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BMC Cancer

Publication date: 2016-01-01
Volume: 16 Pages: 22 -
Publisher: BioMed Central

Author:

Reichardt, Peter
Demetri, George D ; Gelderblom, Hans ; Rutkowski, Piotr ; Im, Seock-Ah ; Gupta, Sudeep ; Kang, Yoon-Koo ; Schöffski, Patrick ; Schuette, Jochen ; Soulières, Denis ; Blay, Jean-Yves ; Goldstein, David ; Fly, Kolette ; Huang, Xin ; Corsaro, Massimo ; Lechuga, Maria Jose ; Martini, Jean-Francois ; Heinrich, Michael C

Keywords:

Science & Technology, Life Sciences & Biomedicine, Oncology, Sunitinib, Imatinib, GIST, KIT, KIT mutation, Imatinib-resistant GIST, Overall survival, Progression-free survival, TYROSINE KINASE INHIBITOR, IMATINIB RESISTANCE, ACQUIRED-RESISTANCE, GROWTH-FACTOR, ACTIVATION, SU11248, EFFICACY, MECHANISMS, GENOTYPE, MESYLATE, Adolescent, Adult, Aged, Aged, 80 and over, Disease-Free Survival, Drug Resistance, Neoplasm, Female, Gastrointestinal Stromal Tumors, Genotype, Humans, Indoles, Male, Middle Aged, Mutation, Prognosis, Protein Kinase Inhibitors, Proto-Oncogene Proteins c-kit, Pyrroles, Receptor, Platelet-Derived Growth Factor alpha, 1112 Oncology and Carcinogenesis, 1117 Public Health and Health Services, Oncology & Carcinogenesis, 3211 Oncology and carcinogenesis, 4202 Epidemiology

Abstract:

Several small studies indicated that the genotype of KIT or platelet-derived growth factor receptor-α (PDGFRA) contributes in part to the level of clinical effectiveness of sunitinib in gastrointestinal stromal tumor (GIST) patients. This study aimed to correlate KIT and PDGFRA mutational status with clinical outcome metrics (progression-free survival [PFS], overall survival [OS], objective response rate [ORR]) in a larger international patient population.