Mechanisms of FLT3 inhibitor resistance in AML: type I vs type II inhibitors
Catherine Smith, MD, University of California San Francisco, San Francisco, CA, presents on the mechanisms of FLT3 inhibitor resistance in acute myeloid leukemia (AML). Dr Smith explains that resistance is polyclonal and segregates by inhibitor type, with on-target kinase domain mutations more common with type II inhibitors such as quizartinib, and off-target RAS pathway mutations more common with type I inhibitors such as gilteritinib. She also explains that combination therapies can drive clonal selection against FLT3-mutated cells, and that monocytic differentiation may contribute to resistance, particularly with venetoclax-based combinations. This presentation took place at the 8th International Workshop on Acute Leukemias (iwAL) in Cambridge, MA.
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