Kinase mutations and imatinib response in patients with metastatic gastrointestinal stromal tumor.

By M. Heinrich, Christopher Corless, G. Demetri, C. Blanke, M. von Mehren, Heikki Joensuu, Laura S. McGreevey, Chang-jie Chen, A. D. Van den Abbeele, Brian J. Druker and 8 more. Journal of Clinical Oncology, 2003

2,287 citations recorded by the source corpus.

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

Clinical Pharmacokinetics of Imatinib (2005, neutral): “[28]”
One vs three years of adjuvant imatinib for operable gastrointestinal stromal tumor: a randomized trial. (2012, background): “Primary tumor diameter, median (range), cm 9 (2-35) 10 (2-40)”
Systems Pharmacology: Network Analysis to Identify Multiscale Mechanisms of Drug Action (2012, background): “KIT oncogene mutations reduce the responsiveness of gastrointestinal stromal tumors to imatinib (40); k-RAS oncogene mutations in colorectal cancer reduce responsiveness to cetuximab (33); and epidermal growth factor receptor mutations in non-small-cell lung cancer alter responsiveness to gefitinib…”
Phase III randomized, intergroup trial assessing imatinib mesylate at two dose levels in patients with unresectable or metastatic gastrointestinal stromal tumors expressing the kit receptor tyrosine kinase: S0033. (2008, background): “Many untreated GISTs express a single mutated oncogenic kinase, usually KIT (85% to 88% of cases), while a smaller percentage of patients possess oncogenic mutations in the platelet-derived growth factor receptor gene (PDGFR ; 5% to 7%) or have no detectable kinase mutations (10%).(4,5) Imatinib mes”