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 Printable version |
KIT and KIT: from biology to clinical use |
Bulletin du Cancer. Volume 99, Number 2, 191-7, Février 2012, Synthèse
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 Résumé
Texte intégral
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Author(s) : Elsa Curtit, Laura Mansi, Erika Viel, Erion Dobi, Loïc Chaigneau, Thierry Nguyen, Xavier Pivot, Jean-Yves Blay, Elsa Kalbacher |
Summary : Scientific knowledge on gastrointestinal stromal tumors (GIST) has highly progressed over the last 10 years. The molecular bases of oncogenic transformation,
KIT activating mutations, were identified in 1998 by Hirota
et al. The product of
KIT proto-oncogene, KIT protein, is a transmembrane receptor with tyrosine kinase activity. Tyrosine kinase inhibitors targeting these mutated activated kinases, namely imatinib and more recently sunitinib, nilotinib, masitinib or sorafenib, have deeply modified GIST prognosis. Molecular biology in GIST is now becoming a routine tool for treatment selection. In patients with advanced GIST, imatinib should be given until progression, and then, other tyrosine kinase inhibitors targeting KIT should be used. In the adjuvant setting, the optimal duration of imatinib treatment remains unknown. |
Keywords : KIT, imatinib, sunitinib, gastrointestinal stromal tumors, tyrosine kinase receptor |
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