|Education||BS, University of Texas at Dallas|
About 30% of acute myeloid leukemia (AML) patients harbor a mutation in the protein tyrosine kinase FMS-like tyrosine kinase 3 (FLT3) that results in its constitutive activation. The most common mutation, internal tandem duplication, confers poor prognosis. FLT3 results in downstream activations of pathways such as JAK/STAT, PI3K/AKT, and MAPK, and its activity in leukemia cells provides a survival and proliferative advantage. Several FLT3 inhibitors are in development for the treatment of AML, but there have been limitations in patient response to these drugs and none have been FDA approved. My project seeks to better understand the mechanisms by which leukemia cells may resist FLT3 inhibitor treatment.