Curtit Elsa, Mansi Laura, Viel Erika, Dobi Erion, Chaigneau Loïc, Nguyen Thierry, Pivot Xavier, Blay Jean-Yves, Kalbacher Elsa
CHU Jean-Minjoz, 3, boulevard Fleming, 25030 Besançon Cedex, France.
Bull Cancer. 2012 Feb 1;99(2):191-7. doi: 10.1684/bdc.2011.1386.
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.
在过去10年中，关于胃肠道间质瘤（GIST）的科学知识有了高度进展。致癌转化的分子基础，即KIT激活突变，于1998年由Hirota等人鉴定出来。KIT原癌基因的产物KIT蛋白是一种具有酪氨酸激酶活性的跨膜受体。针对这些突变激活激酶的酪氨酸激酶抑制剂，即伊马替尼，以及最近的舒尼替尼、尼洛替尼、马西替尼或索拉非尼，已深刻改变了GIST的预后。GIST中的分子生物学现在正成为治疗选择的常规工具。在晚期GIST患者中，应给予伊马替尼直至病情进展，然后使用其他针对KIT的酪氨酸激酶抑制剂。在辅助治疗中，伊马替尼治疗的最佳持续时间仍然未知。
