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@ARTICLE{Anderson:291025,
      author       = {C. J. Anderson and L. Talmane and J. Luft and J. Connelly
                      and M. D. Nicholson and J. C. Verburg and O. Pich and S.
                      Campbell and M. Giaisi$^*$ and P.-C. Wei$^*$ and V. Sundaram
                      and F. Connor and P. A. Ginno$^*$ and T. Sasaki and D. M.
                      Gilbert and N. López-Bigas and C. A. Semple and D. Odom$^*$
                      and S. J. Aitken and M. S. Taylor},
      collaboration = {L. C. E. Consortium},
      othercontributors = {S. Aitken and C. Arnedo-Pac and M. Daunesse and R. M. Drews
                          and A. Ewing and C. Feig and P. Flicek and V. B. Kaiser and
                          E. Kentepozidou and E. López-Arribillaga and M. Lukk and T.
                          F. Rayner and I. Sentís},
      title        = {{S}trand-resolved mutagenicity of {DNA} damage and repair.},
      journal      = {Nature},
      volume       = {630},
      number       = {8017},
      issn         = {0028-0836},
      address      = {London [u.a.]},
      publisher    = {Nature Publ. Group},
      reportid     = {DKFZ-2024-01258},
      pages        = {744-751},
      year         = {2024},
      note         = {2024 Jun;630(8017):744-751},
      abstract     = {DNA base damage is a major source of oncogenic mutations1.
                      Such damage can produce strand-phased mutation patterns and
                      multiallelic variation through the process of lesion
                      segregation2. Here we exploited these properties to reveal
                      how strand-asymmetric processes, such as replication and
                      transcription, shape DNA damage and repair. Despite distinct
                      mechanisms of leading and lagging strand replication3,4, we
                      observe identical fidelity and damage tolerance for both
                      strands. For small alkylation adducts of DNA, our results
                      support a model in which the same translesion polymerase is
                      recruited on-the-fly to both replication strands, starkly
                      contrasting the strand asymmetric tolerance of bulky
                      UV-induced adducts5. The accumulation of multiple distinct
                      mutations at the site of persistent lesions provides the
                      means to quantify the relative efficiency of repair
                      processes genome wide and at single-base resolution. At
                      multiple scales, we show DNA damage-induced mutations are
                      largely shaped by the influence of DNA accessibility on
                      repair efficiency, rather than gradients of DNA damage.
                      Finally, we reveal specific genomic conditions that can
                      actively drive oncogenic mutagenesis by corrupting the
                      fidelity of nucleotide excision repair. These results
                      provide insight into how strand-asymmetric mechanisms
                      underlie the formation, tolerance and repair of DNA damage,
                      thereby shaping cancer genome evolution.},
      cin          = {B400 / B270},
      ddc          = {500},
      cid          = {I:(DE-He78)B400-20160331 / I:(DE-He78)B270-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38867042},
      doi          = {10.1038/s41586-024-07490-1},
      url          = {https://inrepo02.dkfz.de/record/291025},
}