[KIT and KIT: from biology to clinical use].
Fiche publication
Date publication
février 2012
Auteurs
Membres identifiés du Cancéropôle Est :
Dr CHAIGNEAU Loïc, Pr PIVOT Xavier
Tous les auteurs :
Curtit E, Mansi L, Viel E, Dobi E, Chaigneau L, Nguyen T, Pivot X, Blay JY, Kalbacher E
Lien Pubmed
Résumé
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.
Référence
Bull Cancer. 2012 Feb 1;99(2):191-7.