PI3K-AKT-mTOR信号通路抑制剂与肿瘤免疫治疗

发布时间：2018-06-03 08:52

本文选题：PIK-AKT-mTOR + 抑制剂　；参考：《中国肿瘤生物治疗杂志》2017年12期

【摘要】：磷脂酰肌醇3-蛋白激酶B-哺乳动物雷帕霉素靶蛋白(PI3K-AKT-mTOR)信号通路的上游通路主要包括表皮生长因子受体(EGFR)、人类表皮生长因子受体2(HER2)、肝细胞生长因子受体(MET)和成纤维细胞生长因子受体(FGFR)等各类受体的酪氨酸激酶,其受体的突变、扩增常会导致PI3K-AKT-mTOR信号通路的失调,引起肿瘤发生发展。该通路异常激活常伴随着下游关键分子的改变包括PIK3CA、AKT1、PTEN的基因突变,PIK3CA、AKT1、AKT2的基因扩增,肿瘤抑制基因PTEN的缺失等。PI3K-AKT-mTOR信号通路抑制剂主要包括PI3K抑制剂、AKT抑制剂、mTOR抑制剂和双重抑制剂等。PI3K-AKT-mTOR抑制剂对肿瘤免疫微环境、免疫细胞均有显著影响。PI3K-AKT-mTOR抑制剂单药治疗肿瘤具有一定局限性,如联合DC疫苗、免疫检查点抑制剂和CAR-T细胞等免疫疗法可增强抗肿瘤疗效。
[Abstract]:The upstream pathways of the rapamycin target protein (PI3K-AKT-mTOR) signaling pathway of the phosphatidylinositol 3- protein kinase B- include epidermal growth factor receptor (EGFR), human epidermal growth factor receptor 2 (HER2), hepatocyte growth factor receptor (MET) and fibroblast growth factor receptor (FGFR) receptor tyrosine kinase, and so on. The mutation of the receptor often causes maladjustment of the PI3K-AKT-mTOR signaling pathway and causes the development of the tumor. The abnormal activation of this pathway is often accompanied by changes in the downstream key molecules including PIK3CA, AKT1, PTEN mutations, PIK3CA, AKT1, AKT2 gene amplification, and the deletion of the tumor suppressor based on the loss of PTEN. .PI3K-AKT-mTOR inhibitors, such as PI3K inhibitors, AKT inhibitors, mTOR inhibitors and double inhibitors, have significant effects on the tumor immune microenvironment, and immune cells have significant effects on.PI3K-AKT-mTOR inhibitors, such as combined DC vaccines, immunosuppressive agents and CAR-T cells, which can enhance the anti-tumor effect. Curative effect.
【作者单位】：第二军医大学附属长海医院呼吸与危重症医学科;
【基金】：上海市科研计划资助项目(No.15411960400)~~
【分类号】：R730.51

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