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Benjamin Raphael and colleagues report an analysis of altered subnetworks of somatic aberrations in TCGA pan-cancer data sets, including 3,281 samples from 12 cancer types, using a newly developed HotNet2 algorithm. They identify 16 significantly mutated subnetworks and provide a more comprehensive view into altered pathways, including those with known roles in cancer development.
Erik Larsson and colleagues present an analysis pipeline for identifying likely transcription-altering noncoding somatic mutations in cancer using publicly available data from 505 tumor genomes across 14 cancer types. They find that TERT promoter mutations show strong associations to altered transcriptional levels and identify recurrent promoter mutations in DPH3 and PLEKHS1.
William Lee and colleagues present a systematic analysis of noncoding somatic mutations in 863 tumor samples representing over 20 cancer types. They identify new mutation hotspots as well as genes with frequent mutations in their promoter regions, including WDR74 and SDHD.
Trey Ideker and colleagues report a comprehensive genome-wide analysis of head and neck squamous cell carcinoma, reporting that TP53 mutations are frequently accompanied by loss of chromosome 3p. Their data indicate that the combination of these two events has a stronger negative effect on survival rate than either event alone.
Charles Perou and colleagues apply a panel of 52 published gene expression signatures of human breast tumors to expression data from The Cancer Genome Project to identify new proliferation drivers. They find genomic regions that are uniquely amplified in highly proliferative luminal breast tumors, including some that are correlated with poor prognosis.
Jonathan Pritchard, Guy Sella and colleagues report an analysis using population genetic models to show that recent human demography is likely to have had little impact on the average burden of deleterious mutations. They examine two large exome sequence datasets and find that individuals of west African and European ancestry carry similar burdens of damaging mutations.
