In Nature Genetics this week, a collaboration of European investigators present five new loci for breast cancer susceptibility that they discovered in a genome-wide association study of 3,659 family-history cases and 4,897 controls. "Previously identified breast cancer susceptibility loci were also found to show larger effect sizes in this study of familial breast cancer cases than in previous population-based studies, consistent with polygenic susceptibility to the disease," the authors write. Nazneen Rahman, study co-author from The Institute of Cancer Research in the UK, said in a statement that their "results now take the total number of gene regions linked to the risk of breast cancer to 18, but we still don't know which genes are causing this increased risk."
A new study published in Nature Methods outlines the potential of Pacific Biosciences' SMRT [single-molecule real-time] sequencing to detect DNA methylation without bisulfite conversion. "We used these kinetic signatures to identify adenine methylation in genomic samples and found that, in combination with circular consensus sequencing, they can enable single-molecule identification of epigenetic modifications with base-pair resolution," the PacBio team writes, adding that their method — which is "amenable to long read lengths" — could enable researchers to map the methylation patterns of highly repetitive genomic regions.
In Nature this week, researchers in the UK report that by using an inducible system of DNA damage bypass in Saccharomyces cerevisiae, the RAD6 pathway — which ordinarily operates during S phase — is "separable in time and space from genome replication, thus allowing direct visualization and quantification of productive PRR [post-replication repair] tracts." The team writes that "during and after S phase ultraviolet-radiation-induced lesions are bypassed predominantly via translesion synthesis, whereas the error-free pathway functions as a backup system," adding that their study elucidates the distribution of PRR tracts in a cell population and will "allow an in-depth mechanistic analysis of how cells manage the processing of lesions to their genomes during and after replication."
Researchers at the University of Miami Miller School of Medicine and the University of Iowa describe their "approach in which the expression of new, and thereby potent, antigens are induced in tumor cells by inhibiting nonsense-mediated messenger RNA decay." In performing siRNA-mediated inhibition of nonsense-mediated messenger RNA decay in tumor cells, the team found that new antigenic determinants were expressed — as was their immune-mediated rejection.