Acute Myeloid Leukemia (AML) is an aggressive cancer with poor overall survival due to frequent relapse. FMS-like tyrosine kinase (FLT3) is the most commonly mutated genes in AML, and leads to higher relapse rates. Several FLT3 inhibitors have been developed, including gilteritinib. Our lab developed a two-step model of early and late resistance to study the mechanism of resistance and relapse to FLT3 inhibitors. Early resistant AML cells are dependent upon the marrow microenvironment for survival. Over time, intrinsic resistance allows independent growth and results in late resistance, leading to disease relapse.
Details
Title
The FLT3 F691L gatekeeper mutation promotes clinical resistance to Gilteritinib + Venetoclax in AML
Creator
Sharzehi, Setareh : Oregon Health and Science University Joshi, Sunil : Oregon Health and Science University Pittsenbarger, Janet : Oregon Health and Science University Bottomly, Daniel : Oregon Health and Science University McWeeney, Shannon : Oregon Health and Science University Tyner, Jeffrey W. : Oregon Health and Science University Traer, Elie : Oregon Health and Science University
Meeting Name
Research Week, Oregon Health and Science University, 2022