Marquee Sessions and Lectures

Announcement of Awards: Outstanding Service Award, ASH Mentor Awards, ASH Advancing Inclusive Excellence Award, and the Wallace H. Coulter Award for Lifetime Achievement

Sunday, December 7, 2025, 1:30 p.m. - 2:00 p.m.
OCCC - West Hall D2

OUTSTANDING SERVICE AWARD ASH will recognize three patient and community-based organizations – the Sickle Cell Disease Association of America, the Sickle Cell Consortium, and Sick Cells – for their dedication and work to improve and extend the lives of individuals with sickle cell disease. Find out more…

ASH MENTOR AWARDS

ASH will recognize Jorge Di Paola, MD, of Washington University in St. Louis, for his role in helping teach and inspire the next generation of pediatric classical hematologists. Find out more…

ASH will recognize Sophie Lanzkron, MD, MHS, of Thomas Jefferson University, for providing hands-on, lifelong mentorship to physician-scientists passionate about improving care for patients, especially those living with sickle cell disease. Find out more…

ASH ADVANCING INCLUSIVE EXCELLENCE AWARD ASH will recognize Diane Krause, MD, PhD, of Yale School of Medicine, for her commitment to removing barriers that prevent the full participation of all who are interested in hematology. Find out more…

WALLACE H. COULTER AWARD FOR LIFETIME ACHIEVEMENT IN HEMATOLOGY ASH will recognize Rainer Storb, MD, of the Fred Hutchinson Cancer Center, with the Wallace H. Coulter Award for Lifetime Achievement in Hematology, the Society's highest honor. Find out more…

Chair:

Belinda Avalos, MD
President, American Society of Hematology, Advocate Health, Atrium Health Levine Cancer

Speakers:

Jorge Di Paola

Sophie Lanzkron

Diane Krause

Rainer Storb, MD

Announcement of Awards: William Dameshek Prize and Henry M. Stratton Medals

Tuesday, December 9, 2025, 9:30 a.m. - 9:45 a.m.
OCCC - West Hall D2

WILLIAM DAMESHEK PRIZE ASH will recognize Mark Dawson, MD, PhD, of Peter MacCallum Cancer Centre, for his contributions to the understanding of epigenetics, the process by which our DNA is accessed to turn genes on and off, and its relationship to the development of hematologic cancers. Find out more...

HENRY M. STRATTON MEDAL 

ASH will recognize Karina Yazdanbakhsh, PhD, of New York Blood Center Enterprises, with the Medal for basic science for her outstanding research in transfusion medicine, which has led to advances in the understanding and treatment of several classical (non-malignant) blood disorders. Find out more...

ASH will recognize David A. Williams, MD, of Boston Children’s Hospital and Dana-Farber Cancer Institute, Harvard Medical School, with the Medal for clinical science for his vital contributions to the understanding of hematopoietic stem cells and viral vectors, which have led to landmark clinical trials of gene therapy for inherited blood disorders. Find out more...

Chair:

Belinda Avalos, MD
President, American Society of Hematology, Advocate Health, Atrium Health Levine Cancer

Speakers:

Mark Dawson, MBBS, BMedSci, FRACP, FRCPA, PhD

Karina Yazdanbakhsh, PhD

David A. Williams

ASH-EHA Joint Symposium

Sunday, December 7, 2025, 12:30 p.m. - 1:30 p.m.
OCCC - West Hall D2

The ASH-EHA Joint Symposium addresses global issues in hematology and provides insight on how international collaboration can help address these issues. This year marks the 20th anniversary of this shared symposia.

