Scientific Program
The following information is preliminary and subject to change. The full annual meeting schedule (including session dates, times, and locations) will be available in early October.
Scientific Program sessions are developed by ASH鈥檚 18 Scientific Committees and highlight important basic and translational research topics across the field of hematology. The sessions will take place in person and stream simultaneously on the virtual platform (the recording will be available on demand). Sessions will consist of didactic presentations followed by panel discussions and a question-and-answer period with all speakers. Session descriptions for this program will be available in the Annual Meeting App.
JOINT SESSION: Molecular Characterization of Lymphomas in Children, Adolescents, and Young Adults
Scientific Committee on Blood Disorders in Childhood + Scientific Committee on Lymphoid Neoplasia
Dynamic advances in the molecular characterization of lymphomas continue to shape how these malignancies are classified and inform therapeutic targeting. This joint session will provide a state-of-the-science update on next-generation technologies used to explore that special group of lymphoma subtypes that are most prevalent in pediatric, adolescents, and young adults. The speakers represent experts in these methods and will highlight exciting applications in elucidating lymphoma biology (especially age-related differences in pathogenesis), including enhancing clinical management.
Dr. Lisa Roth will discuss ongoing efforts to delineate the genomic landscape of classic Hodgkin lymphoma (cHL). Historically, genetic evaluation of cHL has been limited by the scarcity of Hodgkin and Reed-Sternberg (HRS) cells in cHL tumors. This has been overcome in recent years using fluorescence-activated cell sorting to isolate HRS cells from cHL tissues and evaluation of circulating tumor DNA, which have revealed tumors with high mutational burden, complex structural variants, and genomic subtypes with distinct clinical and molecular characteristics. The applicability of these findings to develop prognostic biomarkers and novel therapeutics will be discussed.
Dr. Tomohiro Aoki聽will discuss emerging single-cell technologies that have enabled better understanding of the comprehensive interactions within the cHL tumor microenvironment at an unprecedented resolution. Considering current pathogenesis models where HRS cells 鈥渞ecruit and re-educate鈥 their microenvironment to create an immuno-suppressive milieu, cHL has emerged as one of the most exciting fields for application of these cutting-edge technologies. Dr. Aoki will summarize new insights gained using CyTOF, single-cell RNA sequencing and multiplexed imaging techniques, and discuss potential implications for clinical decisions.
Dr. Birgit Burkhardt聽will provide a comprehensive update of recurrent genetic variants reported in Burkitt lymphoma (BL) in several recent studies. Covering both endemic and sporadic BL, Dr. Burkhardt will highlight the impact of patient age at diagnosis on molecular characteristics and its implications for pathogenesis. Incorporation of specific variants as potential biomarkers for risk group stratification in upcoming BL clinical trials will also be discussed.
Dr. Bj枚rn Chapuy聽will discuss novel (epi)genomic analyses employed to define molecular heterogeneity in B-cell lymphoma subtypes and identify clinically actionable alterations, with a focus on primary mediastinal large B-cell lymphomas (PBMLs). With biometric features that often overlap with cHL, PMBLs are distinguished by their typical manifestation in young female patients and sensitivity to PD-1 blockade. Dr. Chapuy will present evolving approaches to comprehensive genetic analysis used to inform and test response to therapies that target such mechanisms of immune escape.
Co-Chairs:
狈颈肠辞濒别听碍耻肠颈苍别,听惭顿,惭厂
Weill Cornell Medicine
New York,聽NY
Jean L.聽Koff,聽MD,MSc
Winship Cancer Institute of Emory University
础迟濒补苍迟补,听骋础
Speakers:
Lisa Giulino聽Roth,聽MD
Weill Cornell Medicine
New York,聽NY
Genomic Landscape in Hodgkin Lymphoma
Tomohiro聽Aoki,聽MD, PhD
Princess Margaret Cancer Center
罢辞谤辞苍迟辞,听翱狈,听颁补苍补诲补
Sequencing Technologies in Hodgkin Lymphoma
叠颈谤驳颈迟听叠耻谤办丑补谤诲迟,听惭顿,笔丑顿
University Hospital M眉nster
惭耻别苍蝉迟别谤,听骋别谤尘补苍测
Age-Related Molecular Changes in Burkitt Lymphoma
叠箩枚谤苍听颁丑补辫耻测
Charit茅 - University Medical Center Berlin, Campus Benjamin Franklin
叠别谤濒颈苍,听骋别谤尘补苍测
Functional Genomics of Non-Hodgkin Lymphoma in Children, Adolescents, and Young Adults
JOINT SESSION: Therapeutic Gene Editing of Stem Cells in Classical and Malignant Hematology
Scientific Committee on Bone Marrow Failure + Scientific Committee on Transplantation Biology and Cellular Therapies
Gene editing is a novel technology to change specific nucleotides or knockouts in cells, and these are starting to be used clinically. This joint-scientific committee session will include 4 talks that span from basic science to clinical use of gene-edited stem cell products and CAR-T products in malignant and classical hematology.
