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1 May 2022
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ZNF384-fusion oncoproteins collectively mark a transcriptionally homogeneous subset of leukemia with B-lymphoid and myeloid features. On page 240, Dickerson et al. utilize mouse and human models of acute leukemias with diverse ZNF384 fusions. The fusions drive hematopoietic lineage skewing and transformation, accompanied by FLT3 expression, and sensitivity to FLT3-inhibition. The fusion oncoproteins exhibit differential chromatin binding and recruitment of the mediator complex compared to wild-type ZNF384, associated with deregulated expression of hematopoietic lineage transcription factors, which is further influenced by differential ZNF384 exon usage and splicing observed in human leukemia. These findings highlight a central role for the orchestration of chromatin state by fusion oncoproteins in dysregulation of hematopoietic lineage differentiation, and facilitating oncogenic transformation of hematopoietic stem and progenitor cells. - PDF Icon PDF LinkTable of Contents
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ISSN 2643-3230
EISSN 2643-3249
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