Melamed Rachel D, Wang Jiguang, Iavarone Antonio, Rabadan Raul
Department of Systems Biology, Columbia University College of Physicians and Surgeons, New York, NY, USA Department of Biomedical Informatics, Columbia University College of Physicians and Surgeons, New York, NY, USA.
Institute for Cancer Genetics, Columbia University College of Physicians and Surgeons, New York, NY, USA Department of Pathology and Cell Biology, Columbia University College of Physicians and Surgeons, New York, NY, USA Department of Neurology, Columbia University College of Physicians and Surgeons, New York, NY, USA.
J Mol Cell Biol. 2015 Jun;7(3):203-13. doi: 10.1093/jmcb/mjv026. Epub 2015 May 4.
Tumors are the result of accumulated genomic alterations that cooperate synergistically to produce uncontrollable cell growth. Although identifying recurrent alterations among large collections of tumors provides a way to pinpoint genes that endow a selective advantage in oncogenesis and progression, it fails to address the genetic interactions behind this selection process. A non-random pattern of co-mutated genes is evidence for selective forces acting on tumor cells that harbor combinations of these genetic alterations. Although existing methods have successfully identified mutually exclusive gene sets, no current method can systematically discover more general genetic relationships. We develop Genomic Alteration Modules using Total Correlation (GAMToC), an information theoretic framework that integrates copy number and mutation data to identify gene modules with any non-random pattern of joint alteration. Additionally, we present the Seed-GAMToC procedure, which uncovers the mutational context of any putative cancer gene. The software is publicly available. Applied to glioblastoma multiforme samples, GAMToC results show distinct subsets of co-occurring mutations, suggesting distinct mutational routes to cancer and providing new insight into mutations associated with proneural, proneural/G-CIMP, and classical types of the disease. The results recapitulate known relationships such as mutual exclusive mutations, place these alterations in the context of other mutations, and find more complex relationships such as conditional mutual exclusivity.
肿瘤是基因组改变累积的结果,这些改变协同作用导致细胞生长失控。虽然在大量肿瘤样本中识别复发性改变为确定在肿瘤发生和进展中赋予选择性优势的基因提供了一种方法,但它未能解决这种选择过程背后的基因相互作用。共突变基因的非随机模式是作用于携带这些基因改变组合的肿瘤细胞的选择力的证据。尽管现有方法已成功识别出相互排斥的基因集,但目前尚无方法能系统地发现更普遍的基因关系。我们开发了基于总相关性的基因组改变模块(GAMToC),这是一个信息理论框架,整合了拷贝数和突变数据,以识别具有任何联合改变非随机模式的基因模块。此外,我们还提出了种子-GAMToC程序,该程序揭示了任何假定癌症基因的突变背景。该软件可公开获取。应用于多形性胶质母细胞瘤样本时,GAMToC结果显示了共发生突变的不同子集,提示了不同的癌症突变途径,并为与神经干细胞型、神经干细胞/G-CIMP型和经典型疾病相关的突变提供了新的见解。这些结果重现了已知的关系,如相互排斥的突变,将这些改变置于其他突变的背景下,并发现了更复杂的关系,如条件性相互排斥。