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@ARTICLE{Chen:167736,
      author       = {X. Chen$^*$ and L. Jansen$^*$ and F. Guo$^*$ and M.
                      Hoffmeister$^*$ and J. Chang-Claude$^*$ and H. Brenner$^*$},
      title        = {{S}moking, {G}enetic {P}redisposition, and {C}olorectal
                      {C}ancer {R}isk.},
      journal      = {Clinical and translational gastroenterology},
      volume       = {12},
      number       = {3},
      issn         = {2155-384X},
      address      = {London},
      publisher    = {Nature Publ. Group},
      reportid     = {DKFZ-2021-00502},
      pages        = {e00317},
      year         = {2021},
      note         = {#EA:C070#LA:C070#2021 Mar 1;12(3):e00317},
      abstract     = {Smoking and genetic predisposition are established risk
                      factors for colorectal cancer (CRC). We aimed to assess and
                      compare their individual and joint impact on CRC risk using
                      the novel approach of genetic risk equivalent (GRE).Data
                      were extracted from the Darmkrebs: Chancen der Verhütung
                      durch Screening study, a large population-based case-control
                      study in Germany. A polygenic risk score (PRS) based on 140
                      CRC-related single nucleotide polymorphisms was derived to
                      quantify genetic risk. Multiple logistic regression was used
                      to estimate the individual and joint impact of smoking and
                      PRS on CRC risk, and to quantify the smoking effect in terms
                      of GRE, the corresponding effect conveyed by a defined
                      difference in PRS percentiles.There were 5,086 patients with
                      CRC and 4,120 controls included. Current smokers had a
                      $48\%$ higher risk of CRC than never smokers (adjusted odds
                      ratio 1.48, $95\%$ confidence interval 1.27-1.72). A PRS
                      above the 90th percentile was significantly associated with
                      a 3.6-, 4.3-, and 6.4-fold increased risk of CRC in never,
                      former, and current smokers, respectively, when compared
                      with a PRS below the 10th percentile in never smokers. The
                      interaction between smoking and PRS on CRC risk did not
                      reach statistical significance (P = 0.53). The effect of
                      smoking was equivalent to the effect of having a 30
                      percentile higher level of PRS (GRE 30, $95\%$ confidence
                      interval 18-42).Both smoking and the PRS carry essentially
                      independent CRC risk information, and their joint
                      consideration provides powerful risk stratification.
                      Abstinence from smoking can compensate for a substantial
                      proportion of genetically determined CRC risk.},
      cin          = {HD01 / C070 / C120 / M110 / C020},
      ddc          = {610},
      cid          = {I:(DE-He78)HD01-20160331 / I:(DE-He78)C070-20160331 /
                      I:(DE-He78)C120-20160331 / I:(DE-He78)M110-20160331 /
                      I:(DE-He78)C020-20160331},
      pnm          = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
      pid          = {G:(DE-HGF)POF4-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33646204},
      doi          = {10.14309/ctg.0000000000000317},
      url          = {https://inrepo02.dkfz.de/record/167736},
}