Podcast
Blood Podcast
Hosted by American Society of Hematology · EN
Stay up to date on the latest research and reviews for both clinical and basic hematology with Blood podcast, published weekly in conjunction with each issue of Blood. Additionally, Blood review series podcasts feature in depth discussion with authors of recently published review articles. Subscribe and never miss a new episode.
62episodes
Episodes
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Diffuse large B-cell lymphoma’s long-term effects on immune profiles, plasminogen activation and prevention of venous thromboembolism, and PARP inhibitors in hematological malignancies carrying epigenetic mutations
Sep 1100:18:31Summary readyIn this week's episode we'll learn about persistent changes in immune profiles in patients who have had diffuse large B-cell lymphoma, or DLBCL, and other cancers; that plasminogen activation and plasmin activity do not appear to play a role in routine physiological prevention of venous thromboembolism, or VTE; and about a novel mechanism that makes hematological malignancies carrying epigenetic mutations susceptible to PARP inhibitors.Featured Articles:Large B-cell lymphoma imprints a dysfunctional immune phenotype that persists years after treatmentPlasminogen activation and plasmin activity are not required to prevent venous thrombosis/thromboembolismTransposable elements as novel therapeutic targets for PARPi-induced synthetic lethality in PcG-mutated blood cancer
Summary“Ironing out” Tet2-mutant HSPCs; A CAR-T “license to kill” in T cell leukemia/lymphoma; insights on cHL genetics, through the lens of ctDNA
Sep 400:20:43Summary readyIn this week's episode, we'll learn about how TET2 is often mutated in myeloid malignancies and clonal hematopoiesis. In new work, expansion of Tet2-mutant HSPCs was dependent on Ncoa4, the cargo receptor mediating ferritinophagy. We’ll iron out the implications. After that: a double-oh-seven license to kill in T-cell leukemia/lymphoma. WU-CART-007 is an off-the-shelf CAR T product with manageable safety and encouraging efficacy. With further work, it could become a new option for patients in urgent need of therapy. Finally: a comprehensive genetic study of classical Hodgkin lymphoma using circulating tumor DNA. This new research provides novel and complex insights on genetic subtypes, prognostic biomarkers, neoantigens in the disease environment, and more.Featured Articles:An in vivo barcoded CRISPR-Cas9 screen identifies Ncoa4-mediated ferritinophagy as a dependence in Tet2-deficient hematopoiesisPhase 1/2 trial of anti-CD7 allogeneic WU-CART-007 for patients with relapsed/refractory T-cell malignanciesA comprehensive genetic study of classic Hodgkin lymphoma using circulating tumor DNA
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How I Treat Myeloproliferative Neoplasms
Apr 17, 202500:38:36Summary readyIn this How I Treat series episode Blood Associate Editor, Dr. Jason Gotlib speaks with Drs. Aaron Gerds, Andreas Reiter, and Claire Harrison. The conversation focuses on the work and contributions of these authors to How I Treat Myeloproliferative Neoplasms, and exciting advances in the treatment and management of MPNs. See the full How I Treat series in volume 145 issue 16 of Blood.
SummaryThe decline of transplant for relapsed myeloma; DDAVP response in bleeding disorders; dual DOT1L/EZH2 targeting in DLBCL
Apr 17, 202500:18:49Summary readyIn this week's episode we'll learn about the role of autologous transplant for relapsed myeloma. In an updated analysis of the GMMG ReLApsE trial, salvage autologous transplant offered no survival benefit compared to control chemotherapy. These findings may have clinical implications in an era of alternative, and highly effective, treatment options. After that: Response to DDAVP, or desmopressin, in bleeding disorders. This study is the first large scale meta-analysis to assess the response rate to DDAVP in bleeding disorders. Authors provide new insights into determinants of response, which vary according to the disease type. Finally, turning to diffuse large B cell lymphoma. Germinal center B cells depend on the activity of DOT1 and EZH2 to maintain their pro-proliferative identity. New research shows that combined treatment with DOT1L and EZH2 inhibitors has synergistic activity in vitro.Featured Articles:Salvage autologous transplant in relapsed multiple myeloma: long-term follow-up of the phase 3 GMMG ReLApsE trialDDAVP response and its determinants in bleeding disorders: a systematic review and meta-analysisTargeting DOT1L and EZH2 synergizes in breaking the germinal center identity of diffuse large B-cell lymphoma
SummaryInterleukin-1 signaling pathways in myelodysplastic syndromes, the immune checkpoint regulator VISTA as a target in graft-vs-host disease, and epcoritamab plus chemotherapy in transplant-ineligible relapsed/refractory diffuse large B-cell lymphoma
Apr 10, 202500:20:59Summary readyIn this week's episode we’ll learn about the role of interleukin-1 signaling in the bone marrow microenvironment in the development of myelodysplastic syndromes, the immune checkpoint regulator VISTA as a potential target for preventing graft-vs-host disease, and epcoritamab plus gemcitabine and oxaliplatin in transplant-ineligible relapsed/refractory diffuse large B-cell lymphoma.Featured Articles:IL-1R1 and IL-18 signals regulate mesenchymal stromal cells in an aged murine model of myelodysplastic syndromesTargeting cell-surface VISTA expression on allospecific naïve T cells promotes toleranceEpcoritamab plus GemOx in transplant-ineligible relapsed/refractory DLBCL: results from the EPCORE NHL-2 trial
SummaryAging platelets shift to proinflammatory function; Odronextamab bispecific antibody therapy after CAR T in DLBCL; prizlon-cel, a novel bispecific CAR T, in B-NHL
Apr 3, 202500:15:26Summary readyIn this week's episode we'll learn about tracking the functional profile of aging platelets. Researchers demonstrate that over time, platelet function shifts away from hemostasis and toward a more immunomodulatory role. These finding could have important implications for transfusion medicine and certain platelet-related disease states. After that, use of odronextamab, a CD20×CD3 bispecific antibody, in patients with diffuse large B-cell lymphoma, or DLBCL, progressing after CAR T cell therapy. The study is the first to evaluate the efficacy and safety of this therapy in the post-CAR T cell treatment setting. Finally, we will recap findings from a study of a novel CAR T-cell product that utilizes specificity to two antigens common in diffuse large B-cell lymphoma.Featured Articles:Aging platelets shift their hemostatic properties to inflammatory functionsOdronextamab monotherapy in R/R DLBCL after progression with CAR T-cell therapy: primary analysis of the ELM-1 studyDissection of single-cell landscapes for the development of chimeric antigen receptor T cells in Hodgkin lymphoma
SummaryBlood Bonus Episode: What is a Blood group?
