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@ARTICLE{Park:137587,
      author       = {J. Y. Park and H. B. Bueno-de-Mesquita and P. Ferrari and
                      E. Weiderpass and J. de Batlle and A. Tjønneland and C.
                      Kyro and V. Rebours and M.-C. Boutron-Ruault and F. R.
                      Mancini and V. Katzke$^*$ and T. Kühn$^*$ and H. Boeing and
                      A. Trichopoulou and C. La Vecchia and M. Kritikou and G.
                      Masala and V. Pala and R. Tumino and S. Panico and P. H.
                      Peeters and G. Skeie and S. Merino and E. J. Duell and M.
                      Rodríguez-Barranco and M. Dorronsoro and M.-D. Chirlaque
                      and E. Ardanaz and B. Gylling and J. Schneede and U. Ericson
                      and H. Sternby and K.-T. Khaw and K. E. Bradbury and I.
                      Huybrechts and D. Aune and P. Vineis and N. Slimani},
      title        = {{D}ietary folate intake and pancreatic cancer risk:
                      {R}esults from the {E}uropean {P}rospective {I}nvestigation
                      into {C}ancer and {N}utrition.},
      journal      = {International journal of cancer},
      volume       = {144},
      number       = {7},
      issn         = {0020-7136},
      address      = {Bognor Regis},
      publisher    = {Wiley-Liss},
      reportid     = {DKFZ-2018-01467},
      pages        = {1511-1521},
      year         = {2019},
      abstract     = {Pancreatic cancer (PC) has an exceptionally low survival
                      rate and primary prevention strategies are limited. Folate
                      plays an important role in one-carbon metabolism and has
                      been associated with the risk of several cancers, but not
                      consistently with PC risk. We aimed to investigate the
                      association between dietary folate intake and PC risk, using
                      the standardised folate database across 10 European
                      countries. A total of 477,206 participants were followed up
                      for 11 years, during which 865 incident primary PC cases
                      were recorded. Folate intake was energy-adjusted using the
                      residual method. Hazard ratios (HRs) and $95\%$ confidence
                      intervals (CIs) were estimated using Cox proportional
                      hazards models. In multivariable analyses stratified by age,
                      sex, study centre and adjusted for energy intake, smoking
                      status, BMI, educational level, diabetes status, supplement
                      use and dietary fibre intake, we found no significant
                      association between folate intake and PC risk: the HR of PC
                      risk for those in the highest quartile of folate intake
                      (≥353 μg/d) compared with the lowest (<241 μg/d) was
                      0.81 $(95\%$ CI: 0.51, 1.31; Ptrend = 0.38). In current
                      smokers, a positive trend was observed in PC risk across
                      folate quartiles (HR=4.42 $(95\%$ CI: 1.05, 18.62) for
                      ≥353 μg/d vs. <241 μg/d, Ptrend = 0.01). Nonetheless,
                      there was no significant interaction between smoking and
                      dietary folate intake (Pinteraction = 0.99). We found no
                      association between dietary folate intake and PC risk in
                      this large European study. This article is protected by
                      copyright. All rights reserved.},
      cin          = {C020},
      ddc          = {610},
      cid          = {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:30178496},
      doi          = {10.1002/ijc.31830},
      url          = {https://inrepo02.dkfz.de/record/137587},
}