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@ARTICLE{Wang:143174,
      author       = {X. Wang and J. Y. Dai and D. Albanes and V. Arndt$^*$ and
                      S. I. Berndt and S. Bézieau and H. Brenner$^*$ and D. D.
                      Buchanan and K. Butterbach$^*$ and B. Caan and G. Casey and
                      P. T. Campbell and A. T. Chan and Z. Chen and J.
                      Chang-Claude$^*$ and M. Cotterchio and D. F. Easton and G.
                      G. Giles and E. Giovannucci and W. M. Grady and M.
                      Hoffmeister$^*$ and J. L. Hopper and L. Hsu and M. A.
                      Jenkins and A. D. Joshi and J. W. Lampe and S. C. Larsson
                      and F. Lejbkowicz and L. Li and A. Lindblom and L. Le
                      Marchand and V. Martin and R. L. Milne and V. Moreno and P.
                      A. Newcomb and K. Offitt and S. Ogino and P. D. P. Pharoah
                      and M. Pinchev and J. D. Potter and H. S. Rennert and G.
                      Rennert and W. Saliba and C. Schafmayer and R. E. Schoen and
                      P. Schrotz-King$^*$ and M. L. Slattery and M. Song and C.
                      Stegmaier and S. J. Weinstein and A. Wolk and M. O. Woods
                      and A. H. Wu and S. B. Gruber and U. Peters and E. White},
      title        = {{M}endelian randomization analysis of {C}-reactive protein
                      on colorectal cancer risk.},
      journal      = {International journal of epidemiology},
      volume       = {48},
      number       = {3},
      issn         = {1464-3685},
      address      = {Oxford},
      publisher    = {Oxford Univ. Press},
      reportid     = {DKFZ-2019-00773},
      pages        = {767-780},
      year         = {2019},
      abstract     = {Chronic inflammation is a risk factor for colorectal cancer
                      (CRC). Circulating C-reactive protein (CRP) is also
                      moderately associated with CRC risk. However, observational
                      studies are susceptible to unmeasured confounding or reverse
                      causality. Using genetic risk variants as instrumental
                      variables, we investigated the causal relationship between
                      genetically elevated CRP concentration and CRC risk, using a
                      Mendelian randomization approach.Individual-level data from
                      30 480 CRC cases and 22 844 controls from 33 participating
                      studies in three international consortia were used: the
                      Genetics and Epidemiology of Colorectal Cancer Consortium
                      (GECCO), the Colorectal Transdisciplinary Study (CORECT) and
                      the Colon Cancer Family Registry (CCFR). As instrumental
                      variables, we included 19 single nucleotide polymorphisms
                      (SNPs) previously associated with CRP concentration. The
                      SNP-CRC associations were estimated using a logistic
                      regression model adjusted for age, sex, principal components
                      and genotyping phases. An inverse-variance weighted method
                      was applied to estimate the causal effect of CRP on CRC
                      risk.Among the 19 CRP-associated SNPs, rs1260326 and
                      rs6734238 were significantly associated with CRC risk
                      (P = 7.5 × 10-4, and P = 0.003, respectively).
                      A genetically predicted one-unit increase in the
                      log-transformed CRP concentrations (mg/l) was not associated
                      with increased risk of CRC [odds ratio (OR) = 1.04;
                      $95\%$ confidence interval (CI): 0.97, 1.12; P = 0.256).
                      No evidence of association was observed in subgroup analyses
                      stratified by other risk factors.In spite of adequate
                      statistical power to detect moderate association, we found
                      genetically elevated CRP concentration was not associated
                      with increased risk of CRC among individuals of European
                      ancestry. Our findings suggested that circulating CRP is
                      unlikely to be a causal factor in CRC development.},
      cin          = {C070 / C120 / C020},
      ddc          = {610},
      cid          = {I:(DE-He78)C070-20160331 / I:(DE-He78)C120-20160331 /
                      I:(DE-He78)C020-20160331},
      pnm          = {313 - Cancer risk factors and prevention (POF3-313)},
      pid          = {G:(DE-HGF)POF3-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30476131},
      doi          = {10.1093/ije/dyy244},
      url          = {https://inrepo02.dkfz.de/record/143174},
}