Dr. Justin Eyquem will discuss his latest work using novel gene editing technologies to improve CAR T-cell function and facilitate their manufacturing. He will present new gene edits associated with improved CAR T-cell functional persistence and novel types of vectors for the generation of CAR T cell in vivo.
Dr. Paulo Rio will present the latest results in optimizing novel genome editing tools, including prime editing, to correct hematopoietic stem cells (HSCs) from Fanconi Anemia (FA) patients. She will discuss the latest advances from her lab in optimizing prime editing technology to efficiently target long-term repopulating HSCs and correct the most common FA mutations in both cell lines and primary HSCs from FA patients.
Dr. Pietro Genovese will present the innovative 鈥渆pitope editing鈥 strategy for overcoming on-target/off-tumor toxicities in acute myeloid leukemia (AML) immunotherapy. Epitope mapping and library screenings have identified specific amino acid changes that have avoided antibody binding. These have now been introduced into HSPCs via base-editing techniques. Epitope-edited HSPC鈥檚 were resistant to CAR-T cell therapy, and enabled specific eradication of patient-derived AML xenografts. Dr. Genovese will discuss the potential of precision immunotherapy for relapsed/refractory AML, non-genotoxic conditioning approaches, and advances in multiplex engineering of HSPCs.
Dr. Julia Skokowa will review recent efforts to establish clinical genome editing to correct severe congenital neutropenia-associated mutations as well as gene editing efforts to inhibit mutated genes in patients' HSCs that may be applicable to other bone marrow failure syndromes. She will also discuss key considerations that are particularly important for gene therapy of pre-leukemic bone marrow syndromes, where gene editing of HSCs should be extremely safe so as not to potentiate the leukemogenic transformation of hematopoiesis. Finally, Dr. Skokowa will present her thoughts on the ethics of gene editing for pre-leukemic bone marrow failure.
Co-Chairs:
Marcela V聽Maus,聽MD, PhD
Harvard University/Massachusetts General Hospital
叠辞蝉迟辞苍,听惭础
贬补苍苍补丑听罢补尘补谤测,听惭顿
Tel Aviv University, Israel
Ramat Gan,聽Israel
Speakers:
闯耻蝉迟颈苍听贰测辩耻别尘,听笔丑顿
University of California San Francisco
San Fransisco,聽CA
New Gene Editing Technologies
笔补耻濒补听搁颈辞,听笔丑顿
IIS-FJD, UAM
惭补诲谤颈诲,听厂辫补颈苍
Gene Editing for Fanconi Anemia Bone Marrow Failure
笔颈别迟谤辞听骋别苍辞惫别蝉别,听笔丑顿
Boston Children's Hospital
叠辞蝉迟辞苍,听惭础
Stem Cell Gene Editing
Julia聽Skokowa,聽MD, PhD
University Hospital T眉bingen
罢眉产颈苍驳别苍,听骋别谤尘补苍测
Gene Editing for Severe Congenital Neutropenia 鈥 Current Advances and Critical Considerations
JOINT SESSION: Emerging Therapeutic Strategies Targeting Epigenetic, Transcriptomic, and Metabolic Mechanisms
Scientific Committee on Epigenetics and Genomics + Scientific Committee on Myeloid Neoplasia
Recent developments in therapeutic targeting of various mechanisms of epigenetic, transcriptomic, and metabolic vulnerabilities in cancer utilize novel technologies and may provide future breakthroughs. Given the extensive amount of knowledge derived from high throughput methodologies in the last decade, rational targeting is now possible, with sophisticated mechanistic studies to study the effects of targeting. This session will focus on novel research aimed at identifying and targeting these molecules, including novel targeting approaches such as heterobifunctional molecules and others.
