Article
Characterizing and Overriding the Structural Mechanism of the Quizartinib-Resistant FLT3 "Gatekeeper" F691L Mutation with PLX3397.
Cancer discovery - 1 Jun 2015
Smith Catherine C, Zhang Chao, Lin Kimberly C, Lasater Elisabeth A, Zhang Ying, Massi Evan, Damon Lauren E, Pendleton Matthew, Bashir Ali, Sebra Robert, Perl Alexander, Kasarskis Andrew, Shellooe Rafe, Tsang Garson, Carias Heidi, Powell Ben, Burton Elizabeth A, Matusow Bernice, Zhang Jiazhong, Spevak Wayne, Ibrahim Prabha N, Le Mai H, Hsu Henry H, Habets Gaston, West Brian L, Bollag Gideon, Shah Neil P
Abstract excerpt
UNLABELLED: Tyrosine kinase domain mutations are a common cause of acquired clinical resistance to tyrosine kinase inhibitors (TKI) used to treat cancer, including the FLT3 inhibitor quizartinib. Mutation of kinase "gatekeeper" residues, which control access to an allosteric pocket adjacent to the ATP-binding site, has been frequently implicated in TKI resistance. The molecular underpinnings of gatekeeper...
Read the complete abstract on PubMedTopics
Share this publication in a Topic to start or enrich a Post.