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000156705 1001_ $$0P:(DE-HGF)0$$aICGC/TCGAPan-CancerAnalysisofWholeGenomesConsortium$$b0
000156705 245__ $$aPan-cancer analysis of whole genomes.
000156705 260__ $$aLondon [u.a.]$$bNature Publ. Group52462$$c2020
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000156705 500__ $$a2020 Feb;578(7793):82-93 / siehe Correction: DKFZ Autoren affiliiert im PCAWG Consortium: https://inrepo02.dkfz.de/record/265692   /  https://doi.org/10.1038/s41586-022-05598-w
000156705 520__ $$aCancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale1-3. Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4-5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter4; identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation5,6; analyses timings and patterns of tumour evolution7; describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity8,9; and evaluates a range of more-specialized features of cancer genomes8,10-18.
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000156705 650_7 $$0EC 2.7.7.49$$2NLM Chemicals$$aTERT protein, human
000156705 650_7 $$0EC 2.7.7.49$$2NLM Chemicals$$aTelomerase
000156705 650_2 $$2MeSH$$aCell Proliferation: genetics
000156705 650_2 $$2MeSH$$aCellular Senescence: genetics
000156705 650_2 $$2MeSH$$aChromothripsis
000156705 650_2 $$2MeSH$$aCloud Computing
000156705 650_2 $$2MeSH$$aDNA Mutational Analysis
000156705 650_2 $$2MeSH$$aEvolution, Molecular
000156705 650_2 $$2MeSH$$aFemale
000156705 650_2 $$2MeSH$$aGenome, Human: genetics
000156705 650_2 $$2MeSH$$aGenomics
000156705 650_2 $$2MeSH$$aGerm-Line Mutation: genetics
000156705 650_2 $$2MeSH$$aHigh-Throughput Nucleotide Sequencing
000156705 650_2 $$2MeSH$$aHumans
000156705 650_2 $$2MeSH$$aInformation Dissemination
000156705 650_2 $$2MeSH$$aMale
000156705 650_2 $$2MeSH$$aMutagenesis: genetics
000156705 650_2 $$2MeSH$$aMutation
000156705 650_2 $$2MeSH$$aNeoplasms: classification
000156705 650_2 $$2MeSH$$aNeoplasms: genetics
000156705 650_2 $$2MeSH$$aNeoplasms: pathology
000156705 650_2 $$2MeSH$$aOncogenes: genetics
000156705 650_2 $$2MeSH$$aPromoter Regions, Genetic: genetics
000156705 650_2 $$2MeSH$$aRNA Splicing: genetics
000156705 650_2 $$2MeSH$$aReproducibility of Results
000156705 650_2 $$2MeSH$$aTelomerase: genetics
000156705 650_2 $$2MeSH$$aTelomere: genetics
000156705 773__ $$0PERI:(DE-600)1413423-8$$a10.1038/s41586-020-1969-6$$gVol. 578, no. 7793, p. 82 - 93$$n7793$$p82 - 93$$tNature <London>$$v578$$x1476-4687$$y2020
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