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@ARTICLE{Alexandrov:177478,
      author       = {L. B. Alexandrov and J. Kim and N. J. Haradhvala and M. N.
                      Huang and A. W. Tian Ng and Y. Wu and A. Boot and K. R.
                      Covington and D. A. Gordenin and E. N. Bergstrom and S. M.
                      A. Islam and N. Lopez-Bigas and L. J. Klimczak and J. R.
                      McPherson and S. Morganella and R. Sabarinathan and D. A.
                      Wheeler and V. Mustonen and
                      PCAWGMutationalSignaturesWorkingGroup and G. Getz and S. G.
                      Rozen and M. R. Stratton and PCAWGConsortium},
      title        = {{T}he repertoire of mutational signatures in human cancer.},
      journal      = {Nature},
      volume       = {578},
      number       = {7793},
      issn         = {1476-4687},
      address      = {London [u.a.]},
      publisher    = {Nature Publ. Group},
      reportid     = {DKFZ-2021-02565},
      pages        = {94 - 101},
      year         = {2020},
      note         = {siehe Correction: DKFZ Autoren affiliiert im PCAWG
                      Consortium;https://inrepo02.dkfz.de/record/265690 /
                      https://doi.org/10.1038/s41586-022-05600-5},
      abstract     = {Somatic mutations in cancer genomes are caused by multiple
                      mutational processes, each of which generates a
                      characteristic mutational signature1. Here, as part of the
                      Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium2 of
                      the International Cancer Genome Consortium (ICGC) and The
                      Cancer Genome Atlas (TCGA), we characterized mutational
                      signatures using 84,729,690 somatic mutations from
                      4,645 whole-genome and 19,184 exome sequences that
                      encompass most types of cancer. We identified
                      49 single-base-substitution, 11 doublet-base-substitution,
                      4 clustered-base-substitution and 17 small
                      insertion-and-deletion signatures. The substantial size of
                      our dataset, compared with previous analyses3-15, enabled
                      the discovery of new signatures, the separation of
                      overlapping signatures and the decomposition of signatures
                      into components that may represent associated-but
                      distinct-DNA damage, repair and/or replication mechanisms.
                      By estimating the contribution of each signature to the
                      mutational catalogues of individual cancer genomes, we
                      revealed associations of signatures to exogenous or
                      endogenous exposures, as well as to defective
                      DNA-maintenance processes. However, many signatures are of
                      unknown cause. This analysis provides a systematic
                      perspective on the repertoire of mutational processes that
                      contribute to the development of human cancer.},
      keywords     = {Age Factors / Base Sequence / Exome: genetics / Genome,
                      Human: genetics / Humans / Mutation: genetics / Neoplasms:
                      genetics / Sequence Analysis, DNA},
      cin          = {BE01 / B260 / B330 / HD01 / B360 / C010 / B080 / B370 /
                      B060 / B062 / B066 / W610 / B063 / B087 / W190},
      ddc          = {500},
      cid          = {I:(DE-He78)BE01-20160331 / I:(DE-He78)B260-20160331 /
                      I:(DE-He78)B330-20160331 / I:(DE-He78)HD01-20160331 /
                      I:(DE-He78)B360-20160331 / I:(DE-He78)C010-20160331 /
                      I:(DE-He78)B080-20160331 / I:(DE-He78)B370-20160331 /
                      I:(DE-He78)B060-20160331 / I:(DE-He78)B062-20160331 /
                      I:(DE-He78)B066-20160331 / I:(DE-He78)W610-20160331 /
                      I:(DE-He78)B063-20160331 / I:(DE-He78)B087-20160331 /
                      I:(DE-He78)W190-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32025018},
      pmc          = {pmc:PMC7054213},
      doi          = {10.1038/s41586-020-1943-3},
      url          = {https://inrepo02.dkfz.de/record/177478},
}