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This Week in Cell: Feb 10, 2016

Researchers from Canada and the US report on findings from an effort to characterize functional genomic features in breast cancer cell lines. Using small hairpin RNA-based dropout screens, the team searched for mutations involved in breast cancer survival or proliferation in 77 breast cancer cell lines. Findings from the screen, combined with RNA sequence and proteomic data for these and other breast cancer or mammary cell lines, offer a peek at potential cancer drivers in various breast cancer subtypes and highlight genes that might serve as useful targets for treating breast cancer and/or predicting treatment resistance. "[O]ur integrated functional genomic approach not only can suggest new treatment strategies for breast tumor subtypes," the study's authors say, "but also reveals new features of breast cancer biology."

A Broad Institute-led team describes DNA damage and repair patterns it detected in tumor genomes from 14 cancer types. The researchers used two types of genome partitioning to search 590 tumor genomes for examples of mutational strand asymmetry, when alterations affect one DNA strand more than the other. Indeed, their search uncovered cases of transcriptional asymmetry, replicative asymmetry, and transcription-coupled damage to the non-transcribed strand of DNA — features that differed depending on mutation type and whether these mutations were nudged along by factors such as UV light, smoking, DNA damage defects, and so on. "As more genomes are sequenced," authors of the analysis note, "studying and classifying asymmetries will illuminate the underlying biological mechanisms of DNA damage and repair."

A study by investigators in Germany and elsewhere suggests obesity may be related to epigenetic patterns prompted by mutations interfering with one copy of a gene called Trim28. Following from results of a study done several years ago that implicated Trim28 mutations in weight in mice, the team used RNA sequencing to assess samples from mice lacking one copy of Trim28 that were raised in similar conditions but fell into a metabolically healthy obese group and a normal weight groups. Results from the analysis suggested that obesity occurred when expression of imprinted genes such as Nnat, Peg3, Cdkn1c, and Plagl1 is dialed down — findings supported in humans by the group's array-based gene expression studies of adipose tissue samples from weight-discordant identical twins. GenomeWeb has more on the study, here.