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December 8, 2025BloodOpen Access

Somatic ASXL1 mutations in chronic myelomonocytic leukemia result in loss of imprinting control and overexpression of DLK1 through deregulation of DNA methylation

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Authors

CFChristy FinkeMPMrinal M. Patnaik

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Overview

Observational analysis reveals increased DLK1 expression in chronic myelomonocytic leukemia associated with ASXL1 mutations, suggesting disrupted DNA methylation controls.

Key Points

  • DLK1 overexpression correlates with ASXL1 mutations in chronic myelomonocytic leukemia, disrupting normal imprinting.
  • RNA-seq analysis shows a log2 fold change of +4.85 in DLK1 expression among ASXL1 mutant cases.
  • ChIP-seq analysis indicates altered chromatin states at DLK1 regulatory regions in ASXL1 mutant chronic myelomonocytic leukemia.
  • Loss of methylation at the DLK1-DMR suggests epigenetic silencing is compromised, contributing to leukemia stemness gene expression.

Cite This Study

Finke et al. (2025) studied this question.

synapsesocial.com/papers/69362f4b4fa91c937236d778https://doi.org/10.1182/blood-2025-1457
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Also Consider

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

  1. 1Clone-specific epigenetic regulatory mechanisms in ASXL1-mutant chronic myelomonocytic leukemia2025
  2. 2DNA methylation instability as a biomarker to predict resistance or progression to advanced disease Phase following tyrosine kinase inhibitor therapy in chronic myeloid leukemia2025
  3. 3Prognostic impact of ASXL1 somatic mutation on patients with chronic myeloid leukemia: A systemic review and meta-analysis.2026
  4. 4SMARCC1 loss impairs differentiation and enhances self-renewal in ASXL1-mutant hematopoietic cells2025
  5. 5Unravelling the epigenetic drivers of chip – MDS/CMML – AML progression through novel methylation-sensitive regulatory elements2025