STI571 inactivation of the gastrointestinal stromal tumor c-KIT oncoprotein: biological and clinical implications
By D. Tuveson, Nicholas A. Willis, T. Jacks, J. Griffin, S. Singer, C. Fletcher, J. Fletcher, G. Demetri. Oncogene, 2001
704 citations recorded by the source corpus.
Subfields: Gastroenterology, Neurology, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/889f0c4da285a08090856b85a44d10151866d996
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Citations in the corpus
- Evolution of Cancer Pharmacological Treatments at the Turn of the Third Millennium (2018, background): “Several clinical trials have demonstrated the efficacy and safety of Imatinib in patients affected by CML, ALL, and GIST.”
- Molecular correlates of imatinib resistance in gastrointestinal stromal tumors. (2006, background): “This concentration is 10-fold greater than that necessary to block exon 11 mutant isoforms of KIT in GIST cells.(8,21,31) Activation of AKT was partially but not completely inhibited by imatinib doses of 0.”
- Kinase mutations and imatinib response in patients with metastatic gastrointestinal stromal tumor. (2003, background): “In preclinical studies, imatinib was active against mutant isoforms of KIT commonly found in GIST.(13,16) Subsequent treatment of a patient with metastatic GIST resulted in marked clinical, radiologic, and pathologic improvement.”
- KIT activation is a ubiquitous feature of gastrointestinal stromal tumors. (2001, background): “The KIT/ABL/PDGFR kinase inhibitor, STI571 (Gleevec), is one such therapeutic option, and we have determined that STI571 inhibits oncogenic KIT activation and GIST cell proliferation in vitro and in vivo (32, 33).”
- Efficacy and safety of imatinib mesylate in advanced gastrointestinal stromal tumors. (2002, background): “In both preclinical experiments 13 and a previous case study, 14 inhibition by imatinib had considerable antiproliferative and proapoptotic effects on gastrointestinal stromal tumor cells.”