Co-Chairs:
Dinesh S.聽Rao,聽MD, PhD
University of California Los Angeles
Los Angeles,聽CA
顿补苍颈别濒听厂迟补谤肠锄测苍辞飞蝉办颈,听笔丑顿
Cincinnati Children's Hospital
颁颈苍肠颈苍苍补迟颈,听翱贬
Speakers:
Hannah J聽Uckelmann,聽PhD
Frankfurt Cancer Institute
贵谤补苍办蹿耻谤迟,听骋别谤尘补苍测
Novel Inhibitors of Transcriptional Mechanisms
Gerald R.聽Crabtree,聽MD
Stanford University
厂迟补苍蹿辞谤诲,听颁础
Heterobifunctional Molecules Targeting Epigenetic Mechanisms
叠别苍箩补尘颈苍听颁谤补惫补迟迟,听笔丑顿
The Scripps Research Institute
San Diego,聽CA
Inhibitors of RNAs and RNA Binding Proteins.
颁辞耻谤迟苍别测听闯辞苍别蝉,听笔丑顿
Cincinnati Children's Hospital
颁颈苍肠颈苍苍补迟颈,听翱贬
Targeting Metabolic Vulnerabilities
Metabolic Deregulation in Hematopoietic Neoplasia: Tumor, The Environment, and Therapies.
Scientific Committee on Hematopathology and Clinical Laboratory Hematology
Cellular metabolism and its role in the pathogenesis of hematologic malignancies is an emerging area of research. Recent studies implicate various cellular mechanisms by which oncogenic activation of metabolic pathways contribute to lymphoid and myeloid malignancies as well as their respective tumor environment. In this session, the speakers will discuss the role of deregulated cellular metabolism that contributes to lymphoid and myeloid malignancies and how they may provide novel insights with therapeutic relevance. The metabolic control of T cell differentiation and their function in immunity will also be discussed. This session highlights the opportunities for gaining novel mechanistic insights of hematologic malignancies through global metabolomic studies that has potential to impact the field of T-cell immunology, immunotherapies and facilitate translation to clinical practice.
Chair:
Megan S. S聽Lim,聽MD,PhD
Memorial Sloan Kettering Cancer Center
New York City,聽NY
Speakers:
J眉rgen Maximilian聽Ruland
Technical University of Munich
惭耻苍颈肠丑,听骋别谤尘补苍测
Novel Insights in Metabolic Deregulation in Lymphoid Malignancies
笔补辞濒辞听骋补濒濒颈辫辞濒颈,听惭顿
Queen Mary University of London
London,聽United Kingdom
Targeting Metabolic Deregulation in Acute Myeloid Leukemia
础苍补苍诲补听骋辞濒诲谤补迟丑,听笔丑顿
Allen Institute
厂别补迟迟濒别,听奥础
Metabolic Control of T Cell Differentiation and Function in Tumor Immunity
JOINT SESSION: The Fuel & Physiology of Regeneration
Scientific Committee on Hematopoiesis + Scientific Committee on Stem Cells and Regenerative Medicine
The regulation of hematopoietic stem cell (HSC) regeneration involves a sophisticated interplay between signals from the niche and the nuclear regulatory machinery. Extensive work has been done to identify many key players in both areas. However, conveying the signal to the nucleus is not sufficient without the 鈥渄oers,鈥 the machineries that execute the cellular processes critical for regeneration. Recent studies have identified several vulnerable processes in HSC physiology, such as proteostasis and energy metabolism, which become imbalanced during HSC exhaustion or dysfunction, i.e., processes involved in HSC culture expansion or aging. This session will closely examine the critical physiological processes and their interplay with other regulatory cues, including nutrient-derived signals (minerals and vitamins) crucial for maintaining healthy regeneration without malignant transformation.
Dr. Robert Signer, will discuss how protein homeostasis has emerged as fundamentally and preferentially important in HSCs. He will review how the protein homeostasis network is uniquely configured to promote hematopoietic stem cell self-renewal. Dr. Signer will further discuss how mechanisms of translational control, protein folding, and protein degradation are rewired throughout life to preserve stem cell fitness and will evaluate consequences of protein homeostasis disruption.
Dr. Marie-Dominique Filippi, will discuss the role of metabolism in HSC functions and how HSCs are highly responsive to changes in metabolite availability. New mechanisms will be presented on how HSC metabolic needs are remodeled during regenerative conditions. Additionally, Dr. Filippi will discuss the usage of branch chain amino acids as a new cell-autonomous metabolic checkpoint that influences HSC replicative lifespan.
