The National Institutes of Health's Francis Collins and colleagues from the US, UK, Finland bring together gene expression, DNA methylation, and genetic variants in 265 skeletal muscle biopsies from individuals enrolled in the Finland-United States Investigation of Non-Insulin-Dependent Diabetes Mellitus Genetics (FUSION) study, analyzing these features alongside physiological traits such as height, body mass index, and type 2 diabetes in the FUSION participants. After narrowing in on quantitative trait loci influencing gene expression or methylation, the team used these genetic insights to find hundreds of potential causal associations between methylation and expression in the skeletal muscle samples. The authors also looked at how well the QTL data from FUSION and from the Genotype-Tissue Expression could predict potential disease associations in dozens more tissue types.
A team from France and the US tracks the viruses found in blood samples over time in dozens of kidney transplant recipients, noting that viral infections can contribute to decreased allograft survival and other forms of morbidity. Using a multiplexed VirScan array that relies on a synthetic virome to pick up antibodies against more than 200 known human viruses, the researchers assessed blood serum viruses at baseline and again a year after transplant in 45 kidney recipients. With this approach, they saw antibodies corresponding with 39 viral species — findings that appeared to line up well with results from standard PCR or enzyme-linked immunosorbent assays. "Using VirScan," the authors add, "we found that anti-viral antibody responses were largely conserved in patients during the first year after transplantation, regardless of immunosuppressive treatment."
Researchers from Memorial Sloan Kettering Cancer Center, the Massachusetts Institute of Technology, and elsewhere describe a role for chromosome gains and losses in pushing prostate cancer progression in a subset of high-risk cases. With the help of DNA copy number data generated from more than 300 primary prostate cancers profiled for the Cancer Genome Atlas project, the team came up with a method for quantifying the loss or gain of chromosome arms from tumor transcriptome data. When they applied this approach to transcriptome profiles representing 404 prostate cancers cases followed for 15 years, on average, for the Health Professionals Follow-up Study and the Physicians' Health Study, the authors found tumor aneuploidy in almost one-quarter of the prostate cancer cases—chromosome arm gains and losses that corresponded with a much higher risk of lethal disease than that observed in aneuploidy-free prostate cancers with the same Gleason scores.