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      author       = {A.-L. Mayén and E. K. Aglago and V. Knaze and R. Cordova
                      and C. G. Schalkwijk and K.-H. Wagner and K. Aleksandrova
                      and V. Fedirko and P. Keski-Rahkonen and M. F. Leitzmann and
                      V. Katzke$^*$ and B. Srour$^*$ and M. B. Schulze and G.
                      Masala and V. Krogh and S. Panico and R. Tumino and B.
                      Bueno-de-Mesquita and M. Brustad and A. Agudo and M. D.
                      Chirlaque López and P. Amiano and B. Ohlsson and S. Ramne
                      and D. Aune and E. Weiderpass and M. Jenab and H. Freisling},
      title        = {{D}ietary intake of advanced glycation endproducts and risk
                      of hepatobiliary cancers: {A} multinational cohort study.},
      journal      = {International journal of cancer},
      volume       = {149},
      number       = {4},
      issn         = {0020-7136},
      address      = {Bognor Regis},
      publisher    = {Wiley-Liss},
      reportid     = {DKFZ-2021-01098},
      pages        = {854-864},
      year         = {2021},
      note         = {2021 Apr 25;149(4):854-864},
      abstract     = {Advanced glycation endproducts (AGEs) may contribute to
                      liver carcinogenesis because of their proinflammatory and
                      prooxidative properties. Diet is a major source of AGEs, but
                      there is sparse human evidence on the role of AGEs intake in
                      liver cancer etiology. We examined the association between
                      dietary AGEs and the risk of hepatobiliary cancers in the
                      European Prospective Investigation into Cancer and Nutrition
                      prospective cohort (n = 450 111). Dietary intake of three
                      AGEs, Nε -[carboxymethyl]lysine (CML), Nε
                      -[1-carboxyethyl]lysine (CEL) and Nδ
                      -[5-hydro-5-methyl-4-imidazolon-2-yl]-ornithine (MG-H1), was
                      estimated using country-specific dietary questionnaires
                      linked to an AGEs database. Cause-specific hazard ratios
                      (HR) and their $95\%$ confidence intervals (CI) for
                      associations between dietary AGEs and risk of hepatocellular
                      carcinoma (HCC), gallbladder and biliary tract cancers were
                      estimated using multivariable Cox proportional hazard
                      regression. After a median follow-up time of 14.9 years, 255
                      cases of HCC, 100 cases of gallbladder cancer and 173
                      biliary tract cancers were ascertained. Higher intakes of
                      dietary AGEs were inversely associated with the risk of HCC
                      (per 1 SD increment, HR-CML  = 0.87, $95\%$ CI: 0.76-0.99,
                      HR-CEL  = 0.84, $95\%$ CI: 0.74-0.96 and HR-MH-G1
                       = 0.84, $95\%$ CI: 0.74-0.97). In contrast, positive
                      associations were observed with risk of gallbladder cancer
                      (per 1 SD, HR-CML  = 1.28, $95\%$ CI: 1.05-1.56, HR-CEL
                       = 1.17; $95\%$ CI: 0.96-1.40, HR-MH-G1  = 1.27, $95\%$
                      CI: 1.06-1.54). No associations were observed for cancers of
                      the intra and extrahepatic bile ducts. Our findings suggest
                      that higher intakes of dietary AGEs are inversely associated
                      with the risk of HCC and positively associated with the risk
                      of gallbladder cancer.},
      keywords     = {EPIC study (Other) / advanced glycation endproducts (Other)
                      / bile duct cancers (Other) / gallbladder cancer (Other) /
                      hepatocellular carcinoma (Other)},
      cin          = {C020},
      ddc          = {610},
      cid          = {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:33899229},
      doi          = {10.1002/ijc.33612},
      url          = {https://inrepo02.dkfz.de/record/168847},