Fusion gene depletion eliminates stemness and induces bidirectional differentiation of acute myeloid leukemia.

ABSTRACT:

Abstract

Chromosomal rearrangements that generate novel fusion genes are a hallmark of acute myeloid leukemia (AML). Depletion experiments in cell line models have suggested that their continued expression is required for maintaining their leukemic phenotype and that fusion genes therefore represent ideal cancer-specific therapeutic targets. However, the extent to which this result holds true for the different stages of hematopoietic development in primary cells and whether therapeutic agents can be efficiently delivered to those cells is still unclear. In this study, we demonstrate that primary AML cells harboring the chromosomal translocation t(8;21) are critically dependent on the corresponding fusion gene, RUNX1::RUNX1T1, to suppress differentiation and maintain stemness. Silen

SUBMITTER: Derevyanko PK 

PROVIDER: S-EPMC12824707 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature