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@ARTICLE{Weigl:148362,
      author       = {K. Weigl$^*$ and L. Hsu and P. Knebel and M.
                      Hoffmeister$^*$ and M. Timofeeva and S. Farrington and M.
                      Dunlop and H. Brenner$^*$},
      title        = {{H}ead-to-{H}ead {C}omparison of {F}amily {H}istory of
                      {C}olorectal {C}ancer and a {G}enetic {R}isk {S}core for
                      {C}olorectal {C}ancer {R}isk {S}tratification.},
      journal      = {Clinical and translational gastroenterology},
      volume       = {10},
      number       = {12},
      issn         = {2155-384X},
      address      = {London},
      publisher    = {Nature Publ. Group},
      reportid     = {DKFZ-2019-02918},
      pages        = {e00106},
      year         = {2019},
      note         = {EA:C070LA:C0702019 Dec;10(12):e00106},
      abstract     = {Family history (FH) is associated with increased risk of
                      colorectal cancer (CRC). We aimed to examine the potential
                      for CRC risk stratification by known common genetic variants
                      beyond FH in a large population-based case-control study
                      from Germany.Four thousand four hundred forty-seven cases
                      and 3,480 controls recruited in 2003-2016 were included for
                      whom comprehensive interview, medical, and genomic data were
                      available. Associations with CRC risk were estimated from
                      multiple logistic regression models for FH and a genetic
                      risk score (GRS) based on 90 previously identified risk
                      variants.CRC in a first-degree relative was associated with
                      a 1.71-fold $(95\%$ confidence interval 1.47-2.00) increase
                      in CRC risk. A higher risk increase (odds ratio 2.06, $95\%$
                      confidence interval 1.78-2.39) was estimated for the GRS
                      when it was dichotomized at a cutoff yielding the same
                      positivity rate as FH among controls. Furthermore, the GRS
                      provides substantial additional risk stratification in both
                      people with and especially without FH. Equal or even
                      slightly higher risks were observed for participants without
                      FH with a GRS in the upper $20\%$ compared with participants
                      with FH with a GRS below median. The observed patterns were
                      confirmed in a replication study.In contrast to common
                      perception, known genetic variants do not primarily reflect
                      some minor share of the familial excess risk of CRC, but
                      rather reflect a substantial share of risk independent of
                      FH.},
      cin          = {C070 / L101 / C120},
      ddc          = {610},
      cid          = {I:(DE-He78)C070-20160331 / I:(DE-He78)L101-20160331 /
                      I:(DE-He78)C120-20160331},
      pnm          = {313 - Cancer risk factors and prevention (POF3-313)},
      pid          = {G:(DE-HGF)POF3-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31800541},
      doi          = {10.14309/ctg.0000000000000106},
      url          = {https://inrepo02.dkfz.de/record/148362},
}