This year's topic is Menin Inhibitors: Novel Targeted Agents for Treatment of Acute Myeloid Leukemia (AML). AML is an aggressive heterogeneous disease with limited treatment options. Although most patients with AML receiving intensive chemotherapy can achieve a complete remission, the majority will relapse, with five-year overall survival (without hematopoietic cell transplantation) being 25%. Between 1973 and 2017, no new drugs were approved for the treatment of AML. The identification of unique gene expression profiles in AML has spurred significant advances in our understanding of AML and led to development and the U.S. Food and Drug Administration's (FDA) approval of 12 novel agents since 2017 that target key genetic drivers of specific subtypes of AML. Menin is a member of the KMT2A (lysine methyltransferase 2A, formerly known as MLL1) complex that occupies a broad region around the promoters of a small subset of genes involved in development and cell cycle control. Menin target genes can be essential dependencies for solid and hematopoietic malignancies, especially in rearranged KMT2A (KMT2Ar) and NPM1-mutated AML, in which a stemness transcriptional program involving HOXA/MEIS1 is activated to induce malignant transformation. Small molecule inhibitors of menin have emerged as promising new agents for KMT2Ar or NPM1-mutated AML, and more recently for NUP98 fusions. A total of seven different menin inhibitors have been developed, with two already granted breakthrough therapy designation by the FDA. However, the mechanisms that determine menin-KMT2A occupancy and sensitivity to menin inhibition remain unknown. This session will focus on the rational design and development of menin inhibitors, their mechanisms of action and resistance mechanisms, clinical efficacy, safety, use in combination therapies, biomarkers of response, and appropriate molecular tests to detect measurable residual disease. It will also highlight the application of integrated multiomic platforms including CRISPR screens, proteogenomics, transcriptomics, and single-cell analyses.

Co-Chairs:

Belinda Avalos, MD
President, American Society of Hematology, Advocate Health, Atrium Health Levine Cancer

Konstanze Döhner, MD
University Hospital of Ulm

Speakers:

Scott Armstrong
Dana-Farber Cancer Institute
Design and Development of Menin Inhibitors, Mechanisms of Action, Clinical Trial Results, and Safety

Marc Raaijmakers, MD
Erasmus Medical Center
Review of Menin Inhibitors; Translational Aspects and Clinical Trial

Best of ASH

Tuesday, December 9, 2025, 11:30 a.m. - 1:00 p.m.
OCCC - West Hall D2

Best of ASH (BOA) highlights the most cutting-edge science presented in the oral abstract sessions during the Annual Meeting. This year’s session will consist of talks arranged in overarching themes and will be presented by the 2025 Scientific Program Co-Chairs: Betty Pace, MD, (Augusta University) and Esther Obeng, MD, PhD, (St. Jude Children's Research Hospital).

Co-Chairs:

Betty Pace, MD
Augusta University

Esther Obeng, MD, PhD
The Children's Hospital Corporation

Business Meeting and Ceremonial Passing of the ASH President's Gavel

Tuesday, December 9, 2025, 11:15 a.m. - 11:30 a.m.
OCCC - West Hall D2

This ceremonial session will mark the conclusion of Dr. Belinda Avalos' term serving as the ASH President in 2025.  Dr. Avalos will be recognized for her service to ASH by the ASH President-Elect, Dr. Robert Negrin.  Dr. Avalos will then pass the ceremonial gavel to Dr. Negrin as he begins his year of service to ASH as the 2026 ASH President.  This ceremony will be the conclusion of the in-person annual meeting.

E. Donnall Thomas Lecture and Prize

Monday, December 8, 2025, 9:00 a.m. - 10:00 a.m.
OCCC - West Hall D2

Nancy Speck, PhD, is being honored for her pivotal work in hematopoiesis and leukemogenesis. Her discovery of the transcription factor complex "core binding factor" has enabled significant conceptual insights into embryonic blood cell formation. One subunit of core binding factor is the transcription factor RUNX1, encoded by a gene responsible for blood cell creation. This factor is mutated in individuals with familial platelet disorder with associated myeloid malignancy — a condition that predisposes patients to developing myelodysplastic syndromes and leukemia.

Core binding factor consists of RUNX1, a DNA-binding subunit, and CBFb, a non-DNA-binding subunit. Both subunits are essential for the formation of the first blood cells in the embryo, and both are mutated in leukemia. Dr. Speck's lecture will describe the discovery of core binding factor, its essential role in blood cell formation, and the mutations that contribute to inherited and acquired forms of leukemia.

