Researchers at Stanford University School of Medicine present in PLoS Computational Biology this week an integrative method for the data-driven discovery of candidate genes for human pain sensitivity that takes "advantage of the vast amount of existing disease-related clinical literature and gene expression microarray data stored in large international repositories." To develop this, the researchers first ranked thousands of diseases according to their disease-specific pain indices. Then, integrating publicly available gene expression profile data for 121 of those diseases, the researchers selected candidate genes with expression variation that significantly correlated with disease-specific pain index across diseases. "Our results demonstrate the utility of a novel paradigm that integrates publicly available disease-specific gene expression data with clinical data curated from Medline to facilitate the discovery of pain-relevant genes," the authors write. "This data-derived list of pain gene candidates enables additional focused and efficient biological studies validating additional candidates."
Over in PLoS Genetics, a team led by investigators at the Fred Hutchinson Cancer Research Center reports that human colorectal cancer tissue they studied showed a decreased prevalence of non-clonal de novo single base substitutions in the mtDNA. This finding, the authors write, raises "the intriguing possibility that fidelity of mitochondrial genome is, in fact, increased in cancer as a result of a decrease in reactive oxygen species-mediated mtDNA damage."
And in PLoS One, researchers at North Carolina State University identify genes affecting sensitivity and resistance to reactive oxygen species-induced locomotor decline in Drosophila melanogaster genome-wide association analysis. "Candidate genes associated with variation in sensitivity to MSB [3 mM menadione sodium bisulfite]-induced oxidative stress form networks of genes involved in neural development, immunity, and signal transduction," the NC State team writes. "Many of these genes have human orthologs, highlighting the utility of genome-wide association in Drosophila for studying complex human disease."
