Primary and secondary kinase genotypes correlate with the biological and clinical activity of sunitinib in imatinib-resistant gastrointestinal stromal tumor.
By M. Heinrich, R. Maki, Christopher Corless, C. Antonescu, Amy Harlow, D. Griffith, Ajia Town, A. McKinley, W. Ou, J. Fletcher and 5 more. Journal of Clinical Oncology, 2008
728 citations recorded by the source corpus.
Subfields: Gastroenterology, Pulmonary and Respiratory Medicine, Rheumatology
View Paper: https://www.semanticscholar.org/paper/552145a3294dc06baebd573b6872fa4d441ad467
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Citations in the corpus
- Gastrointestinal stromal tumours: origin and molecular oncology (2011, background): “Despite the poor clinical prognosis of exon 11-mutant KIT GISTs in the absence of imatinib treatment, this mutant is highly sensitive to imatinib in vitro , with a half-maximal inhibitory concentration (IC 50 ) of 50 of ∼1,000 nM for each”