some patients develop myeloid leukaemia?

EHA 2015

Play Episode Listen Later Aug 6, 2015 5:21


"Myeloid leukaemia is a disease of bad luck," Dr George Vassiliou (Cambridge Cancer Centre, Cambridge, UK) tells ecancertv at EHA 2015. It's common for people - particularly those over the age of 90 - to accumulate the genetic mutations that lead to leukaemia, but the body's systems usually keep the disease in check. He explains these mechanisms and connects the influences of genetics, cancer evolution and the environment with respect to leukaemia. Watch Dr Vassiliou explain more about these mutations here. ecancer's filming at EHA has been kindly supported by Amgen through the ECMS Foundation. ecancer is editorially independent and there is no influence over content.

EHA 2015
First randomised evidence for kinase inhibitor activity in acute myeloid leukaemia

EHA 2015

Play Episode Listen Later Aug 6, 2015 6:30


Dr Ehninger (University Hospital Dresden, Dresden, Germany) presents on the results of a phase II randomised study on the safety and efficacy of sorafenib in leukaemia at a press conference at EHA 2015.

EHA 2015
Evidence for kinase inhibitor activity in acute myeloid leukaemia

EHA 2015

Play Episode Listen Later Aug 6, 2015 6:32


Dr Ehninger (University Hospital Dresden, Dresden, Germany) talks to ecancertv at EHA 2015 about the results of a phase II randomised study on the safety and efficacy of sorafenib in leukaemia. Read the news story or watch the press conference video for more. ecancer's filming at EHA has been kindly supported by Amgen through the ECMS Foundation. ecancer is editorially independent and there is no influence over content.

EHA 2015
Measuring molecular responses to tyrosine kinase inhibitors in chronic myeloid leukaemia

EHA 2015

Play Episode Listen Later Aug 6, 2015 6:08


Prof Branford (Adelaide University Adelaide, Australia) talks to ecancertv at EHA 2015 about differences in molecular responses to tyrosine kinase inhibitors in chronic myeloid leukaemia and how decisions can be made about stopping the treatment.

Understanding Childhood Cancer With Dr Geoff
Acute Myeloid Leukaemia 1: What is this disease? The first weeks.

Understanding Childhood Cancer With Dr Geoff

Play Episode Listen Later Aug 4, 2015 27:47


Acute myeloid leukaemia is the second main form of leukaemia in childhood. This podcast explains what the disease is, and the tests and treatments done at initial diagnosis.

19th European Haematology Association (EHA) Congress
Novel targeting in acute myeloid leukaemia

19th European Haematology Association (EHA) Congress

Play Episode Listen Later Jul 15, 2014 8:35


Prof Martinelli talks to ecancertv at EHA 2014 about the use of novel targets in acute myeloid leukaemia.

19th European Haematology Association (EHA) Congress
Philadelphia chromosome and the role it plays in chronic myeloid leukaemia

19th European Haematology Association (EHA) Congress

Play Episode Listen Later Jul 15, 2014 6:41


Prof Harrison talks to ecancertv at EHA 2014 about the Philadelphia chromosome and the role it plays in triggering chronic myeloid leukaemia (CML).