BackgroundOf late, high-throughput microarray and sequencing data have been extensively used to monitor biomarkers and biological processes related to many diseases. Under this circumstance, the support vector machine (SVM) has been popularly used and been successful for gene selection in many applications. Despite surpassing benefits of the SVMs, single data analysis using small- and mid-size of data inevitably runs into the problem of low reproducibility and statistical power. To address this problem, we propose a meta-analytic support vector machine (Meta-SVM) that can accommodate multiple omics data, making it possible to detect consensus genes associated with diseases across studies.ResultsExperimental studies show that the Meta-SVM is superior to the existing meta-analysis method in detecting true signal genes. In real data applications, diverse omics data of breast cancer (TCGA) and mRNA expression data of lung disease (idiopathic pulmonary fibrosis; IPF) were applied. As a result, we identified gene sets consistently associated with the diseases across studies. In particular, the ascertained gene set of TCGA omics data was found to be significantly enriched in the ABC transporters pathways well known as critical for the breast cancer mechanism.ConclusionThe Meta-SVM effectively achieves the purpose of meta-analysis as jointly leveraging multiple omics data, and facilitates identifying potential biomarkers and elucidating the disease process.Electronic supplementary materialThe online version of this article (doi:10.1186/s13040-017-0126-8) contains supplementary material, which is available to authorized users.
In genomic data analysis, it is commonplace that underlying regulatory relationship over multiple genes is hardly ascertained due to unknown genetic complexity and epigenetic regulations. In this paper, we consider a joint mean and constant covariance model (JMCCM) that elucidates conditional dependent structures of genes with controlling for potential genotype perturbations. To this end, the modified Cholesky decomposition is utilized to parametrize entries of a precision matrix. The JMCCM maximizes the likelihood function to estimate parameters involved in the model. We also develop a variable selection algorithm that selects explanatory variables and Cholesky factors by exploiting the combination of the GCV and BIC as benchmarks, together with Rao and Wald statistics. Importantly, we notice that sparse estimation of a precision matrix (or equivalently gene network) is effectively achieved via the proposed variable selection scheme and contributes to exploring significant hub genes shown to be concordant to a priori biological evidence. In simulation studies, we confirm that our model selection efficiently identifies the true underlying networks. With an application to miRNA and SNPs data from yeast (a.k.a. eQTL data), we demonstrate that constructed gene networks reproduce validated biological and clinical knowledge with regard to various pathways including the cell cycle pathway.
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