Article
Imatinib resistance and microcytic erythrocytosis in a KitV558Δ;T669I/+ gatekeeper-mutant mouse model of gastrointestinal stromal tumor.
Proceedings of the National Academy of Sciences of the United States of America - 21 Aug 2012
Bosbach Benedikt, Deshpande Shayu, Rossi Ferdinand, Shieh Jae-Hung, Sommer Gunhild, de Stanchina Elisa, Veach Darren R, Scandura Joseph M, Manova-Todorova Katia, Moore Malcolm A S, Antonescu Cristina R, Besmer Peter
Abstract excerpt
Most gastrointestinal stromal tumors (GISTs) harbor a gain-of-function mutation in the Kit receptor. GIST patients treated with the tyrosine kinase inhibitor imatinib frequently develop imatinib resistance as a result of second-site Kit mutations. To investigate the consequences of second-site Kit mutations on GIST development and imatinib sensitivity, we engineered a mouse model carrying in the endogenous Kit...
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