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• W3025728513 abstract "FLT3-ITD mutations occur in 20-30% of AML patients and are associated with aggressive disease. Patients with relapsed FLT3-mutated disease respond well to 2nd generation FLT3 TKIs but inevitably relapse within a short timeframe. In this setting, until overt relapse occurs, the bone marrow microenvironment facilitates leukemia cell survival despite continued on-target inhibition. We demonstrate that human bone marrow derived conditioned medium (CM) protects FLT3-ITD+ AML cells from the 2nd generation FLT3 TKI quizartinib and activates STAT3 and STAT5 in leukemia cells. Extrinsic activation of STAT5 by CM is the primary mediator of leukemia cell resistance to FLT3 inhibition. Combination treatment with quizartinib and dasatinib abolishes STAT5 activation and significantly reduces the IC50 of quizartinib in FLT3-ITD+ AML cells cultured in CM. We demonstrate that CM protects FLT3-ITD+ AML cells from the inhibitory effects of quizartinib on glycolysis and that this is partially reversed by treating cells with the combination of quizartinib and dasatinib. Using a doxycycline-inducible STAT5 knockdown in the FLT3-ITD+ MOLM-13 cell line, we show that dasatinib-mediated suppression of leukemia cell glycolytic activity is STAT5-independent and provide a preclinical rationale for combination treatment with quizartinib and dasatinib in FLT3-ITD+ AML." @default.
• W3025728513 created "2020-05-21" @default.
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• W3025728513 date "2020-05-14" @default.
• W3025728513 modified "2023-10-17" @default.
• W3025728513 title "Dasatinib overcomes stroma-based resistance to the FLT3 inhibitor quizartinib using multiple mechanisms" @default.
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• W3025728513 doi "https://doi.org/10.1038/s41375-020-0858-1" @default.
• W3025728513 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7606260" @default.
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• W3025728513 hasPublicationYear "2020" @default.
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