Dr. Nina Cabezas-Wallscheid, will discuss how mouse and human HSCs and multipotent progenitors are metabolically regulated from intrinsic to dietary-derived metabolites. Through her work using integrated low-input multi-layer omics data, she will highlight research demonstrating distinct metabolic and epigenetic hubs that are essential in HSCs (and not for their downstream progenitors)
Dr. Britta Will, will discuss integrating nutrients into HSC regulation and iron homeostasis in HSCs. Her lab has uncovered a key role of the readily accessible intracellular labile iron pool in instructing HSC self-renewal. More recently, she has focused on identifying the molecular mechanisms of action, particularly focusing on metabolic and non-enzymatic pathways that rely on iron.
Co-Chairs:
Hanna聽Mikkola,聽MD PhD
University of California, Los Angeles
Los Angeles,聽CA
Keisuke聽Ito,聽MD, PhD
Albert Einstein College of Medicine
叠谤辞苍虫,听狈驰
Speakers:
搁辞产别谤迟听厂颈驳苍别谤,听笔丑顿
University of California San Diego
La Jolla,聽CA
Proteomic Health in Hematopoietic Stem Cells
惭补谤颈别-顿辞尘颈苍颈辩耻别听贵颈濒颈辫辫颈,听笔丑顿
Cincinnati Children's Hospital Research Foundation
颁颈苍肠颈苍苍补迟颈,听翱贬
Energy Management in Hematopoietic Stem Cells
狈颈苍补听颁补产别锄补蝉-奥补濒濒蝉肠丑别颈诲,听笔丑顿
ETH Z眉rich
窜眉谤颈肠丑,听厂飞颈迟锄别谤濒补苍诲
Integrating Nutrients to Hematopoietic Stem Cell Regulation
叠谤颈迟迟补听奥颈濒濒,听笔丑顿
Albert Einstein College of Medicine
叠谤辞苍虫,听狈驰
Iron Homeostasis in Hematopoietic Stem Cells.
Paradigm Shifts in Hemostasis: From Mechanisms to Therapies and Back
Scientific Committee on Hemostasis
Coagulation is not a linear process that ends at clot formation. Rather, coagulation is a network of ever-growing complexity with many mechanisms and pathways for regulation and feedback. The consequences of coagulation extend well beyond clot formation and into processes related to immunity, inflammation, vascular biology and regeneration. This session will highlight three examples for how bi-directional interactions from bench to bedside and back have paved the way to paradigm shifts in mechanistic insights, diagnosis, and treatment options for bleeding disorders and thrombotic complications.
Dr. Annette von Drygalski will discuss the most recent therapeutic paradigms in hemophilia. The continued unraveling of genetic and biochemical mechanisms underlying impaired blood clotting remains critical to inform the development of groundbreaking therapeutic strategies for Hemophilia A and B. Such strategies include extended half-life clotting factor preparations, non-factor-based molecules modifying hemostasis and, lastly, gene therapy. The new therapies have great potential to improve joint bleed prevention and reduce the sequelae of hemophilic arthropathy, which remains one of the most prominent aspects of clinical management in daily practice. Dr. von Drygalski will discuss pathophysiological mechanisms contributing to hemophilic arthropathy, new imaging modalities and joint outcome measures, paving the way for more targeted and individualized treatment strategies.
Dr. Dani毛l Verhoef will discuss the discovery and (pre)clinical development of a modified [PR1] recombinant form of coagulation factor X, called VMX-C001, which can bypass factor Xa direct oral anticoagulants (DOACs) in patients requiring immediate reversal of anticoagulation. It carries a unique 16 amino acid insertion that was derived from a snake venom factor X that makes VMX-C001 insensitive to inhibition by FXa DOACs. A single intravenous administration of VMX-C001 was shown to restore coagulation assays in animals and human volunteers on FXa-DOACs. VMX-C001 also prevented rivaroxaban induced bleeding in a primate liver injury model. VMX-C001 holds promise as an effective FXa DOAC reversal agent given its favorable half-life, short infusion time, FXa DOAC independent dosing and lack of a prothrombotic effect.
Dr. Cristina Puy will present a comprehensive exploration of coagulation factor XI dynamic interaction with diverse ligands, substrates, and endothelial cell receptors. Delving into the intricate mechanisms, Dr. Puy will elucidate factor XI pivotal role in modulating endothelial cell permeability and barrier function, shedding light on its implications in thrombotic and inflammatory conditions. This presentation will deepen our understanding of factor XI multifaceted involvement in health and disease.
