Call for Late-Breaking Abstracts

Late-breaking abstracts should highlight novel and substantive studies of high impact. The late-breaking abstract deadline is not intended to be merely an extension of the general submission deadline and will focus on capturing abstracts with ground-breaking and novel data that otherwise could not be presented at the annual meeting.

Late-breaking abstract submissions are now closed.

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.

The ASH Program Committee recognizes that some exciting research results may not have been available by the general abstract submission deadline of August 4, 2026. Hence, ASH offers a late-breaking abstract submission pathway to offer the opportunity for presentation of selected timely, novel and substantive studies of high impact. The goal is to enrich the ASH annual meeting with outstanding work completed after the general abstract submission deadline.

All abstract submissions must be made electronically through ASH’s online abstract submission system. The late-breaking abstracts site opens on October 14, 2026, and the deadline for late-breaking abstract submission is October 28, 2026, at 11:59 p.m. Pacific time.

To aid in your submission our Call For Abstracts Reference Guide and Late-Breaking Abstract Submission FAQs are available to download.

Other Key Information for Abstract Authors:

During submission, authors of late-breaking abstracts will need to explain why their abstract was not ready by the regular deadline (August 4) and why it deserves to be considered as late-breaking. This information will be available to reviewers.
Only six abstracts will be accepted and presented in the Late-Breaking abstracts session on Tuesday, December 15. Authors should realize that selection for presentation is extremely competitive, with the quality and general significance of the presented Late-Breaking abstracts equivalent to Plenary Sessions.
There is a $150 nonrefundable handling fee for submitting a late-breaking abstract. Payment must be made by credit card; Visa, MasterCard, and American Express are accepted. Purchase orders and checks will not be accepted.
Late-breaking abstracts will undergo regular peer-review evaluation.
The six accepted abstracts will be published online on December 11 and in the Late-Breaking Abstracts supplemental issue of Blood. Submissions not accepted for presentation will not be published in any form.

Key Dates and Deadlines

Call for late-breaking abstract submissions	October 14, 2026 to October 28, 2026, at 11:59 p.m. Pacific time
Regular abstracts available online	November 4, 2026, at 9:00 a.m. Eastern time
Late-breaking abstracts available online	December 7, 2026, at 9:00 a.m. Eastern time

Eligibility

Late-Breaking Abstract Policies

Submissions

No revisions in abstract content can be made after the abstract submission deadline (October 28). This includes changes to the spelling of authors’ names and the order of co-authors.
Please proofread your abstract to ensure that it does not contain spelling, grammar, or scientific mistakes, as it will be reproduced exactly as submitted.
Abstracts should be written in clear and concise English so that reviewers are able to focus solely on the scientific merits of the submission. We encourage non-English-speaking authors to have their abstracts checked for grammar and spelling before submission
There is a $150 nonrefundable handling fee for submitting a late-breaking 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 for the meeting.
During submission, ASH staff are authorized to communicate with the corresponding author. After acceptance, ASH staff will only communicate with the presenting author regarding any abstract-related matters, including requests for withdrawal which must be submitted in writing. Any queries or requests from co-authors or non-authors, including pharmaceutical companies or medical communications companies, must go through the presenting author.

Presentation

Late-Breaking Abstract Submission Policies

How to Submit a Late-Breaking Abstract

The late-breaking abstract submission site is open October 14–October 28, 2026.

All abstracts must be submitted by October 28 at 11:59 p.m. Pacific time. 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 $150 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 late-breaking 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 so that you can download free browser software.
If this is the first time that you are submitting an abstract for the ASH annual meeting, please be sure to check the box that indicates this during submission.
Once you have submitted the title of the abstract, a draft of your abstract will be saved, and you will be able to return to the site to edit and update the submission at any time until October 28, 2026, at 11:59 p.m. Pacific time. You will receive an e-mail providing a link to your 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 helpdesk@m-events.com. It is advisable not to leave submission of the abstract to the final day or hours, giving time for ASH staff and the submission system helpdesk to assist you with any technical problems during the submission process.

Preparing an Abstract for Submission

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:

All authors approve of submitting this work for presentation and publication;
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); OR the submitter has gained permission from the copyright holder of the previously published abstract for the abstract to be displayed in the ASH meeting mobile app and online program.
All authors have read the ASH Conflict-of-Interest Policy and have acted in accordance with that policy;
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;
The presenting author 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;
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.
The author(s) are aware that the withdrawal deadline for ASH Annual Meeting abstracts is October 28, 2026, and understand that abstracts cannot be withdrawn after October 28.

Sample Abstract

A sample abstract is provided for your 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.

Figures and tables are not permitted.
The title should be in sentence case.
The abstract text may not go over 4,500 characters, including spaces.

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 (Zbtb7a^F/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 (ZBTB7A^Δ/Δ) HUDEP-2 cells. ZBTB7A^Δ/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 ZBTB7A^Δ/Δcells. Strikingly, differential enrichment of ATAC-signals in ZBTB7A^Δ/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 helpdesk@m-events.com.

ASH Annual Meeting Registration and Housing

Please note that submitting an abstract 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.
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.