@article{IR,
      author = {Sharzehi, Setareh and Joshi, Sunil and Pittsenbarger,  Janet and Bottomly, Daniel and McWeeney, Shannon and Tyner,  Jeffrey W. and Traer, Elie},
      url = {http://digitalcollections.ohsu.edu/record/9581},
      title = {The FLT3 F691L gatekeeper mutation promotes clinical  resistance to Gilteritinib + Venetoclax in AML},
      publisher = {Oregon Health and Science University},
      abstract = {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.},
      number = {IR},
      doi = {https://doi.org/10.6083/8049g5745},
      recid = {9581},
      address = {2022},
}