Chair:
Laurent O.聽Mosnier,聽PhD
The Scripps Research Institute
La Jolla,聽CA
Speakers:
Annette聽von Drygalski,聽MD, PharmD, RMSK
University of California San Diego (UCSD)
SAN DIEGO,聽CA
Paradigm Shifts in Hemophilia.
Dani毛l聽Verhoef,聽MSc, PhD
VarmX B.V.
尝别颈诲别苍,听狈别迟丑别谤濒补苍诲蝉
Paradigm Shifts in the Reversal of DOACs
Cristina聽Puy Garcia,聽PhD
Oregon Health and Science University
笔辞谤迟濒补苍诲,听翱搁
New Mechanisms That May Fuel the Paradigm Shifts of the Future
Host Factors Driving Anti-Leukemia Immunotherapy Outcomes
Scientific Committee on Immunology and Host Defense
This session will cover how the immune microenvironment of the host interacts with leukemia cells and how the donor immune system can exert graft-versus-leukemia (GVL) effects. The speakers will focus on the characterization of immune effector cells and leukemia cells using high resolution RNA and protein analysis, the characterization of metabolites that impact the GVL effect and kinase inhibition strategies to overcome immune escape mechanisms of leukemia cells.
Dr. Catherine Wu will discuss the components critical to devising effective immunotherapy for the treatment of myeloid leukemia, namely the identification of myeloid malignancy antigen targets, and the detection of critical immune cell effectors. The analysis of GvL responses following allogeneic stem cell transplant for AML/MDS, through single cell transcriptome and spatial analysis of marrow specimens, is a particularly instructive setting from which to detect key antigens and cell subpopulations implicated in anti-leukemia responses. The insights gained from the study of such GVL settings promise to provide a roadmap for devising new immunotherapeutic approaches for myeloid malignancies.
Dr. Takanori Teshima will discuss mechanisms of leukemia relapse after allogeneic hematopoietic stem cell transplantation and novel strategies to prevent relapse by inhibiting immune escape of leukemic cells, restoring immune cell dysfunction, and turning 鈥淐OLD鈥 into 鈥淗OT鈥 immune microenvironment. In addition, novel strategies to separate GVL from GVHD by controlling migration and activation of donor T cells in the vicinity of leukemic cells.
Chair:
搁辞产别谤迟听窜别颈蝉别谤,听惭顿
Universit盲tsklinikum Freiburg
贵谤别颈产耻谤驳,听骋别谤尘补苍测
Speakers:
Catherine J.聽Wu,聽MD
Harvard Medical School
叠辞蝉迟辞苍,听惭础
Immune Microenvironment and GVL Effects
罢补办补苍辞谤颈听罢别蝉丑颈尘补,听惭顿,笔丑顿
Hokkaido University
厂补辫辫辞谤辞,听贬辞办办补颈诲辞,听闯补辫补苍
Firing Up COLD Tumor Microenvironment to Facilitate GVL
贵谤补苍锄颈蝉办补听叠濒补别蝉肠丑办别,听惭顿,笔丑顿
German Cancer Research Center (DKFZ)
贬别颈诲别濒产别谤驳,听骋别谤尘补苍测
Immune Metabolism in T Cells Acting Against Leukemia Cells
Crosstalk Between Iron Homeostasis and Metabolism
Scientific Committee on Iron and Heme
Maintaining iron balance is fundamental to preserve metabolic functions and energy requirements. This session reflects the current understanding of the reciprocal relationship existing between iron homeostasis and energetic metabolism. It aims to highlight the regulatory role of heme and iron on glucose and lipid metabolism as well as the impact of metabolism on the modulation of the iron status. Novel findings will be presented about the physiologic and pathologic implications of iron-mediated regulation of metabolism, and metabolite-driven control of iron and heme homeostasis. The session will focus on b-thalassemia, sickle cell disease and obesity, and will have broad relevance to all hematologic and non-hematological diseases.
Dr. Antonella Nai will discuss the role of Transferrin Receptor2 (TFR2) in the reciprocal regulation between iron homeostasis, erythropoiesis, and glucose metabolism. TFR2 is an iron sensor acting as a brake of erythropoietin signaling in erythroid cells. Its genetic inactivation in the hematopoietic compartment enhances erythropoiesis and improves anemia in 脽-thalassemia. She will present unpublished data demonstrating that Tfr2 deficiency increases the metabolic activity of erythroid cells, thus promoting glucose consumption and reducing blood glycemia. This is particularly relevant in 脽-thalassemia, whereby glucose intolerance and diabetes are common and invalidating complications.
