DNTTIP1 drives leukaemogenesis through MiDAC‐mediated epigenetic silencing of BMF

Key Points

Leukaemogenesis is driven by DNTTIP1 through MiDAC-mediated epigenetic silencing of BMF, leading to cell death inhibition.
DNTTIP1 is notably overexpressed in acute leukaemia patients, correlating with a poorer prognosis.
Pharmacological disruption of the DNTTIP1-HDAC1/2-BMF axis effectively impairs leukaemogenesis, providing potential treatment avenues.
Epigenetic alterations in this pathway highlight significant therapeutic targets for future studies in acute leukaemia.

Abstract

DNTTIP1 is overexpressed in acute leukaemia and associated with poor prognosis. DNTTIP1 acts as a scaffold for the MiDAC complex, recruiting HDAC1/2 to silence BMF and inhibit leukaemic cell death. Pharmacological disruption of the DNTTIP1-HDAC1/2-BMF axis impairs leukaemogenesis.

DNTTIP1 drives leukaemogenesis through MiDAC‐mediated epigenetic silencing of BMF

Key Points

Abstract

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