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Kinase Mutations and Imatinib Response in Patients With Metastatic Gastrointestinal Stromal Tumor
Journal of Clinical Oncology · 2003 · Vol. 21(23) · pp. 4342–4349
Michael C. Heinrich✉(Oregon Health & Science University)Christopher L. Corless(Oregon Health & Science University)George D. Demetri(Oregon Health & Science University)Charles D. Blanke(Oregon Health & Science University)Margaret von Mehren(Oregon Health & Science University)Heikki Joensuu(Oregon Health & Science University)Laura McGreevey(Oregon Health & Science University)Chang-Jie Chen(Oregon Health & Science University)Annick D. Van den Abbeele(Oregon Health & Science University)Brian Druker(Oregon Health & Science University)Beate Kiese(Oregon Health & Science University)Burton Eisenberg(Oregon Health & Science University)Peter Roberts(Oregon Health & Science University)Samuel Singer(Oregon Health & Science University)Christopher D.�M. Fletcher(Oregon Health & Science University)Sandra Silberman(Oregon Health & Science University)Saša Dimitrijević(Oregon Health & Science University)Jonathan A. Fletcher(Oregon Health & Science University)
Abstract
Activating mutations of KIT or PDGFRA are found in the vast majority of GISTs, and the mutational status of these oncoproteins is predictive of clinical response to imatinib. PDGFRA mutations can explain response and sensitivity to imatinib in some GISTs lacking KIT mutations.
Gastrointestinal Tumor Research and TreatmentSarcoma Diagnosis and TreatmentSoft tissue tumor case studiesPDGFRAImatinibExonImatinib mesylateCancer researchGiSTMutationMedicinePoint mutationStromal tumor
MeSH terms
Imatinib MesylateAnimalsAntineoplastic AgentsBenzamidesDNA Mutational AnalysisDNA, NeoplasmExonsGastrointestinal NeoplasmsCricetinaeHumansImmunoenzyme TechniquesMutationPhosphorylationPiperazinesPrognosis
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