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Studies presented here demonstrate that as compared with AML cells lacking mtRUNX1, their isogenic counterparts harboring mtRUNX1 display impaired ribosomal biogenesis and differentiation, as well as exhibit reduced levels of wild-type RUNX1, PU.1, and c-Myc. Compared with AML cells with only wild-type RUNX1, AML cells expressing mtRUNX1 were also more sensitive to the protein translation inhibitor homoharringtonine (omacetaxine) and BCL2 inhibitor venetoclax. Homoharringtonine treatment repressed enhancers and their BRD4 occupancy and was associated with reduced levels of c-Myc, c-Myb, MCL1, and Bcl-xL. Consistent with this, cotreatment with omacetaxine and venetoclax or BET inhibitor induced synergistic in\u00a0vitro lethality in AML expressing mtRUNX1. Compared with each agent alone, cotreatment with omacetaxine and venetoclax or BET inhibitor also displayed improved in\u00a0vivo anti-AML efficacy, associated with improved survival of immune-depleted mice engrafted with AML cells harboring mtRUNX1. These findings highlight superior efficacy of omacetaxine-based combination therapies for AML harboring mtRUNX1.<\/jats:p>","DOI":"10.1182\/blood.2021013156","type":"journal-article","created":{"date-parts":[[2021,10,3]],"date-time":"2021-10-03T15:10:30Z","timestamp":1633273830000},"page":"907-921","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":84,"title":["Effective therapy for AML with RUNX1 mutation by cotreatment with inhibitors of protein translation and BCL2"],"prefix":"10.1182","volume":"139","author":[{"given":"Christopher P.","family":"Mill","sequence":"first","affiliation":[{"name":"Department of Leukemia,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Warren","family":"Fiskus","sequence":"additional","affiliation":[{"name":"Department of Leukemia,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9003-0390","authenticated-orcid":false,"given":"Courtney 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