Efficacy and safety of imatinib mesylate in advanced gastrointestinal stromal tumors.
By G. Demetri, M. von Mehren, C. Blanke, A. D. Van den Abbeele, B. Eisenberg, P. Roberts, M. Heinrich, D. Tuveson, S. Singer, M. Janicek and 11 more. New England Journal of Medicine, 2002
4,306 citations recorded by the source corpus.
Subfields: Gastroenterology, Hematology
View Paper: https://www.semanticscholar.org/paper/59dd3f5ff40a7a95ad10210c6b4a1de8707367ad
How researchers see this paper
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In Gastroenterology
- Heikki Joensuu
- Christopher Corless
- M. Heinrich
- J. Lasota
- M. Miettinen
- J. Fletcher
- Leslie Sobin
- C. Fletcher
In Hematology
- A. D’Andrea
- Benjamin L. Ebert
- Adi F. Gazdar
- M. Heinrich
- Levi A. Garraway
- P. Jänne
- H. Shigematsu
- Christopher Corless
Citations in the corpus
- The secret ally: immunostimulation by anticancer drugs (2012, background): “Of note, imatinib also efficiently inhibits tyrosine kinases other than BCR–ABL, including KIT and platelet-derived growth factor receptor (PDGFR); a pharmacological profile that led to the approval of imatinib by the US Food and Drug Administration (FDA) for the treatment of tumours with activating”
- Gastrointestinal stromal tumors: The incidence, prevalence, clinical course, and prognostication in the preimatinib mesylate era (2005, neutral): “Clinical-symptomatic 199 (69) 106/93 67 (10–92) Gastric (120), duodenum (12), jejunum-ileum (50), colon (6), rectum (10), mesenterium (1) 8.”
- Somatic mutations of the HER2 kinase domain in lung adenocarcinomas. (2005, background): “The inhibitors include imatinib mesylate (Gleevec, STI571), a small molecule inhibitor of the Abl and KIT tyrosine kinases (TK) for patients with chronic myelogenous leukemia or gastrointestinal stromal tumors (3, 4), and gefitinib (Iressa, ZD1839) and erlotinib (Tarceva, OSI-774) inhibitors of epid”
- Gastrointestinal stromal tumours: origin and molecular oncology (2011, background): “Overall, imatinib achieved disease control in 70–85% of patients with advanced KIT-positive GISTs, and the median progression-free survival was 20–24 month”
- Pre-existence and clonal selection of MET amplification in EGFR mutant NSCLC (2010, positive): “(Demetri et al., 2002; Druker et al., 2001; Inoue et al., 2006; 84 Cancer Cell 17, 77–88, January 19, 2010 ª2010 Elsevier Inc. Mok et al., 2009; Sequist et al., 2008).”