Dr. Speck is a first-generation college graduate whose decades of research have had a profound impact on both classical and malignant hematology.

Chair:

Belinda Avalos, MD
President, American Society of Hematology, Advocate Health, Atrium Health Levine Cancer

Speaker:

Nancy Speck, PhD
University of Pennsylvania
Core Binding Factor in Blood Cell Formation and Leukemia

Ernest Beutler Lecture and Prize

Monday, December 8, 2025, 1:30 p.m. - 2:30 p.m.
OCCC - West Hall D2

Myeloproliferative Neoplasms: How JAK2 Became Key to Better Diagnosis, Prognosis, and Targeted Therapy

The JAK2-V617F mutation described by four laboratories in 2005 was not only the first causative driver gene associated with myeloproliferative neoplasms (MPNs), but also the most frequent mutation acquired in approximately 70% of all patients with MPNs, close to 95% of patients within the subgroup of polycythemia vera (PV), and around 50% of patients with essential thrombocythemia (ET) or primary myelofibrosis (PMF). With the later discoveries of acquired mutations in calreticulin (CALR) and thrombopoietin receptor (myeloproliferative leukemia) genes in patients with ET and PMF, we can now detect one of these three driver gene mutations in approximately 90% of all patients with MPNs. Additional somatic mutations in genes such as TET2 and ASLX1, which modify the course of the disease, can be detected in some patients with MPNs and are also relevant across other myeloid neoplasms.

Analyses of blood and bone marrow of patients with MPNs and studies of genetic mouse models of MPNs established that the JAK2-V617F mutation is originally acquired in a single hematopoietic stem cell. Recent genomic analyses showed that the mutational event occurs several decades before the diagnosis of an MPN. Clonal hematopoiesis (CH) with presence of the JAK2-V617F mutation can be detected in approximately 3% of otherwise healthy older individuals, suggesting that the acquisition of JAK2-V617F is not the rate-limiting step, and there must be factors limiting the conversion of CH to MPNs.

Because JAK2 is a tyrosine kinase, small molecular inhibitors that compete for the ATP binding domain were rapidly developed, with the JAK1/JAK2 inhibitor ruxolitinib at the vanguard. The U.S. Food and Drug Administration’s approval for myelofibrosis (MF) came for demonstrating clinical benefit from rapid reduction of splenomegaly and symptoms quantified for the first time by MPN-specific, patient-reported outcomes (the Myelofibrosis Symptom Assessment Form and the MPN Symptom Assessment Form). The ensuing years have also shown benefit of ruxolitinib on survival for MF. Subsequently, three additional JAK inhibitors — each with their own incremental benefits — have been approved (fedratinib in 2019, pacritinib in 2022, and momelotinib in 2023). A new generation of more mutant selective JAK2 inhibitors (INCB160058, AJ1-11095) is currently in early clinical trials. Ruxolitinib has moved beyond MPNs to impact a spectrum of inflammatory conditions, including chronic graft-versus-host disease, atopic dermatitis, and vitiligo.

Dr. Radek C. Skoda will describe how the JAK2-V617F mutation drives hematopoiesis causing MPNs and recent advances in understanding of how this mutation activates the JAK2 kinase, opening new ways to find candidate drugs preferentially targeting the mutated JAK2 protein.

Dr. Ruben Mesa will summarize how the single-agent JAK inhibitors significantly helped decrease the burden of MPNs and the role of current agents, the next generation of new inhibitors, and combination approaches, as well as the impact JAK inhibitors have had on non-neoplastic inflammatory disorders.

Chair:

Belinda Avalos, MD
President, American Society of Hematology, Advocate Health, Atrium Health Levine Cancer

Speakers:

Radek Skoda, MD
Baylor College of Medicine
Basic Science

Ruben A. Mesa, MD
Atrium Health Wake Forest
Clinical/Translational Science

Ham-Wasserman Lecture

Saturday, December 6, 2025, 12:30 p.m. - 1:30 p.m.
OCCC - West Hall D2

The Ham-Wasserman Lecture was named in honor of two past presidents of ASH, Thomas Hale Ham and Louis R. Wasserman, distinguished hematologists who contributed extensively to the Society. The Ham-Wasserman lecture is traditionally given by an individual from outside the United States who has made a major contribution to our understanding of an area that relates to hematology.

