{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,6,2]],"date-time":"2023-06-02T18:51:03Z","timestamp":1685731863025},"reference-count":69,"publisher":"Springer Science and Business Media LLC","issue":"7793","license":[{"start":{"date-parts":[[2020,2,5]],"date-time":"2020-02-05T00:00:00Z","timestamp":1580860800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"},{"start":{"date-parts":[[2020,2,5]],"date-time":"2020-02-05T00:00:00Z","timestamp":1580860800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Nature"],"published-print":{"date-parts":[[2020,2,6]]},"abstract":"Abstract<\/jats:title>The discovery of drivers of cancer has traditionally focused on protein-coding genes1\u20134<\/jats:sup>. Here we present analyses of driver point mutations and structural variants in non-coding regions across 2,658\u00a0genomes from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium5<\/jats:sup> of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). For point mutations, we developed a statistically rigorous strategy for combining significance levels from multiple methods of driver discovery that overcomes the limitations of individual methods. For structural variants, we present two methods of driver discovery, and identify regions that are significantly affected by recurrent breakpoints and recurrent somatic juxtapositions. Our analyses confirm previously reported drivers6,7<\/jats:sup>, raise doubts about others and identify novel candidates, including point mutations in the 5\u2032 region of TP53<\/jats:italic>, in the 3\u2032 untranslated regions of NFKBIZ<\/jats:italic> and TOB1<\/jats:italic>, focal deletions in BRD4<\/jats:italic> and rearrangements in the loci of AKR1C genes. We show that although\u00a0point mutations and structural variants that drive cancer are less frequent in non-coding genes and regulatory sequences than in protein-coding genes, additional examples of these drivers will be found as more cancer genomes become available.<\/jats:p>","DOI":"10.1038\/s41586-020-1965-x","type":"journal-article","created":{"date-parts":[[2020,2,5]],"date-time":"2020-02-05T19:03:29Z","timestamp":1580929409000},"page":"102-111","update-policy":"http:\/\/dx.doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":327,"title":["Analyses of non-coding somatic drivers in 2,658\u00a0cancer whole genomes"],"prefix":"10.1038","volume":"578","author":[{"given":"Esther","family":"Rheinbay","sequence":"first","affiliation":[]},{"given":"Morten Muhlig","family":"Nielsen","sequence":"additional","affiliation":[]},{"given":"Federico","family":"Abascal","sequence":"additional","affiliation":[]},{"given":"Jeremiah 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P.B. receives grant funding from Novartis from an unrelated project; R.B. owns equity in Ampressa Therapeutics and receives grant funding from Novartis; G.G. receives research funds from IBM and Pharmacyclics and is an inventor on patent applications related to MuTect, ABSOLUTE, MutSig, MSMuTect, MSMutSig and POLYSOLVER; B.J.R. is a consultant at and has ownership interest (including stock, patents and so on) in Medley Genomics; O.S. is currently an employee of Cedilla Therapeutics); and Y.L. is currently an employee of Seven Bridges Genomics.","order":1,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"}}]}}