Dr. Wei Ying will focus on the connection between iron homeostasis and lipid metabolism. He will present findings related to the role of iron homeostasis in regulating hepatocyte lipogenesis and neighboring cell responses, including hepatic stellate cells, and describe how alterations of these mechanisms drive non-alcoholic fatty liver disease, steatohepatitis and obesity.
Dr. Leitinger will share how heme triggers a unique bioenergetic switch in macrophages, characterized by a metabolic shift from oxidative phosphorylation towards glucose consumption, and its critical role in the effective clearance and detoxification of heme in sickle cell disease. Based on the previous identification of the phosphofructokinase PFKFB3 as key mediator of the metabolic switching in heme-detoxifying macrophages, he will present data about a potential therapeutic strategy involving the inhibition of PFKFB3 in a mouse model of sickle cell disease. Furthermore, the general clinical relevance of these processes for patients with hemolytic disorders will be discussed.
Chair:
贵谤补苍肠别蝉肠补听痴颈苍肠丑颈,听笔丑顿
New York Blood Center
New York,聽NY
Speakers:
础苍迟辞苍别濒濒补听狈补颈,听笔丑顿
IRCCS San Raffaele Scientific Institute
惭颈濒补苍,听滨迟补濒测
Iron, Erythropoiesis, and Glucose Metabolism
奥别颈听驰颈苍驳,听笔丑顿
University of California San Diego
La Jolla,聽CA
Iron and Lipid Metabolism
狈辞谤产别谤迟听尝别颈迟颈苍驳别谤
University of Virginia
颁丑补谤濒辞迟迟别蝉惫颈濒濒别,听痴础
Heme and Macrophage Metabolism.
JOINT SESSION: Newly Described Functions in the Vascular Space
Scientific Committee on Megakaryocytes and Platelets + Scientific Committee on Thrombosis and Vascular Biology
Dysregulated interactions between platelets, immune cells, endothelial cells, and their plasma environment underlie numerous age-related diseases. This joint session will provide an integrated view of the vascular space and will highlight the cellular and molecular mechanisms underlying diseases that primarily afflict the elderly. Specifically, the session will also on novel discoveries addressing how platelet and endothelial aging may affect neurodegenerative disorders and thrombotic disease, and immune thrombocytopenia (ITP), and will shed light into the role of fibrinolytic factors in shaping the pro-atherogenic plasma lipid profile.
Dr. Claus Nerlov, will discuss how aging affects hematopoietic stem cells (HSCs). He will describe how increased HSC platelet bias due to how age-related increases in TGFbeta signaling is an evolutionarily conserved feature of murine and human hematopoiesis. The role of HSC platelet bias in suppressing lymphoid cell production during aging and how TGFbeta receptor inhibition can increase the ability of aged HSCs to support antiviral immunity will also be discussed.聽聽
Dr. Nichola Cooper, will discuss the current understanding of ITP pathogenesis and how the results from novel treatments in ITP may depict different disease types in ITP. ITP is a common bleeding disorder with an increase in incidence after age 60. Understanding the disease phenotype and evolution is needed to improve patient outcomes. However, the diagnosis remains presumptive, and treatment is largely empiric, with many patients rotating through several treatments before having a platelet response.
Dr. Lisa Lesniewski will discuss the phenotype of the aging vasculature and the hematopathology underlying mechanisms and potential therapeutic strategies being explored to reverse arterial aging to reduce cardiovascular (CVD) risk in older adults. This is important since several factors contributing to dysfunction of the endothelium (i.e., oxidative stress and inflammation, deregulated nutrient sensing, and cellular senescence) increase with aging and could impact CVD risk.
Dr. Ze Zheng will discuss research demonstrating that hepatocytes are an unappreciated source of tissue-type plasminogen activator (tPA), sense metabolic stresses, and impact the production of tPA and its inhibitor PAI1, thereby influencing the extent of fibrinolysis in obesity. She will introduce findings that tPA binds directly to hepatocyte apoB, preventing it from being loaded with lipids and assembled into lipoproteins. Conversely, tPA's inhibitor, PAI1, has the opposite effect, sequestering free tPA and preventing its interaction with apoB to promote VLDL assembly and increase apoB-lipoprotein cholesterol levels.
