KIT activation is a ubiquitous feature of gastrointestinal stromal tumors.

By B. Rubin, S. Singer, Connie W. Tsao, A. Duensing, Marcia L. Lux, Robert Ruiz, M. Hibbard, Chang-jie Chen, S. Xiao, D. Tuveson and 3 more. Cancer Research, 2001

1,009 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/610e7caa3f6c89dcc8749c1e717dadc218ccc7c2

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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”
• Gastrointestinal stromal tumours: origin and molecular oncology (2011, background): “First, phosphorylated KIT is almost always detectable in GIST tumour extract”
• Gastrointestinal stromal tumors: The incidence, prevalence, clinical course, and prognostication in the preimatinib mesylate era (2005, unknown): “Clinical-symptomatic 199 (69) 106/93 67 (10–92) Gastric (120), duodenum (12), jejunum-ileum (50), colon (6), rectum (10), mesenterium (1) 8.”
• Kinase mutations and imatinib response in patients with metastatic gastrointestinal stromal tumor. (2003, background): “PDGFRA proteins that likely contribute to tumor proliferation or survival.(35,36) In the present study, GISTs lacking a detectable”
• 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)”
• Clinical Pharmacokinetics of Imatinib (2005, background): “[2,10-16] Approximately 35% of GISTs activates a number of signalling pathways (e.”
• The novel marker, DOG1, is expressed ubiquitously in gastrointestinal stromal tumors irrespective of KIT or PDGFRA mutation status. (2004, background): “In the vast majority of GISTs, high levels of KIT expression are accompanied by a KIT gene mutation in exons 9, 11, 13, or 17.(11,12) Recently, a subset of GISTs have been found to have PDGFRA mutations rather than KIT mutations.”