Article
KIT kinase mutants show unique mechanisms of drug resistance to imatinib and sunitinib in gastrointestinal stromal tumor patients.
Proceedings of the National Academy of Sciences of the United States of America - 3 Feb 2009
Gajiwala Ketan S, Wu Joe C, Christensen James, Deshmukh Gayatri D, Diehl Wade, DiNitto Jonathan P, English Jessie M, Greig Michael J, He You-Ai, Jacques Suzanne L, Lunney Elizabeth A, McTigue Michele, Molina David, Quenzer Terri, Wells Peter A, Yu Xiu, Zhang Yan, Zou Aihua, Emmett Mark R, Marshall Alan G, Zhang Hui-Min, Demetri George D
Abstract excerpt
Most gastrointestinal stromal tumors (GISTs) exhibit aberrant activation of the receptor tyrosine kinase (RTK) KIT. The efficacy of the inhibitors imatinib mesylate and sunitinib malate in GIST patients has been linked to their inhibition of these mutant KIT proteins. However, patients on imatinib can acquire secondary KIT mutations that render the protein insensitive to the inhibitor. Sunitinib has shown...
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