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Recurrent mutations, including NPM1c, activate a BRD4-dependent core transcriptional program in acute myeloid

M A Dawson1, E J Gudgin2, S J Horton3

  • 11] Department of Haematology, Cambridge Institute for Medical Research and Addenbrookes Hospital, University of Cambridge, Cambridge, UK [2] Wellcome Trust-Medical Research Council Cambridge Stem Cell Institute, Cambridge, UK [3] Gurdon Institute and Department of Pathology, University of Cambridge, Cambridge UK.

Leukemia
|November 14, 2013
PubMed
Summary

Bromodomain and extra-terminal (BET) inhibitors show promise for treating acute myeloid leukemia (AML). Targeting a core transcriptional program, particularly in NPM1-mutated AML, offers a potential therapeutic strategy.

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