【摘要】 在功能获得性突变所致的KIT或PDGFRA受体酪氨酸激酶异常活化与胃肠间质瘤(GIST)的发病关系阐明后,酪氨酸激酶抑制剂甲璜酸伊马替尼(imatinib)在进展期GIST中显现出很高的有效性,使GIST的治疗发生了革命性的改变。然而,GIST中对imatinib的早期或晚期耐药已经成为日益严重的临床问题。因此,对耐药的分子机制的进一步了解就成为当前研究的焦点,本文综述了目前对imatinib耐药的分子机制的认识,这些认识可能引导新的治疗策略的产生。更多还原

【Abstract】 After the identification of abnormal activation of KIT/PDGFRA receptor tyrosine kinase as a key factor in the pathogenesis of gastrointestinal stromal tumour (GIST),imatinib,a tyrosine kinase inhibitor (TKI),has been shown to be highly effective in patients with advanced GIST and has certainly revolutionalized the treatment of GIST.However,early or late resistance of tumours to imatinib is an in- creasing clinical problem.In recent years,major progress has been made in the elucidation of mecha- nisms conferring resistance to imatinib.This review focuses on the mechanisms of imatinib resistance that have been elucidated so far,which may lead to the identification of novel clinical strategies.更多还原