Call for Abstracts

Abstract submissions for the 2026 ASH Annual Meeting are now closed.

Prospective abstract submitters should take note of several changes for the 2026 ASH Annual Meeting.

  • No figures or tables may be included in abstract submissions. While only text is allowed in abstracts, figures and/or tables may be included in the oral and poster presentations for abstracts accepted to the program.
  • ASH requests that posters and oral presentations reporting information about clinical trials include relevant demographic information, when available, about the participants in those clinical trials. Demographic information such as sex, race, ethnicity, age, disability, or other relevant factors of the subjects enrolled in the clinical trials strengthens the science, as it is important to ensure that the characteristics of the trial population adequately reflect the broader population at risk for the disease under investigation. If some or all relevant demographic information is not available, poster and oral presenters should disclose in their presentations the limitations that led to such data not being collected in the trial.

Information for Authors

The 68th Annual Meeting of the American Society of Hematology (ASH) will be held Saturday, December 12, through Tuesday, December 15, 2026, in New Orleans, Louisiana. The meeting will be in person, with a virtual attendance option, however, presenting authors are required to be on-site in New Orleans. The goal of the ASH annual meeting is to present the best new basic, translational, clinical and epidemiological research in all areas of hematology. The meeting content will also be accessible to virtual meeting attendees via an online platform.

Eligibility

Abstract Policies

Trials in Progress (no outcome data)

Abstract Submission Guidelines

How to Submit an Abstract


All abstracts must be submitted by August 4, 2026, at 11:59 p.m., Pacific time. All Submissions that are incomplete by the deadline will be rejected.

  • Abstracts must be submitted online through the official online abstract submission system. Abstracts sent via e-mail to ASH will not be accepted.
  • There is a $95 non-refundable handling fee for submission of each abstract. Payment must be made by credit card; Visa, MasterCard, and American Express are accepted. Purchase orders and checks will not be accepted. The abstract submission fee does not include registration for the annual meeting; therefore, all authors planning to attend the ASH annual meeting must register.
  • Electronic submission works optimally with Microsoft Internet Explorer 7+, Mozilla Firefox 3.0+, and Safari or MAC OS 10.4+. Netscape Navigator 7.7+ is supported, but its use is discouraged since not all features are available. The online abstract submission system will provide links for free browser downloads.
  • If this is the first time that you are submitting an abstract for the ASH annual meeting, please be sure to check the box indicating so during submission.
  • Once authors have submitted the title of the abstract, a draft will be saved, and the submitting author will be able to return to the site to edit and update the submission at any time until August 4, 2026, at 11:59 p.m., Pacific time. The submitting author will receive an e-mail providing a link to their submission.
  • Abstracts cannot be submitted and will not be reviewed without proper payment and completion of the “Submission Information” and “Disclosure” sections of the online abstract submission program.
  • Any technical questions regarding navigation of the submission site itself should be directed to ash@confex.com. It is advisable not to leave submission of the abstract to the final day or hours, giving time for ASH staff to assist with any technical problems during the submission process.

Submitting an Abstract

Presentation

Abstract Achievement Awards

These $500 merit-based awards are provided to trainee investigators with high-scoring annual meeting abstracts, of which they are the first or senior author and presenter, to defray travel expenses associated with their presentation at the annual meeting. Recipients will be notified by email by late October. The list of award recipients will also be posted on the ASH website by November.

Individuals are encouraged to review the website before sending an inquiry to ASH.

Winners must register for and attend the meeting in person and present their abstract in person to receive their award. For accurate identification, it is strongly encouraged that you use the same email address for abstract submission that you use to register for the annual meeting.

Abstract Achievement Award and Outstanding Abstract Achievement Award applicants will be notified by late October if they have been selected for an award. A list of winners will also be posted online at that time.

Individuals who have not received notification by November 1 may contact awards@hematology.org for information regarding their award status.