Co-Chairs:
Lijun聽Xia,聽MD, PhD
Oklahoma Medical Research Foundation
Oklahoma City,聽OK
贬补谤迟尘耻迟听奥别颈濒别谤,听笔丑顿
Versiti Blood Research Institute
惭颈濒飞补耻办别别,听奥滨
Speakers:
颁濒补耻蝉听狈别谤濒辞惫,听笔丑顿
University of Oxford
Oxford,聽United Kingdom
Platelets and Aging
狈颈肠丑辞濒补听颁辞辞辫别谤,听惭顿
Imperial College
London,聽ENG,聽United Kingdom
New Insights in MK/PLT Functions and Diseases.
尝颈蝉补听尝别蝉苍颈别飞蝉办颈,听笔丑顿
University of Utah Health
Salt Lake City,聽UT
Age-Related Endothelial Function
窜别听窜丑别苍驳,听惭叠叠厂,笔丑顿
Medical College of Wisconsin; Versiti Blood Research Institute
惭颈濒飞补耻办别别,听奥滨
Novel Functions of Fibrinolytic Factors in Shaping the Pro-Atherogenic Lipid Profile in Plasma.
Leveraging Single Cell Multi-Omics to Understand Mechanisms of Myeloid Lineage Expansion in Aging and Disease.
Scientific Committee on Myeloid Biology
Single cell multi-omic studies of normal and malignant hematopoiesis highlight how hematology remains an ideal testing ground for technologic innovation. Continued advancements in single cell sequencing and the analysis of these complex datasets have informed functional experiments that have enabled the field to improve its understanding of hematopoietic stem cell behavior and myeloid differentiation in response to aging, inflammation, and malignant transformation. This session will showcase innovative transcriptomic and functional genomic studies of the pathways that govern myeloid differentiation in response to aging, inflammation, and malignancy. The talks will focus on how advances in single cell lineage tracing have improved the fields鈥 understanding of hematopoietic stem cell commitment to the myeloid lineage early in life; explore how aging and inflammatory conditions impact myelopoiesis; and address how the tumor microenvironment can impact the function of mature myeloid cells.
Chair:
Esther A.聽Obeng,聽MD,PhD
St. Jude Children's Research Hospital
惭别尘辫丑颈蝉,听罢狈
Speakers:
贰濒颈蝉补听尝补耻谤别苍迟颈,听笔丑顿
University of Cambridge
Cambridge,聽ENG,聽United Kingdom
Hematopoietic Stem Cell Commitment to the Myeloid Lineage
John E.聽Dick,聽PhD
Princess Margaret Cancer Centre, University Health Network
罢辞谤辞苍迟辞,听翱狈,听颁础狈
Hematopoietic Stem Cell and Myeloid Progenitor Cell Response to Inflammation
Allon Moshe聽Klein,聽PhD
Harvard Medical School
叠辞蝉迟辞苍,听惭础
Myeloid Progenitor and Mature Neutrophil Responses in Cancer.
Proteo-Genomics to Better Study Multiple Myeloma Biology and Evolution
Scientific Committee on Plasma Cell Neoplasia
Cancer proteogenomics provides new biological and diagnostic knowledge that can improve our understanding of malignant transformation and therapeutic outcomes. This area is new in plasma cell neoplasia. In this session the speakers will discuss how proteogenomics can lead to a better study of multiple myeloma (MM) biology and support the development of novel therapeutic targets in MM.聽
Dr. Jan Kr枚nke will discuss the impact of proteogenomic studies on our understanding of MM biology. He will outline how proteomics improve risk stratification, and reveal deregulated proteins and pathways that can be exploited for new therapies in MM.聽
Dr. Francesco Maura will present the genomic landscape of MM and its precursor conditions, with a particular focus on the temporal acquisition of various combinations of genomic drivers. He will highlight the relevance of these genomic patterns in predicting MM progression and identifying the most effective immunotherapy for MM patients.聽
Dr. Fabiana Perna will describe a strategy for probing the MM surface proteome (surfaceome) with mass-spectrometry and transcriptomic analyses to identify novel immunotherapeutic targets. She will discuss the contribution that the surfaceome makes to MM biology as well as the pre-clinical development of novel chimeric antigen receptor platforms for MM.
