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Updated: Dec 18, 2025

Identification of Key Factors Regulating Self-renewal and Differentiation in EML Hematopoietic Precursor Cells by RNA-sequencing Analysis
Published on: November 11, 2014
Chromatin Complexes Maintain Self-Renewal of Myeloid Progenitors in AML: Opportunities for Therapeutic Intervention
Hannah J Uckelmann1, Scott A Armstrong1
1Department of Pediatric Oncology, Dana-Farber Cancer Institute, Division of Hematology/Oncology, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.
Abstract:
Specific subgroups of acute myeloid leukemia (AML), including those containing MLL rearrangements and NPM1c mutations, possess characteristic stem cell-like gene expression profiles. These expression programs are highly dependent on components of the MLL histone methyltransferase complex, including Menin and DOT1L. Understanding the chromatin-based mechanisms through which cancer cells subvert certain aspects of normal stem cell biology helped identify specific vulnerabilities and translate them into targeted therapy approaches. Exciting progress has been made in the development of small-molecule inhibitors targeting this epigenetic machinery in leukemia cells and prompted the development of clinical trials in patients with hematologic malignancies.
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