PI3K/Akt信号转导通路与胶质母细胞瘤靶向治疗研究进展  

PI3K/Akt signaling pathway and targeted therapy for glioblastoma

作　　者：陈念慈[1] 王明昊[2] 王亮尹 王恩华[3] 

机构地区：[1]中国医科大学,97期9班七年制沈阳110001 [2]中国医科大学附属第一医院神经外科,沈阳110001 [3]中国医科大学基础医学院病理学教研室,沈阳110001

出　　处：《解剖科学进展》2015年第1期94-97,共4页Progress of Anatomical Sciences

摘　　要：胶质母细胞瘤(GBM)是脑部肿瘤中最常见和恶性程度最高的肿瘤。GBM多伴发表皮生长因子受体(EGFR)的过表达或突变。EGFR的异常可导致下游信号转导通路的激活。大量研究显示,磷脂酰肌醇3-激酶(PI3K)信号转导通路是参与GBM发生和恶性演进的重要核心通路之一。本文阐述GBM中PUK/Akt/mTORfq号转导通路的活化过程,分析通过抑制该通路进行GBM靶向治疗的机理,介绍PI3K抑制剂在临床前期研究中的进展,归纳导致疗效降低的原因及可能的解决方案。Giloblastoma（GBM） is the most common and malignant glioma in the brain tumor and often with over expression and/or mutation of EGFR. The alteration of epidermal growth factor receptor（EGFR） leads to activation of many downstream singnal pathways. PI3K pathway is one of the core pathways involving the carcinogenesis and development of GBM. We described the activation of the PI3K/Akt/mTOR pathway in GBM, explored why inhibition of this pathway may serve as a compelling therapeutic target for the disease, and tried to provide an update of the data on PI3K inhibitors in clinical trials from earlier investigation, summarized some reasons that may attenuate the therapeutic effect and some promising solutions.

关 键 词：胶质母细胞瘤 PI3K/AKT 信号转导 靶向药物 脑部肿瘤 磷脂酰肌醇 胶质瘤 恶性程度 下游信号 临床前期 

分 类 号：R739.41[医药卫生—肿瘤]