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@ARTICLE{Matejcic:142089,
      author       = {M. Matejcic and F. Lesueur and C. Biessy and A. L. Renault
                      and N. Mebirouk and S. Yammine and P. Keski-Rahkonen and K.
                      Li and B. Hémon and E. Weiderpass and V. Rebours and M. C.
                      Boutron-Ruault and F. Carbonnel and R. Kaaks$^*$ and V.
                      Katzke$^*$ and T. Kuhn$^*$ and H. Boeing and A. Trichopoulou
                      and D. Palli and C. Agnoli and S. Panico and R. Tumino and
                      C. Sacerdote and J. R. Quirós and E. J. Duell and M. Porta
                      and M. J. Sánchez and M. D. Chirlaque and A. Barricarte and
                      P. Amiano and W. Ye and P. H. Peeters and K. T. Khaw and A.
                      Perez-Cornago and T. J. Key and H. B. Bueno-de-Mesquita and
                      E. Riboli and P. Vineis and I. Romieu and M. J. Gunter and
                      V. Chajès},
      title        = {{C}irculating plasma phospholipid fatty acids and risk of
                      pancreatic cancer in a large {E}uropean cohort.},
      journal      = {International journal of cancer},
      volume       = {143},
      number       = {10},
      issn         = {0020-7136},
      address      = {Bognor Regis},
      publisher    = {Wiley-Liss},
      reportid     = {DKFZ-2018-02319},
      pages        = {2437 - 2448},
      year         = {2018},
      abstract     = {There are both limited and conflicting data on the role of
                      dietary fat and specific fatty acids in the development of
                      pancreatic cancer. In this study, we investigated the
                      association between plasma phospholipid fatty acids and
                      pancreatic cancer risk in the European Prospective
                      Investigation into Cancer and Nutrition (EPIC) cohort. The
                      fatty acid composition was measured by gas chromatography in
                      plasma samples collected at recruitment from375 incident
                      pancreatic cancer cases and375 matched controls.
                      Associations of specific fatty acids with pancreatic cancer
                      risk were evaluated using multivariable conditional logistic
                      regression models with adjustment for established pancreatic
                      cancer risk factors. Statistically significant inverse
                      associations were found between pancreatic cancer incidence
                      and levels of heptadecanoic acid (ORT3-T1 [odds ratio for
                      highest versus lowest tertile] =0.63; $95\%CI[confidence$
                      interval] = 0.41-0.98; ptrend = 0.036), n-3 polyunsaturated
                      α-linolenic acid (ORT3-T1 = 0.60; $95\%CI$ = 0.39-0.92;
                      ptrend = 0.02) and docosapentaenoic acid (ORT3-T1 = 0.52;
                      $95\%CI$ = 0.32-0.85; ptrend = 0.008). Industrial
                      trans-fatty acids were positively associated with pancreatic
                      cancer risk among men (ORT3-T1 = 3.00; $95\%CI$ = 1.13-7.99;
                      ptrend = 0.029), while conjugated linoleic acids were
                      inversely related to pancreatic cancer among women only
                      (ORT3-T1 = 0.37; $95\%CI$ = 0.17-0.81; ptrend = 0.008).
                      Among current smokers, the long-chain n-6/n-3
                      polyunsaturated fatty acids ratio was positively associated
                      with pancreatic cancer risk (ORT3-T1 = 3.40; $95\%CI$ =
                      1.39-8.34; ptrend = 0.007). Results were robust to a range
                      of sensitivity analyses. Our findings suggest that higher
                      circulating levels of saturated fatty acids with an odd
                      number of carbon atoms and n-3 polyunsaturated fatty acids
                      may be related to lower risk of pancreatic cancer. The
                      influence of some fatty acids on the development of
                      pancreatic cancer may be sex-specific and modulated by
                      smoking.},
      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:30110135},
      doi          = {10.1002/ijc.31797},
      url          = {https://inrepo02.dkfz.de/record/142089},
}