FLT3 mutations, generally associated with a poor prognosis, are found in approximately one-third of patients with acute myeloid leukemia (AML) and represent an attractive therapeutic target. FLT3 inhibitors undergoing clinical evaluation include first-generation relatively non-specific small molecules and second-generation compounds with higher potency and selectivity against mutant FLT3. Recently presented results from a prospective randomized clinical trial will likely lead to a change in the standard of care for younger patients with FLT3-mutated AML: addition of the multi-targeted FLT3 inhibitor midostaurin to standard induction and consolidation chemotherapy. Thus, personalized therapies for this subset of AML will soon be possible.
Key points
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Patients with FMS-like tyrosine kinase 3 gene ( FLT3 )–in-frame internal tandem duplication (ITD)–positive mutant acute myeloid leukemia (AML) generally have a poor prognosis.
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Midostaurin, a multitargeted kinase inhibitor, may soon be routinely added to chemotherapy in newly diagnosed mutant FLT3.
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Newer, more-specific FLT3 inhibitors, including some that target both FLT3 -ITD and FLT3 –tyrosine kinase domain (TKD), are being aggressively evaluated.
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