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@ARTICLE{Tomasova:153793,
      author       = {K. Tomasova and M. Kroupa and A. Forsti$^*$ and P. Vodicka
                      and L. Vodickova},
      title        = {{T}elomere maintenance in interplay with {DNA} repair in
                      pathogenesis and treatment of colorectal cancer.},
      journal      = {Mutagenesis},
      volume       = {35},
      number       = {3},
      issn         = {1464-3804},
      address      = {Oxford},
      publisher    = {Oxford Univ. Press},
      reportid     = {DKFZ-2020-00459},
      pages        = {261-271},
      year         = {2020},
      note         = {2020 Jul 11;35(3):261-271},
      abstract     = {Colorectal cancer (CRC) continues to be one of the leading
                      malignancies and causes of tumour-related deaths worldwide.
                      Both impaired DNA repair mechanisms and disrupted telomere
                      length homeostasis represent key culprits in CRC initiation,
                      progression and prognosis. Mechanistically, altered DNA
                      repair results in the accumulation of mutations in the
                      genome and, ultimately, in genomic instability. DNA repair
                      also determines the response to chemotherapeutics in CRC
                      treatment, suggesting its utilisation in the prediction of
                      therapy response and individual approach to patients.
                      Telomere attrition resulting in replicative senescence,
                      simultaneously by-passing cell cycle checkpoints, is a
                      hallmark of malignant transformation of the cell. Telomerase
                      is almost ubiquitous in advanced solid cancers, including
                      CRC, and its expression is fundamental to cell
                      immortalisation. Therefore, there is a persistent effort to
                      develop therapeutics, which are telomerase-specific and
                      gentle to non-malignant tissues. However, in practice, we
                      are still at the level of clinical trials. The current state
                      of knowledge and the route, which the research takes, gives
                      us a positive perspective that the problem of molecular
                      models of telomerase activation and telomere length
                      stabilisation will finally be solved. We summarise the
                      current literature herein, by pointing out the crosstalk
                      between proteins involved in DNA repair and telomere length
                      homeostasis in relation to CRC.},
      subtyp        = {Review Article},
      cin          = {B062},
      ddc          = {610},
      cid          = {I:(DE-He78)B062-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32083302},
      doi          = {10.1093/mutage/geaa005},
      url          = {https://inrepo02.dkfz.de/record/153793},
}