Electronic Signature

Completion of all required disclosure information in the online abstract submission system serves as an agreement and is accepted in lieu of a faxed signature. It certifies the ASH abstract submitter's understanding of the rules for participation contained in the online abstract submission program and affirms that:

  1. All authors approve of submitting this work for presentation and publication.
  2. The author(s) transfer(s) all copyright ownership of the named abstract to the American Society of Hematology (except when one or more authors are U.S. Government employees).
  3. All authors have read the ASH Conflict-of-Interest Policy and have acted in accordance with that policy.
  4. The author(s) agree(s) to materially confine the presentation to information in the abstract if accepted for presentation. If an author has more than one abstract accepted, each presentation will be materially confined to the information in the abstract selected for the specific session.
  5. The presenting author or other designated will be available to present the abstract in person if selected for the program. The author(s) will immediately notify ASH if the presenting author must be changed.
  6. The data in the abstract have not been accepted for publication before the abstract submission closing date; nor will they be materially presented at a meeting of 3,000 or more participants before the ASH annual meeting (note the exception for abstracts submitted to other ASH meetings in the Eligibility section above.); and are not to be presented at an ASH Friday Satellite Symposium. If the data have been made available on a preprint server, all ASH policies summarized above regarding preprints have been and will be followed.
  7. The author(s) are aware that the withdrawal deadline for ASH Annual Meeting abstracts is September 16, 2026, and understand that abstracts cannot be withdrawn after this date.

Sample Abstract

A sample abstract is provided for reference below. Note that the title, authors, and institutions are entered in separate fields in the submission form, not in the abstract body, as they are not included in the character count.

The LRF/ZBTB7A transcription factor Is a BCL11A-independent repressor of fetal hemoglobin Takeshi Masuda, PhD1, Xin Wang, PhD2, Manami Maeda, M.D., PhD1, Matthew C. Canver, B.S.3, Falak Sher, PhD3, Alister P.W. Funnell, PhD4, Chris Fisher, PhD5, Maria Suciu5, Gabriella E. Martyn4, Laura J. Norton4, Ruijia Zhu1, Ryo Kurita, PhD6, Yukio Nakamura, MD, PhD6, Jian Xu, PhD7, Douglas R. Higgs, FRS5, Merlin Crossley, DPhil4, Daniel E. Bauer, MD, PhD3, Stuart H. Orkin, M.D.8, Peter V. Kharchenko, PhD2 and Takahiro Maeda, MD, PhD1

1Division of Hematology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 2Department of Biomedical Informatics, Harvard Medical School, Boston, MA 3Pediatric Hematology-Oncology, Boston Children's Hospital, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 4School of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, Australia 5MRC Molecular Hematology Unit, Weatherall Institute of Molecular Medicine, Oxford University, Oxford, United Kingdom 6Cell Engineering Division, RIKEN BioResource Center, Tsukuba, Japan 7Children's Medical Center Research Institute, University of Texas Southwestern Medical Center, Dallas, TX 8Department of Pediatric Hematology-Oncology, Boston Children's Hospital, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA

Induction of fetal-type hemoglobin (HbF: α2γ2) is a promising means to treat hemoglobinopathies; however, precisely how HbF expression is silenced in adult erythroid cells is not fully understood. Such knowledge is essential to develop mechanism-based, targeted approaches to reactivate HbF production. Here, we show that Leukemia/lymphoma Related Factor (LRF), encoded by the ZBTB7A gene, is a novel and potent repressor of HbF production.

To assess the effects of LRF loss on the mouse erythroid transcriptome, we performed RNA-Seq analysis using splenic erythroblasts from control and LRF conditional knockout (Zbtb7aF/F Mx1-Cre+) mice. LRF-deficient adult erythroblasts showed significant induction of Hbb-bh1, but not Hbb-y. The results were validated at the protein levels via isoelectric focusing of peripheral blood (PB) hemolysates and MALDI-TOFMS analysis. LRF loss also reactivated human fetal globin expression in vivo in LRF conditional KO mice harboring the human β-globin gene cluster as a yeast artificial chromosome transgene (β-YAC).

