Neuroblastoma is a highly complex and heterogeneous cancer in children. Acquired genomic alterations including MYCN amplification, 1p deletion and 11q deletion are important risk factors and biomarkers in neuroblastoma. Here, we performed a co-expression-based gene network analysis to study the intrinsic association between specific genomic changes and transcriptome organization. We identified multiple gene coexpression modules which are recurrent in two independent datasets and associated with functional pathways including nervous system development, cell cycle, immune system process and extracellular matrix/space. Our results also indicated that modules involved in nervous system development and cell cycle are highly associated with MYCN amplification and 1p deletion, while modules responding to immune system process are associated with MYCN amplification only. In summary, this integrated analysis provides novel insights into molecular heterogeneity and pathogenesis of neuroblastoma. This article is part of a Special Issue entitled: Accelerating Precision Medicine through Genetic and Genomic Big Data Analysis edited by Yudong Cai & Tao Huang.
The underlying mechanisms of eating disorders (EDs) are very complicated and still poorly understood. The pathogenesis of EDs may involve the interplay of multiple genes. To investigate the dysregulated gene pathways in EDs we analyzed gene expression profiling in dorsolateral prefrontal cortex (DLPFC) tissues from 15 EDs cases, including 3 with anorexia nervosa (AN), 7 with bulimia nervosa (BN), 2 AN-BN cases, 3 cases of EDs not otherwise specified, and 102 controls. We further used a weighted gene co-expression network analysis to construct a gene co-expression network and to detect functional modules of highly correlated genes. The functional enrichment analysis of genes in co-expression modules indicated that an altered mitochondrial oxidative phosphorylation process may be involved in the pathogenesis of EDs.
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