Chair:
笔补辞濒补听狈别谤颈,听惭顿,笔丑顿
Arnie Charbonneau Cancer Institute, University of Calgary
颁补濒驳补谤测,听础叠,听颁补苍补诲补
Speakers:
闯补苍听碍谤辞苍办别,听惭顿
Charit茅 鈥 Universit盲tsmedizin Berlin, corporate member of Freie Universit盲t Berlin, Humboldt Universit盲t zu Berlin, and Berlin Institute of Health
叠别谤濒颈苍,听骋别谤尘补苍测
Defining the Proteomic Landscape of Multiple Myeloma
贵谤补苍肠别蝉肠辞听惭补耻谤补,听惭顿
University of Miami
Palmetto Bay,聽FL
Genomic Drivers Involved in Myeloma Progression and Development of Resistance
Fabiana聽Perna,聽MD, PhD
H. Lee Moffitt Cancer Center and Research Institute
罢补尘辫补,听贵尝
Proteo-Genomics to Better Study Cell Surfaceome in Multiple Myeloma
Ineffective Erythropoiesis: Insights Into Molecular Mechanisms and Disease Pathophysiology
Scientific Committee on Red Cell Biology
Ineffective erythropoiesis is the leading cause of red cell-related diseases, including anemia, which stands as the most prevalent hematologic disease, affecting millions of individuals worldwide. Understanding the underlying mechanisms of ineffective erythropoiesis is pivotal for advancing diagnostic and therapeutic approaches in hereditary anemias and adult-onset conditions. This session will explore recent breakthroughs in research related to ineffective erythropoiesis, focusing on areas of hemoglobinopathies, malaria infection, and myeloid neoplasms. By bringing together experts at the forefront of these investigations, the session will not only enhance understanding of the pathogenesis of ineffective erythropoiesis but also catalyze the development of innovative approaches to treat related diseases.
Chair:
笔别苍驳听闯颈,听惭顿,笔丑顿
Northwestern University Medical School
颁丑颈肠补驳辞,听滨尝
Speakers:
Wassim聽El Nemer,聽PhD
French Blood Establishment (EFS)
惭补谤蝉别颈濒濒别,听贵谤补苍肠别
Post-Transcriptional and Signaling Mechanisms in Ineffective Erythropoiesis in Hemoglobinopathies
Elizabeth S.聽Egan,聽MD, PhD
Stanford University School of Medicine
厂迟补苍蹿辞谤诲,听颁础
Plasmodium Falciparum Influences Erythropoiesis
厂别谤驳别颈听顿辞耻濒补迟辞惫,听笔丑顿
Division of Hematology, Department of Medicine
厂别补迟迟濒别,听奥础
Ineffective Erythropoiesis in Myeloid Neoplasms
Understanding the Impact of Donor and Recipient Metabolic Variability on Blood Transfusion Outcomes
Scientific Committee on Transfusion Medicine
Blood transfusion requires the donation of blood products from a diverse array of individuals with unique genetics and environmental inputs. This results in the quality and overall behavior of the blood products being less standardized and predictable, with direct consequences on transfused recipients. This session will focus on how recently recognized unique genetic and environmental backgrounds of both the blood donor and the transfusion recipient influence the outcomes of patients. Newly applied metabolic tools reveal metabolic variability in donors and recipients, shedding light on fundamental aspects of these differential responses of transfusion in patients, which could guide future strategies for more personalized and effective blood transfusions.
Chair:
Cassandra Dorothy聽Josephson,聽MD
Johns Hopkins All Children鈥檚 Hospital
St. Petersburg,聽FL
Speakers:
础苍驳别濒辞听顿'础濒别蝉蝉补苍诲谤辞,听笔丑顿
University of Colorado Anschutz Medical Campus
础耻谤辞谤补,听颁翱
Blood Donor Genetics and Biology Impact Red Blood Cell Transfusion Outcomes
惭辞谤颈迟锄听厂迟辞濒濒补,听惭顿
Bloodworks and University of Washington, Pathology and Laboratory Medicine
厂别补迟迟濒别,听奥础
Unveiling Platelet Metabolism: Implications for Storage and Transfusion
颁丑别谤测濒听尝辞产辞,听笔丑顿
Laboratory of Blood-Borne Parasites, Lindsley F. Kimball Research Institute, New York Blood Center
New York,聽NY
Impact of RBC Metabolism on the Disease Outcomes of Transfusion Dependent Patients
66th ASH Annual Meeting and exposition
Registration for ASH members will open on July 17, 2024, at 11:00 a.m. Eastern time.
Registration for non-members, groups, exhibitors, and media opens on August 7, 2024.