Liang Aijun, Zhou Bin, Sun Wei
Department of Neurosurgery, Jiangxi Provincial People's Hospital, No. 92, Aiguo Road, Nanchang, 330006 Jiangxi Province China.
Cancer Cell Int. 2017 Oct 13;17:90. doi: 10.1186/s12935-017-0458-y. eCollection 2017.
Cancers are caused by the acquisition of somatic mutations. Numerous efforts have been made to characterize the key driver genes and pathways in glioma, however, the etiology of glioma is still not completely known. This study was implemented to characterize driver genes in glioma independently of somatic mutation frequencies.
Driver genes and pathways were predicted by OncodriveCLUST, OncodriveFM, Icages, Drgap and Dendrix in glioma using 31,958 somatic mutations from TCGA, followed by an integrative characterization of driver genes.
Overall, 685 driver genes and 215 driver pathways were determined by the five tools. , , , and showed the strongest expression correlation with other genes in the co-expression network of glioma tissues. , , , and are at the core of the protein-protein interaction network. 133 driver genes were up-regulated and associated to poor prognosis, 43 driver genes were down-regulated and related to favorable clinical outcome in glioma patients. The driver genes such as and might serve as candidate prognostic biomarkers and therapeutic targets in glioma.
The set of new cancer genes and pathways sheds insights into the tumorigenesis of glioma and paves the way for developing driver gene-targeted therapy and prognostic biomarkers in glioma.
癌症是由体细胞突变的获得引起的。人们已经做出了许多努力来表征胶质瘤中的关键驱动基因和通路，然而，胶质瘤的病因仍不完全清楚。本研究旨在独立于体细胞突变频率来表征胶质瘤中的驱动基因。
使用来自TCGA的31958个体细胞突变，通过OncodriveCLUST、OncodriveFM、Icages、Drgap和Dendrix在胶质瘤中预测驱动基因和通路，随后对驱动基因进行综合表征。
总体而言，这五种工具确定了685个驱动基因和215条驱动通路。在胶质瘤组织的共表达网络中，[此处原文缺失具体基因名称]与其他基因表现出最强的表达相关性。[此处原文缺失具体基因名称]处于蛋白质-蛋白质相互作用网络的核心。133个驱动基因上调并与不良预后相关，43个驱动基因下调并与胶质瘤患者的良好临床结果相关。诸如[此处原文缺失具体基因名称]等驱动基因可能作为胶质瘤的候选预后生物标志物和治疗靶点。
这组新的癌症基因和通路为胶质瘤的肿瘤发生提供了见解，并为开发针对驱动基因的治疗方法和胶质瘤的预后生物标志物铺平了道路。
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