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@ARTICLE{King:277102,
      author       = {S. D. King and S. Veliginti and M. C. G. J. Brouwers and Z.
                      Ren and W. Zheng and V. W. Setiawan and L. R. Wilkens and
                      X.-O. Shu and A. A. Arslan and L. E. Beane Freeman and P. M.
                      Bracci and F. Canzian$^*$ and M. Du and S. J. Gallinger and
                      G. G. Giles and P. J. Goodman and C. A. Haiman and M.
                      Kogevinas and C. Kooperberg and L. Le Marchand and R. E.
                      Neale and K. Visvanathan and E. White and D. Albanes and G.
                      Andreotti and A. Babic and S. I. Berndt and L. K. Brais and
                      P. Brennan and J. E. Buring and K. G. Rabe and W. R. Bamlet
                      and S. J. Chanock and C. S. Fuchs and J. M. Gaziano and E.
                      L. Giovannucci and T. Hackert and M. M. Hassan and V.
                      Katzke$^*$ and R. C. Kurtz and I.-M. Lee and N. Malats and
                      N. Murphy and A. L. Oberg and I. Orlow and M. Porta and F.
                      X. Real and N. Rothman and H. D. Sesso and D. T. Silverman
                      and I. M. Thompson and J. Wactawski-Wende and X. Wang and N.
                      Wentzensen and H. Yu and A. Zeleniuch-Jacquotte and K. Yu
                      and B. M. Wolpin and E. J. Duell and D. Li and R. J. Hung
                      and S. Perdomo and M. L. McCullough and N. D. Freedman and
                      A. V. Patel and U. Peters and E. Riboli and M. Sund and A.
                      Tjønneland and J. Zhong and S. K. Van Den Eeden and P.
                      Kraft and H. A. Risch and L. T. Amundadottir and A. P. Klein
                      and R. Z. Stolzenberg-Solomon and S. O. Antwi},
      title        = {{G}enetic susceptibility to nonalcoholic fatty liver
                      disease and risk for pancreatic cancer: {M}endelian
                      randomization.},
      journal      = {Cancer epidemiology, biomarkers $\&$ prevention},
      volume       = {32},
      number       = {9},
      issn         = {1055-9965},
      address      = {Philadelphia, Pa.},
      publisher    = {AACR},
      reportid     = {DKFZ-2023-01267},
      pages        = {1265-1269},
      year         = {2023},
      note         = {2023 Sep 1;32(9):1265-1269},
      abstract     = {There are conflicting data on whether nonalcoholic fatty
                      liver disease (NAFLD) is associated with susceptibility to
                      pancreatic cancer (PC). Using Mendelian randomization (MR),
                      we investigated the relationship between genetic
                      predisposition to NAFLD and risk for PC.Data from
                      genome-wide association studies within the Pancreatic Cancer
                      Cohort Consortium (PanScan; cases n=5090, controls n=8733)
                      and the Pancreatic Cancer Case Control Consortium (PanC4;
                      cases n=4,163, controls n=3,792) were analyzed. We used data
                      on 68 genetic variants with four different MR methods
                      (inverse variance weighting [IVW], MR-Egger, simple median,
                      and penalized weighted median) separately to predict genetic
                      heritability of NAFLD. We then assessed the relationship
                      between each of the four MR methods and PC risk, using
                      logistic regression to calculate odds ratios (ORs) and
                      $95\%$ confidence intervals (CIs), adjusting for PC risk
                      factors, including obesity and diabetes.No association was
                      found between genetically predicted NAFLD and PC risk in the
                      PanScan or PanC4 samples (e.g., PanScan, IVW OR=1.04, $95\%$
                      CI: 0.88-1.22, MR-Egger OR=0.89, $95\%$ CI: 0.65-1.21;
                      PanC4, IVW OR=1.07, $95\%$ CI: 0.90-1.27, MR-Egger OR=0.93,
                      $95\%$ CI: 0.67-1.28). None of the four MR methods indicated
                      an association between genetically predicted NAFLD and PC
                      risk in either sample.Genetic predisposition to NAFLD is not
                      associated with PC risk.Given the close relationship between
                      NAFLD and metabolic conditions, it is plausible that any
                      association between NAFLD and PC might reflect host
                      metabolic perturbations (e.g., obesity, diabetes, or
                      metabolic syndrome) and does not necessarily reflect a
                      causal relationship between NAFLD and PC.},
      cin          = {C055 / C020},
      ddc          = {610},
      cid          = {I:(DE-He78)C055-20160331 / 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:37351909},
      doi          = {10.1158/1055-9965.EPI-23-0453},
      url          = {https://inrepo02.dkfz.de/record/277102},
}