MCL1 Promotes Fatty Acid β-Oxidation in Therapy-Resistant AML through Cytoplasmic Sequestration of the Transcriptional Repressor IRF2BP2

Despite extensive efforts aimed toward the development of improved molecular therapies targeting acute myeloid leukemia (AML), clinical outcomes remain poor. Notably, targeting BCL2 with venetoclax (Ven) in combination with azacitidine (Aza) has clinically delivered significant responses in newly di...

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Bibliographic Details
Published in:Blood 2024-11, Vol.144, p.39-39
Main Authors: Althoff, Mark J, Minhajuddin, Mohd, Stevens, Brett M, Gillen, Austin E, Miller, Regan, Vujovic, Ana, Patel, Sweta B, Showers, William, Gipson, Stephanie, Dzieciatkowska, Monika, Ellegast, Jana M, Wright, Tristen, Stegmaier, Kimberly, Opferman, Joseph T, Jordan, Craig T
Format: Article
Language:English
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Summary:Despite extensive efforts aimed toward the development of improved molecular therapies targeting acute myeloid leukemia (AML), clinical outcomes remain poor. Notably, targeting BCL2 with venetoclax (Ven) in combination with azacitidine (Aza) has clinically delivered significant responses in newly diagnosed AML patients. Still, both upfront refractory and relapsed diseases are a major obstacle. Of particular importance, a unique subset of Ven/Aza-resistant AML are preferentially reliant on expression of the BCL2 family member MCL1 (5-fold increase in transcript, p
ISSN:0006-4971
DOI:10.1182/blood-2024-206516