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Paper Details

FLT3 D835 mutations confer differential resistance to type II FLT3 inhibitors.
Leukemia
139
2015
-, Asp-, Asp-Phe-Gly, D835, D835 mutations, D835E, D835Y, FLT3, FLT3 D835, FLT3 tyrosine kinase, ITD, PLX3397, acute myeloid leukemia, crenolanib, internal tandem, patients, ponatinib, quizartinib, sorafenib, tyrosine, tyrosine kinase domain
Drug Resistance, Neoplasm, Humans, Molecular Docking Simulation, Mutation, Protein Conformation, Protein Kinase Inhibitors, fms-Like Tyrosine Kinase 3
Author NameAffiliation
Catherine C SmithUniversity of California san francisco
Catherine C SmithHelen Diller Family Comprehensive Cancer Center, University of California san francisco
Kimberly C LinUniversity of California san francisco
Adrian SteculaUniversity of California san francisco
Andrej Sali (CM4AI)University of California san francisco
Andrej Sali (CM4AI)Department of Pharmaceutical Chemistry, University of California san francisco
Andrej Sali (CM4AI)California Institute for Quantitative Biosciences, University of California san francisco
Andrej Sali (CM4AI)University of California san francisco
Andrej Sali (CM4AI)California Institute for Quantitative Biosciences, University of California san francisco
Andrej Sali (CM4AI)Department of Pharmaceutical Chemistry, University of California san francisco
Neil P ShahUniversity of California san francisco
Neil P ShahHelen Diller Family Comprehensive Cancer Center, University of California san francisco
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