Study uncovers molecular "switch" behind chemoresistance in blood cancer
The study identifies a DNA‑methylation–driven upregulation of the RUNX1C isoform that induces quiescence in acute myeloid leukemia (AML), conferring chemoresistance; targeting RUNX1C with antisense oligonucleotides restores chemotherapy sensitivity in preclinical models.
The research describes how DNA methylation at the RUNX1 locus drives expression of the RUNX1C isoform, which activates BTG2 expression and forces AML cells into a dormant state that evades chemotherapy. In vitro and mouse studies using antisense oligonucleotides to inhibit RUNX1C reversed quiescence, enhanced chemotherapeutic killing and reduced relapse in AML models.
Elucidating RUNX1C‑mediated chemoresistance provides a target to eliminate dormant leukemia cells, potentially lowering relapse rates and improving long‑term survival for AML patients.
Bizonyítékszint: Állatkísérletes. Állatmodellben vizsgálták.
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