Chiara Bonini, MD, will speak on the topic, Gene Transfer and Genome Editing of T Cells for Cancer Immunotherapy.

Adoptive T-cell therapy has emerged as a transformative modality in cancer immunotherapy, building upon foundational principles established in allogeneic hematopoietic stem cell transplantation (allo-HSCT). In this setting,  gene transfer strategies — such as suicide gene insertion — have enabled safer use of donor lymphocytes by providing on-demand control of T-cell activity. With this initial gene therapy approach, several lessons on the function, persistence, safety, and efficacy of engineered T cells were learned. More recently, advances in genome editing technologies have enabled the precise manipulation of T cell genome and function, including the disruption of endogenous T-cell receptors (TCRs) and the insertion of tumor-specific receptors, such as chimeric antigen receptors (CARs) and tumor-specific TCRs. Integration of T-cell manufacturing protocols optimized for persistence and resistance to immune suppression, largely facilitated by multiplex genome editing, has positioned engineered T cells as programmable and persistent innovative therapeutics. Key milestones, challenges, and innovations in T-cell gene engineering, from allo-HSCT to next-generation, TCR-edited immunotherapies, will be discussed.

Chair:

Belinda Avalos, MD
President, American Society of Hematology, Advocate Health, Atrium Health Levine Cancer

Speaker:

Chiara Bonini, MD
Vita-Salute San Raffaele University
Gene Transfer and Genome Editing of T Cells for Cancer Immunotherapy

Late-Breaking Abstracts Session

Tuesday, December 9, 2025, 7:30 a.m. - 9:00 a.m.
OCCC - West Hall D2

This highly anticipated session highlights the Joint Program Committees' selections of the highest-impact abstracts, featuring substantive, novel, and groundbreaking data that were not available by the general abstract submission deadline and would otherwise not be presented at the ASH annual meeting.

Co-Chairs:

Payal Desai, MD
Levine Cancer Institute, Atrium Health, Wake Forest School of Medicine Charlotte

Rayne Rouce, MD

Plenary Scientific Session

Sunday, December 7, 2025, 2:00 p.m. - 4:00 p.m.
OCCC - West Hall D2

Co-Chairs:

Belinda Avalos, MD
President, American Society of Hematology, Advocate Health, Atrium Health Levine Cancer

Robert Negrin, MD

Speakers:

Kerry A. Rogers, MD
Ohio State University Hospital
Plenary Introducer 1

Othman Al-Sawaf, MD, PhD
University Hospital of Cologne
Fixed-duration versus continuous targeted treatment for previously untreated chronic lymphocytic leukemia: Results from the randomized CLL17 trial

Julie Makani
Plenary Introducer 2

Anoosha Habibi, MD/ Associated Professor
Outcomes of pregnancies in sickle cell patients treated with hydroxyurea : Findings from the escort-HU cohort studies

Laura K. Hilton, PhD
Plenary Introducer 3

Sanket Shah
Sasp-driven immune evasion defines a novel African ancestry-associated DLBCL subtype with distinctive molecular and immune vulnerabilities

R. Coleman Lindsley, MD, PhD
Dana-Farber Cancer Institute
Plenary Introducer 4

Irenaeus Chi-Chung Chan, M.Sc.
CDK4/6 inhibition mitigates chemotherapy-induced expansion of TP53-mutant clonal hematopoiesis

Jacquelyn M. Powers
Plenary Introducer 5

Haris Sohail
Deciphering the dilemma: Intravenous (IV) iron use in iron deficiency anemia during acute infections

Andrew Wei, MBBS,PhD
The Walter and Eliza Hall Institute of Medical Research
Plenary Introducer 6

