Hematopoietic niche drives FLT3-ITD acute myeloid leukemia resistance to quizartinib via STAT5-and hypoxia-dependent upregulation of AXL
Internal tandem duplication in Fms-like tyrosine kinase 3 (FLT3-ITD) is the most frequent mutation observed in acute myeloid leukemia (AML) and correlates with poor prognosis.FLT3 tyrosine kinase inhibitors are promising for targeted therapy.Here, we investigated mechanisms dampening the response to the FLT3 inhibitor quizartinib, which is specific