伊马替尼治疗胃肠道间质瘤耐药的相关分子机制研究进展

Research progress on the molecular mechanisms of imatinib resistance in gastrointestinal stromal tumors

研究胃肠道间质瘤(gastrointestinal stromal tumor,GIST)伊马替尼耐药的机制,开发新的治疗靶点和治疗方案,对改善GIST患者的长期预后具有重要意义。本文从GIST的分子特征、伊马替尼耐药机制、非编码RNA、溶酶体、关键蛋白和成纤维细胞生长因子2(fibroblast growth factor-2,FGF-2)等方面对GIST伊马替尼耐药机制的研究进行了综述。研究表明,不同的耐药机制网络之间是相互联系的。伊马替尼治疗和联合抑制多种耐药机制有望成为GIST治疗的新选择。此外,基于耐药机制的识别实施个体化治疗将为伊马替尼耐药的GIST患者提供新的辅助治疗选择,从而延缓GIST的进展。

Understanding mechanism of imatinib resistance in gastrointestinal stromal tumors(GIST)and developing new therapeutic targets and schemes to address this resistance exhibit great potential to improve the long-term prognosis of patients with GIST.This review summarizes exiting research into the molecular characteristics of GIST and mechanisms of imatinib resistance acting via non-coding RNA,lysosomes,key protein molecules,fibroblast growth factor-2(FGF-2),and other modulators.Research shows that different drug resistance mechanism networks are closely connected and interrelated.Combining imatinib therapy with multiple drugs that inhibit the resistance mechanism shall present new options treating GIST thereby improving prognosis.Identification and implementation of individualized treatment strategies based on drug resistance mechanisms will provide new adjuvant treatment options for patients with GIST resistant to imatinib,thus delaying progression of GIST.