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December 8, 2025BloodOpen Access

Clone-specific epigenetic regulatory mechanisms in ASXL1-mutant chronic myelomonocytic leukemia

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Authors

TLTerra L. LashoAMAmelia MazzoneCFChristy Finke

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Overview

Observational analysis revealed enhanced chromatin accessibility in ASXL1-mutant CMML, pointing to epigenetic therapies targeting BRD4.

Key Points

  • ASXL1-mutant CMML shows unique chromatin accessibility, favoring leukemogenic gene expression.
  • Key regulatory regions marked by H3K4me3 are enriched in ASXL1-mutant cells, impacting treatment outcomes.
  • Analysis using GoT-ChA-seq unveiled differential accessibility of enhancers in ASXL1-mutant versus wildtype cells.
  • Targeting BRD4 with EP31670 in ASXL1-mutant samples resulted in significant therapeutic responses at low drug dosages.

Cite This Study

Lasho et al. (2025) studied this question.

synapsesocial.com/papers/69362f5d4fa91c937236dc66https://doi.org/10.1182/blood-2025-234
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Somatic ASXL1 mutations in chronic myelomonocytic leukemia result in loss of imprinting control and overexpression of DLK1 through deregulation of DNA methylation2025
  2. 2Prognostic impact of ASXL1 somatic mutation on patients with chronic myeloid leukemia: A systemic review and meta-analysis.2026
  3. 3Epigenetic dysregulation of the polycomb axis in Acute Myeloid Leukemia: Clinical and prognostic correlates2025
  4. 4SMARCC1 loss impairs differentiation and enhances self-renewal in ASXL1-mutant hematopoietic cells2025
  5. 5RUNX1 mutations define a high-risk biological subset of chronic myelomonocytic leukemia and cooperate with ASXL1 mutations to drive leukemic transformation2025