Mar 31, 202500:14:59Summary readyIn this bonus episode of the Blood podcast, we'll hear from Dr. Nicole Thornton, senior author of the article “Deletions in the MAL gene result in loss of Mal protein, defining the rare inherited AnWj-negative blood group phenotype”, speaks with Blood Associate Editor Dr. Erica Wood about the discovery of the genetic basis for the inherited AnWj-negative blood group phenotype. The discovery that Mal protein is expressed on red blood cell membranes of AnWj-positive, but not AnWj-negative individuals, and that homozygous deletion in MAL causes the AnWj-negative blood group phenotype, helps answer a decades-old mystery related to the high prevalence red blood cell antigen AnWj and forms the basis of a new blood group system.
SummaryItacitinib in haploidentical hematopoietic cell transplantation, diagnosis and management of purpura fulminans, and lack of evidence for sickle cell crisis-associated mortality in individuals with sickle cell trait
Mar 27, 202500:19:16Summary readyIn this week's episode, we’ll learn more about using itacitinib for the prevention of graft vs host disease in haploidentical transplants, diagnosis and management of purpura fulminans, and results of a systematic review seeking evidence for sickle cell crisis-associated mortality in individuals with sickle cell trait. Featured Articles:Itacitinib for prevention of graft-versus-host disease and cytokine release syndrome in haploidentical transplantationHow I diagnose and treat acute infection–associated purpura fulminansSickle cell trait does not cause “sickle cell crisis” leading to exertion-related death: a systematic review
SummaryTime-limited triplet therapy in relapsed/refractory CLL; patient-reported outcomes in chronic GVHD-related sclerosis; myeloid bias mechanisms in hematopoiesis
Mar 20, 202500:19:07Summary readyIn today's episode, we'll discuss time-limited triplet therapy in relapsed or refractory CLL. Zanubrutinib, venetoclax and obinutuzumab induced deep remissions, and was well tolerated, even in very high-risk patients, and those with prior exposure to targeted therapies. After that: researchers chronicle the development of a patient-reported outcome measure for sclerosis associated with chronic GVHD—graft-versus-host disease. The new symptom scale—currently undergoing validation studies—may provide valuable information regarding severity, functional impact, and response to therapy. Finally, a study of changes in population dynamic rates that underlie inflammation-associated myeloid bias. The work demonstrates the use of mathematical models to deliver critical biological insights and uncover underlying mechanisms.Featured Articles:MRD-guided zanubrutinib, venetoclax, and obinutuzumab in relapsed CLL: primary end point analysis from the CLL2-BZAG trialDevelopment of the Lee Symptom Scale–Skin Sclerosis for chronic GVHD–associated sclerosisPopulation dynamics modeling reveals that myeloid bias involves both HSC differentiation and progenitor proliferation biases
SummaryAzacitidine plus venetoclax in high-risk myelodysplastic syndromes, post-CAR T-cell hematotoxicity in B-cell acute lymphoblastic leukemia (B-ALL), and inotuzumab ozogamicin resistance in B-ALL
Mar 13, 202500:21:28Summary readyIn this week's episode we’ll learn more about azacitidine-venetoclax combination therapy for first-line treatment of high-risk myelodysplastic syndromes; a new risk-scoring system for post-CAR T-cell hematotoxicity in B-cell acute lymphoblastic leukemia, also known as B-ALL; and a novel mechanism for inotuzumab ozogamicin resistance in B-ALL.Featured Articles:Efficacy and safety of venetoclax plus azacitidine for patients with treatment-naive high-risk myelodysplastic syndromesDevelopment of ALL-Hematotox: predicting post-CAR T-cell hematotoxicity in B-cell acute lymphoblastic leukemiaDNTT-mediated DNA damage response drives inotuzumab ozogamicin resistance in B-cell acute lymphoblastic leukemia
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