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@ARTICLE{Ahmad:212514,
      author       = {O. Ahmad$^*$ and A. Försti$^*$},
      title        = {{T}he complementary roles of genome-wide approaches in
                      identifying genes linked to an inherited risk of colorectal
                      cancer.},
      journal      = {Hereditary cancer in clinical practice},
      volume       = {21},
      number       = {1},
      issn         = {1731-2302},
      address      = {Heidelberg},
      publisher    = {Springer},
      reportid     = {DKFZ-2023-00199},
      pages        = {1},
      year         = {2023},
      note         = {#LA:B062#EA:B062#},
      abstract     = {The current understanding of the inherited risk of
                      colorectal cancer (CRC) started with an observational
                      clinical era in the late 19th century, which was followed by
                      a genetic era starting in the late 20th century. Genome-wide
                      linkage analysis allowed mapping several high-risk genes,
                      which marked the beginning of the genetic era. The current
                      high-throughput genomic phase includes genome-wide
                      association study (GWAS) and genome-wide sequencing
                      approaches which have revolutionized the conception of the
                      inherited risk of CRC. On the one hand, GWAS has allowed the
                      identification of multiple low risk loci correlated with
                      CRC. On the other, genome-wide sequencing has led to the
                      discovery of a second batch of high-to-moderate-risk genes
                      that correlate to atypical familial CRC and polyposis
                      syndromes. In contrast to other common cancers, which are
                      usually dominated by a polygenic background, CRC risk is
                      believed to be equally explained by monogenic and polygenic
                      architectures, which jointly contribute to a quarter of
                      familial clustering. Despite the fact that genome-wide
                      approaches have allowed the identification of a continuum of
                      responsible high-to-moderate-to-low-risk variants, much of
                      the predisposition and familial clustering of CRC has not
                      yet been explained. Other genetic, epigenetic and
                      environmental factors might be playing important roles as
                      well. In this review we aim to provide insights on the
                      complementary roles played by different genomic approaches
                      in allowing the current understanding of the genetic
                      architecture of inherited CRC.},
      subtyp        = {Review Article},
      keywords     = {CRC (Other) / Cancer predisposition (Other) / GWAS (Other)
                      / Genome-wide (Other) / High-risk gene (Other) / Inherited
                      Cancer (Other) / Low-risk gene (Other) / WGS (Other)},
      cin          = {B062 / HD01},
      ddc          = {610},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)HD01-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36707860},
      pmc          = {pmc:PMC9883872},
      doi          = {10.1186/s13053-023-00245-5},
      url          = {https://inrepo02.dkfz.de/record/212514},
}