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- B C Kuenen and H M Pinedo.
- VU Medisch Centrum, afd. Geneeskundige Oncologie, De Boelelaan 1117, 1081 HV Amsterdam. b.kuenen@vumc.nl
- Ned Tijdschr Geneeskd. 2003 Oct 18; 147 (42): 2044-5.
AbstractOne of the undoubted major breakthroughs in the recent treatment of cancer is imatinib, a tyrosine-kinase inhibitor of the bcr-abl fusion protein, the stem-cell factor receptor c-kit (KIT) and the platelet-derived growth-factor receptor. The successes obtained with imatinib in the treatment of chronic myeloid leukaemia (CML), gastrointestinal stroma-cell tumours (GIST), and dermatofibrosarcoma protuberans, demonstrate that targeted therapy with a rationally designed, small, synthetic molecule can be highly successful. However, experience so far with imatinib in KIT-positive tumours indicates that imatinib seems only to be effective in those tumours with a gain-of-function mutation in c-kit. There are arguments in favour of investigating a combined therapy of imatinib and classical chemotherapy.
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