摘要
胃肠间质瘤(GIST)是胃肠道最常见的间叶源性肿瘤,多数GIST发病机制是c-Kit基因发生功能获得性突变,表达Kit蛋白并持续激活其下游信号通路使肿瘤细胞持续增殖。作为酪氨酸激酶抑制剂,伊马替尼在GIST中的应用使得靶向治疗成为手术治疗以外最为重要的治疗方式,已深刻影响了GIST的治疗模式。Foxp3^+Treg是体内重要的调节性T细胞,通过抑制CTL、NK细胞等肿瘤抑制细胞的功能,负向调节机体的抗肿瘤免疫反应。研究显示,伊马替尼不仅可通过靶向治疗机制,也可能通过抑制Foxp3^+Treg细胞而增强机体对肿瘤的免疫反应,从免疫途径发挥治疗GIST的作用。笔者就伊马替尼对GIST患者外周血中Foxp3^+Treg细胞及其亚群影响的相关研究作一综述。
Gastrointestinal stromal tumor（GIST） is the most common mesenchymal tumor of the gastrointestinal tract. The mechanism for most GIST is considered to be the gain-of-function mutations of the c-Kit gene and Kit protein expression which cause the sustained activation of its down-stream signaling pathways and thereby the continuous proliferation of the tumor cells. As a tyrosine kinase inhibitor, application of imatinib has allowed the targeted therapy to become an important therapeutic option besides surgical treatment for GIST, and significantly influenced the treatment mode of GIST. Foxp3＋Treg cells are important regulatory T population, and they negatively control the anti-tumor immune responses through suppressing the anti-tumor cells such as CTL and NK cells. Studies have revealed that imatinib inhibits GIST through not only targeted mechanism but also immunological mechanisms by suppressing the Foxp3＋Treg cells and enhancing the anti-tumor immune responses. Here, the authors present research progress of the effects of imatinib on the peripheral blood Foxp3＋Treg cells and their subpopulations in patients with GIST.
作者
陈小龙
冯立波
巫晓龙
左忠林
陈鹏
刘亿
邹庆伟
刘庆
夏冬
CHEN Xiaolong;FENG Libo;WU Xiaolong;ZUO Zhonglin;CHEN Peng;LIU Yi;ZOU Qingwei;LIU Qing;XIA Dong(Department of the Gastrointestinal Surgery, the Affiliated Hospital, Southwest Medical University, Luzhou, Sichuan 646000, Chin)
出处
《中国普通外科杂志》
CAS
CSCD
北大核心
2018年第4期494-499,共6页
China Journal of General Surgery
基金
四川省教育厅资助项目(16ZA0197)
