title: CCR 20th Anniversary Commentary: A Genetic Mechanism of Imatinib Resistance in Gastrointestinal Stromal Tumor-Where Are We a Decade Later?
abstract: In the June 1, 2005, issue of Clinical Cancer Research, Antonescu and colleagues defined second-site KIT mutations in gastrointestinal stromal tumor (GIST) as the leading mechanism of acquired resistance to imatinib. Secondary mutations were detectable mainly in KIT exon 11 mutant GISTs after prolonged initial clinical responses. These findings played a critical role in designing the next generation of tyrosine kinase inhibitors.
authors.affiliation: Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York, New York. antonesc@mskcc.org.
authors.forename: Cristina R
authors.initials: CR
authors.lastname: Antonescu
authors.affiliation: Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, New York.
authors.forename: Ronald P
authors.initials: RP
authors.lastname: DeMatteo
mesh_terms: D019008:Drug Resistance, Neoplasm / Q000235:genetics*; D005260:Female; D046152:Gastrointestinal Stromal Tumors / Q000188:drug therapy*; D006801:Humans; D008297:Male; D009154:Mutation; D010879:Piperazines / Q000627:therapeutic use*; D011743:Pyrimidines / Q000627:therapeutic use*
chemical_list: D010879:Piperazines; D011743:Pyrimidines