To determine whether LRF loss could induce HbF in human erythroid cells, we employed human CD34+ hematopoietic stem and progenitor (HSPC)-derived primary erythroblasts and determined γ-globin expression levels upon shRNA-mediated LRF knockdown (KD). HbF levels in LRF KD cells (49-70%) were much greater than those seen in parental or scrambled-shRNA transduced cells. We next employed a novel human immortalized erythroid line (HUDEP-2). This line possesses an advantage over lines currently used for globin switching studies because it expresses predominantly adult hemoglobin (HbA: α2β2), with very low background HbF expression. Using CRISPR/cas9 gene modification, we knocked out ZBTB7A in HUDEP-2 cells and performed RNA-Seq analysis. As expected, γ-globin (HBG1 and HBG2) transcripts, but not those of embryonic ε-globin (HBE1), were markedly induced in ZBTB7A KO (ZBTB7AΔ/Δ) HUDEP-2 cells. ZBTB7AΔ/Δ cells exhibited HbF levels greater than 60%, while that of parental cells was less than 3%. Notably, the HbF reactivation occurred without changes in levels of transcripts encoding known HbF repressors, including BCL11A, the principal known switching factor.

We next performed chromatin-immunoprecipitation and sequencing (ChIP-Seq) with an anti-LRF antibody using HSPC-derived proerythroblasts and HUDEP-2 cells. The most enriched motif identified in either was concordant with that previously identified in vitro using CAST analysis (Maeda et. al. Nature 2005), confirming antibody specificity. Supporting a direct role of LRF at the β-globin cluster, we observed several significant enrichment of LRF-ChIP binding signals at adult (HBB), fetal (HBG1) globin loci and the upstream hypersensitivity (HS) sites within the locus control region (LCR). ATAC-Seq (for assay for transposase-accessible chromatin with high-throughput sequencing) analysis revealed strong chromatin accessibility at the γ-globin locus in ZBTB7AΔ/Δcells. Strikingly, differential enrichment of ATAC-signals in ZBTB7AΔ/Δ cells was evident only at the γ-locus. Thus, while LRF binds to the HBB locus and HS sites as well as to the HBG1 locus, LRF depletion specifically opens chromatin at the γ-globin locus.

Finally, to determine whether LRF and BCL11A suppress γ-globin expression via distinct mechanisms, we established LRF/BCL11A double knockout HUDEP-2 cells. Strikingly, HUDEP-2 lines lacking both LRF and BCL11A exhibited almost a complete switch in expression from adult- to fetal-type globin, suggesting that these two factors cumulatively represent the near entirety of γ-globin repressive activity in adult erythroid cells. Our findings reveal a novel molecular mechanism regulating γ-globin silencing and may open a new window for therapeutic targeting in the treatment of hemoglobinopathies.

Contact Information

Send related correspondence and questions regarding abstract submission policies or notifications to ASHabstracts@hematology.org.

Any technical questions regarding navigation of the submission site itself should be directed to ash@confex.com.

ASH Annual Meeting Registration and Housing

  • Please note that submitting an abstract (or having it accepted to the meeting) does not register you for the ASH annual meeting.
  • To register, you must complete and return an Attendee Registration Form or register online through the ASH website.
  • For ASH members, Early-Bird Registration will be available July 22, 2026. During this time, ASH members can access the online meeting registration and hotel reservation program before it is open to the general public.
  • Please note that Early-Bird Registration is available online only, and you must register for the annual meeting before making your hotel reservations.
  • Information about registration, hotel reservation, and the meeting program will be available online in July 2026.
  • Non-members will be able to find all relevant annual meeting information on the ASH website and can access the online registration and hotel reservation program beginning August 12, 2026.
  • To register as a non-member in training and receive the discounted advance registration rate, you must register and submit your trainee verification via the online registration site by December 1, 2026. Trainee verification will not be accepted at on-site registration in New Orleans and the discounted rate will not apply.