Drug combination shows potential in aggressive leukemia
Purpose: Acute myeloid leukemia is an aggressive disease with a poor outcome. We investigated mechanisms by which the anti-AML activity of ABT-199 could be potentiated by dual mTORC1/TORC2 inhibition. Methods: Venetoclax/INK128 synergism was assessed in various AML cell lines and primary patient AML samples in vitro.
Synergism was associated with p-AKT and p-4EBP1 down-regulation and dependent upon MCL-1 downregulation and BAK/BAX up-regulation as MCL-1 overexpression and BAX/BAK knock out abrogated cell death. Constitutive AKT activation opposed synergism between venetoclax and PI3K or AKT inhibitors, but not INK128. Combination treatment also synergistically induced cell death in venetoclax- resistant AML cells. Similar events occurred in primary patient-derived leukemia samples but not normal CD34+ cells.
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