Amir T. Fathi, MD
Massachusetts General Hospital
Results from paradigm - a phase 2 randomized multi-center study comparing azacitidine and venetoclax to conventional induction chemotherapy for newly diagnosed fit adults with acute myeloid leukemia

Presidential Symposium

Tuesday, December 9, 2025, 9:45 a.m. - 11:15 a.m.
OCCC - West Hall D2

Clonal Hematopoiesis and the Path to Myeloid Malignancy

Diverse hematopoietic stem and progenitor cell (HSPC) clones contribute to normal hematopoiesis and aging is associated with the acquisition of myeloid malignancy-associated mutations that confer a fitness advantage to some of the clones and are detectable in the peripheral blood of otherwise healthy individuals. Those with detectable clonal hematopoiesis (CH) of indeterminate potential (CHIP), which occurs in 10% to 20% of people over age 70, have an increased risk of myeloid malignancy and other comorbidities.

Although CHIP was described just 10 years ago, improved technologies have led to its increasing recognition and association with poor survival upon malignant transformation. The mechanisms that promote malignant transformation of CHIP are poorly understood, underscoring the urgent need for additional studies and identification of molecules (natural and synthetic) that affect gene expression, chromatin accessibility, and cytokine/chemokine receptor expression and signaling. Both cell-intrinsic and extrinsic processes appear to be involved and are context-dependent. The scarcity of detailed published data regarding germline predisposition (bone marrow failures, telomeres, ETV6 variants, etc.) underscores the need for additional investigation for proper genetic counseling, surveillance, and personalized medicine. New analytic platforms combining single-cell sequencing, epigenomics, spatial transcriptomics, proteomics, and synthetic chemistry along with flow cytometry, mass spectrometry, and functional assays will be critical to unraveling CH, CHIP, and malignant transformation.

Dr. Churpek will describe the currently known hereditary hematologic malignancy predisposition syndromes that increase risk for myeloid malignancies. She will illustrate how individual syndromes and their causative genetic variants reveal insights into mechanisms governing normal hematopoiesis. Further, she will summarize the growing body of literature that has begun to elucidate the prevalence and patterns of syndrome-specific CH. She will illustrate how specific CH variants can serve as proof of variant pathogenicity and at the same time reveal how different strategies to overcome these specific blocks in hematopoiesis either rescue the defect without (i.e., adaptively) or with (i.e., maladaptively) increasing risk for myeloid malignancies.

Dr. Pietras will address the intersection between metabolism and inflammation as a driver of hematopoietic stem and progenitor cell (HSPC) selection in the context of clonal hematopoiesis (CH). He will discuss the growing set of evidence for the role of microenvironmental inflammation as a trigger for reduced relative fitness of normal HSPC in the bone marrow, and the mechanisms by which mutant clones may use these signals to activate distinct cellular programs that facilitate their expansion. He will focus on advances in understanding how changes in cellular metabolism represent a key mechanism by which HSPC harboring CH mutations maintain increased cellular fitness, and will discuss potential opportunities for targeting metabolic pathways as a means of reducing selection for mutant HSPC clones.

Dr. DiPersio will discuss the synergistic effects of combining novel CXCR4 and VLA-4 inhibitors for stem cell mobilization and ex vivo gene therapy and the use of JAK inhibitors to reduce graft-versus-host disease and promote donor allogeneic HSC engraftment across major histocompatibility complex barriers after antibody-based conditioning regimens. Finally, Dr. DiPersio will address the need for prospective, well-controlled studies to investigate new strategies for risk-adapted prophylaxis and salvage therapies for post-transplant relapse.

Chair:

Belinda Avalos, MD
President, American Society of Hematology, Advocate Health, Atrium Health Levine Cancer

Speakers:

Jane Churpek, MD, MS
University of Wisconsin-Madison
Germline Predisposition for Myeloid Neoplasms

Eric Pietras, PhD
University of Colorado
Role of the Microenvironment in Leukemogenesis

John F. DiPersio, MD
Washington University School of Medicine
Novel Therapeutic Approaches