KIT extracellular and kinase domain mutations in gastrointestinal stromal tumors.

By Marcia L. Lux, B. Rubin, Tara L. Biase, Chang-jie Chen, Timothy Maclure, G. Demetri, S. Xiao, Samuel Singer, C. D. Fletcher, Jonathan A. Fletcher. American Journal of Pathology, 2000

650 citations recorded by the source corpus.

Subfields: Gastroenterology, Immunology, Surgery

View Paper: https://www.semanticscholar.org/paper/b4e17a93e8732bc93f8f27b333f5dce6b5e0be19

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Citations in the corpus

Glivec (STI571, imatinib), a rationally developed, targeted anticancer drug (2002, background): “Oncogenic c-KIT mutations in GISTs have been localized to the extracellular domain, kinase domains 1 and 2 and predominantly in the juxtamembrane domain of the c-KIT protei”
Kinase mutations and imatinib response in patients with metastatic gastrointestinal stromal tumor. (2003, methodology): “The cells were then collected, and protein lysates were prepared and analyzed for KIT or PDGFRA activation as previously described.(4,11) Experiments involving recombinant DNA were performed using BL2 procedures in accordance with National Institutes of Health Guidelines for Research Involving Recom”
Gastrointestinal stromal tumours: origin and molecular oncology (2011, background): “Aside from exon 11 mutations, between 7% and 10% of GISTs have a mutation in an extracellular domain that is encoded by exon 9 (Ref”
Regorafenib (BAY 73‐4506): A new oral multikinase inhibitor of angiogenic, stromal and oncogenic receptor tyrosine kinases with potent preclinical antitumor activity (2011, result): “Constitutive kinase activation of these receptor kinases is reported to lead to tumorigenicity of the GIST cell line GIST 882 and thyroid cell line TT, respectively.(24,25) In general, the level of inhibition observed in the cellular assay closely correlated with that observed in the biochemical ass”
STI571 inactivation of the gastrointestinal stromal tumor c-KIT oncoprotein: biological and clinical implications (2001, background): “The mechanisms of GIST c-KIT activation appear to be varied, as suggested by the ®nding of oncogenic mutations in the extracellular, juxtamembrane, and kinase domains (Lux et al., 2000; Lasota et al., 2000).”
Gastrointestinal stromal tumors – definition, clinical, histological, immunohistochemical, and molecular genetic features and differential diagnosis (2000, background): “Recently, Lux et al. [ 33 ] sequenced KIT transcripts from GISTs and found mutations in the extracellular do-”
KIT activation is a ubiquitous feature of gastrointestinal stromal tumors. (2001, methodology): “The exon 9 and 13 mutations, which have been reported previously (25), resulted in alanine-tyrosine duplication and lysine to glutamate substitution, respectively.”
Gastrointestinal Stromal Tumors, Intramural Leiomyomas, and Leiomyosarcomas in the Duodenum: A Clinicopathologic, Immunohistochemical, and Molecular Genetic Study of 167 Cases (2001, background): “We did not find any mutations in exon 13 or exon 17, indicating that such mutations must be very rare, although each type has been occasionally reported.(12,20)”
Soft Tissue Sarcomas (2001, background): “Most of the mutations result from in-frame deletions or point mutations that lead to ligand-independent activation of the tyrosine kinase of c-Kit.(103,105,112) The resulting constitutive c-Kit tyrosine kinase activity has been shown to promote tumor growth in vitro, and thus, it may be the key even”
Clinical Pharmacokinetics of Imatinib (2005, background): “[2,10-16] Approximately 35% of GISTs activates a number of signalling pathways (e.”
Gastrointestinal Stromal Tumors of the Stomach: A Clinicopathologic, Immunohistochemical, and Molecular Genetic Study of 1765 Cases With Long-term Follow-up (2005, neutral): “All cases 355 (33) 179 (17) 20 407 (27) 21 51 (3)”