Mutations in the FMS-like tyrosine kinase 3 (FLT3) gene are seen in 30% of all acute myeloid leukemia (AML) cases, most commonly involving the internal tandem duplication region (FLT3-ITD) which constitutively activate its kinase activity and thus, allows for leukemia cell proliferation and survival. A particularly poor prognosis is conferred by mutant FLT3, increasing relapse risk, and decreasing overall survival. For this reason, FLT3 genetic testing is advised at diagnosis, and the development of FLT3 inhibitors represent a significant research area over the past decade. Integration of these inhibitors, such as midostaurin and gilteritinib, have helped to improve outcomes of patients with AML but challenges remain, especially treatment resistance.

In this podcast, Naval Daver, MD, The University of Texas MD Anderson Cancer Center, Houston, TX chairs an insightful discussion on FLT3 mutated AML as part of the AML sessions, together with Amir Fathi, MD, MPH, Massachusetts General Hospital, Boston, MA; Jessica Altman, MD, Northwestern University, Chicago, IL; and Eunice Wang, MD, Roswell Park Comprehensive Cancer Center, Buffalo, NY. They discuss novel treatment combinations for FLT3 mutated cancer, as well as treatment options for front-line and post-transplant maintenance settings, and mechanisms of resistance.

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