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@ARTICLE{Bhandari:177482,
      author       = {V. Bhandari and C. H. Li and R. G. Bristow and P. C.
                      Boutros and PCAWGConsortium},
      title        = {{D}ivergent mutational processes distinguish hypoxic and
                      normoxic tumours.},
      journal      = {Nature Communications},
      volume       = {11},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2021-02569},
      pages        = {737},
      year         = {2020},
      note         = {siehe Correction: DKFZ Autoren affiliiert im PCAWG
                      Consortium:https://inrepo02.dkfz.de/record/212440
                      /https://doi.org/10.1038/s41467-022-32339-4},
      abstract     = {Many primary tumours have low levels of molecular oxygen
                      (hypoxia), and hypoxic tumours respond poorly to therapy.
                      Pan-cancer molecular hallmarks of tumour hypoxia remain
                      poorly understood, with limited comprehension of its
                      associations with specific mutational processes, non-coding
                      driver genes and evolutionary features. Here, as part of the
                      ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG)
                      Consortium, which aggregated whole genome sequencing data
                      from 2658 cancers across 38 tumour types, we quantify
                      hypoxia in 1188 tumours spanning 27 cancer types. Elevated
                      hypoxia associates with increased mutational load across
                      cancer types, irrespective of underlying mutational class.
                      The proportion of mutations attributed to several mutational
                      signatures of unknown aetiology directly associates with the
                      level of hypoxia, suggesting underlying mutational processes
                      for these signatures. At the gene level, driver mutations in
                      TP53, MYC and PTEN are enriched in hypoxic tumours, and
                      mutations in PTEN interact with hypoxia to direct tumour
                      evolutionary trajectories. Overall, hypoxia plays a critical
                      role in shaping the genomic and evolutionary landscapes of
                      cancer.},
      keywords     = {Cell Hypoxia: genetics / Genes, myc / Genome, Human /
                      Genomic Structural Variation / Humans / Mutation /
                      Neoplasms: genetics / Neoplasms: pathology / PTEN
                      Phosphohydrolase: genetics / Polymorphism, Single Nucleotide
                      / Tumor Hypoxia: genetics / Tumor Microenvironment: genetics
                      / Tumor Suppressor Protein p53: genetics / Whole Genome
                      Sequencing / TP53 protein, human (NLM Chemicals) / Tumor
                      Suppressor Protein p53 (NLM Chemicals) / PTEN
                      Phosphohydrolase (NLM Chemicals) / PTEN protein, human (NLM
                      Chemicals)},
      cin          = {B080 / B240 / B370 / B330 / HD01 / B060 / B360 / BE01 /
                      B062 / B066 / B063 / W190 / B260 / W610 / B087},
      ddc          = {500},
      cid          = {I:(DE-He78)B080-20160331 / I:(DE-He78)B240-20160331 /
                      I:(DE-He78)B370-20160331 / I:(DE-He78)B330-20160331 /
                      I:(DE-He78)HD01-20160331 / I:(DE-He78)B060-20160331 /
                      I:(DE-He78)B360-20160331 / I:(DE-He78)BE01-20160331 /
                      I:(DE-He78)B062-20160331 / I:(DE-He78)B066-20160331 /
                      I:(DE-He78)B063-20160331 / I:(DE-He78)W190-20160331 /
                      I:(DE-He78)B260-20160331 / I:(DE-He78)W610-20160331 /
                      I:(DE-He78)B087-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32024819},
      pmc          = {pmc:PMC7002770},
      doi          = {10.1038/s41467-019-14052-x},
      url          = {https://inrepo02.dkfz.de/record/177482},
}