Raising H3K9 methylation curbs leukemic stem cell proliferation
Targeting this epigenetic modification in mouse models and patient samples reduces leukemogenesis in young and aged cells.
Researchers analyzed murine hematopoietic stem and progenitor cells, mouse leukemia models, human leukemic cell lines, and patient samples to study histone changes during leukemogenesis. They focused on the methylation of histone 3 at lysine 9, known as H3K9 methylation, which shifts during normal stem cell aging. The team discovered that these age-associated alterations in H3K9 methylation link directly to a pre-malignant phenotype. In addition, leukemic cells rely on low levels of H3K9 methylation to sustain their proliferation in vitro. Artificially increasing H3K9 methylation reduced leukemogenesis in both young and aged murine leukemic cells, as well as in patient-derived cells.
Why it matters
Epigenetic changes accumulate in blood stem cells over time and drive age-related hematological malignancies like acute myeloid leukemia. Understanding how specific histone modifications alter stem cell behavior could reveal selective therapies for aging-associated cancers.
Caveats
The study relies heavily on laboratory cell cultures and mouse models alongside patient samples, and the abstract does not report specific sample sizes or in vivo human outcomes.
- Epigenetic alterations
- Stem cell exhaustion
- Histone modification and chromatin remodelling
- Acute myeloid leukemia
- H3K9 methylation
- Homo sapiens
- Mus musculus
The paper
Increasing H3K9 Methylation Level Reduces the Proliferation of Leukemic Stem Cells
Walter B, Zjablovskaja P, Montserrat-Vazquez S et al.
Cancers · 14 Sep 2026