Zhang Yuping, Linder M Henry, Shojaie Ali, Ouyang Zhengqing, Shen Ronglai, Baggerly Keith A, Baladandayuthapani Veerabhadran, Zhao Hongyu
Department of Statistics, Institute for Systems Genomics, Center for Quantitative Medicine, Institute for Collaboration on Health, Intervention, and Policy, The Connecticut Institute for the Brain and Cognitive Sciences, University of Connecticut, Storrs, CT 06269, USA.
Department of Statistics, University of Connecticut, Storrs, CT 06269, USA.
Stat Biosci. 2018 Apr;10(1):86-106. doi: 10.1007/s12561-017-9193-0. Epub 2017 May 4.
Complex diseases such as cancers usually result from accumulated disturbance of pathways instead of the disruptions of one or a few major genes. As opposed to single-platform analyses, it is likely that integrating diverse molecular regulatory elements and their interactions can lead to more insights on pathway-level disturbances of biological systems and their potential consequences in disease development and progression. To explore the benefit of pathway-based analysis, we focus on mutli-platform genomics, epigenomics and transcriptomics (-omics, for short) from 11 cancer types collected by the Cancer Genome Atlas (TCGA) project. Specifically, we use a well-studied oncogenetic pathway, the BRAF pathway, to investigate the relevant copy number variants, methylations and gene expressions, and quantify their effects on discovering tumor-specific aberrations across multiple tumor lineages. We also perform simulation studies to further investigate the effects of network topology and multiple omics on dissecting pathway disturbances. Our analysis shows that adding molecular regulatory elements such as copy number variants (CNVs) and/or methylations to the baseline mRNA molecules can improve our power of discovering tumorous aberrances. Also, incorporating copy number variants with the baseline mRNA molecules can be more beneficial than incorporating methylations. Moreover, employing regulatory topologies can improve the discoveries of tumorous aberrances. Finally, our analysis reveals similarities and differences among diverse cancer types based on disturbance of the BRAF pathway.
诸如癌症之类的复杂疾病通常是由通路的累积紊乱而非一个或几个主要基因的破坏所致。与单平台分析不同,整合多种分子调控元件及其相互作用可能会使我们对生物系统的通路水平紊乱及其在疾病发生和发展中的潜在后果有更多的了解。为了探索基于通路分析的益处,我们聚焦于癌症基因组图谱(TCGA)项目收集的11种癌症类型的多平台基因组学、表观基因组学和转录组学(简称为“组学”)。具体而言,我们使用一条经过充分研究的致癌通路——BRAF通路,来研究相关的拷贝数变异、甲基化和基因表达,并量化它们对发现多个肿瘤谱系中肿瘤特异性畸变的影响。我们还进行了模拟研究,以进一步探究网络拓扑结构和多组学对剖析通路紊乱的影响。我们的分析表明,在基线mRNA分子中加入诸如拷贝数变异(CNV)和/或甲基化等分子调控元件,可以提高我们发现肿瘤畸变的能力。此外,将拷贝数变异与基线mRNA分子相结合可能比加入甲基化更有益。而且,采用调控拓扑结构可以改善对肿瘤畸变的发现。最后,我们的分析揭示了基于BRAF通路紊乱的不同癌症类型之间的异同。