MLL fusion protein–driven AML is selectively inhibited by targeted disruption of the MLL-PAFc interaction
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Key Points The PAFc subunit, Cdc73, is required for the proliferation and proper epigenetic regulation of proleukemic oncogenes in AML cells. Disrupting the MLL-PAFc interaction selectively inhibits the growth of MLL-associated leukemic cells without altering normal hematopoietic stem cell function.
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2017 ◽
Vol 1
(26)
◽
pp. 2520-2528
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