Circulating plasma phospholipid fatty acids and risk of pancreatic cancer in a large European cohort

  • M. Matejcic
    International Agency for Research on Cancer Lyon France
  • F. Lesueur
    Genetic Epidemiology of Cancer team, Inserm, U900 Paris France
  • C. Biessy
    International Agency for Research on Cancer Lyon France
  • A.L. Renault
    Genetic Epidemiology of Cancer team, Inserm, U900 Paris France
  • N. Mebirouk
    Genetic Epidemiology of Cancer team, Inserm, U900 Paris France
  • S. Yammine
    International Agency for Research on Cancer Lyon France
  • P. Keski‐Rahkonen
    International Agency for Research on Cancer Lyon France
  • K. Li
    International Agency for Research on Cancer Lyon France
  • B. Hémon
    International Agency for Research on Cancer Lyon France
  • E. Weiderpass
    Genetic Epidemiology Group Folkhälsan Research Center Helsinki Finland
  • V. Rebours
    Department of Gastroenterology and Pancreatology Beaujon Hospital, University Paris 7 Clichy France
  • M.C. Boutron‐Ruault
    INSERM, Centre for Research in Epidemiology and Population Health U1018, Health across Generations Team, Institut Gustave Roussy Villejuif France
  • F. Carbonnel
    INSERM, Centre for Research in Epidemiology and Population Health U1018, Health across Generations Team, Institut Gustave Roussy Villejuif France
  • R. Kaaks
    Division of Cancer Epidemiology German Cancer Research Center (DKFZ) Heidelberg Germany
  • V. Katzke
    Division of Cancer Epidemiology German Cancer Research Center (DKFZ) Heidelberg Germany
  • T. Kuhn
    Division of Cancer Epidemiology German Cancer Research Center (DKFZ) Heidelberg Germany
  • H. Boeing
    Epidemiology German Institute of Human Nutrition Potsdam‐Rehbruecke (DIfE) Nuthetal Germany
  • A. Trichopoulou
    Hellenic Health Foundation Athens Greece
  • D. Palli
    Molecular and Nutritional Epidemiology Unit Cancer Research and Prevention Institute – ISPO Florence Italy
  • C. Agnoli
    Epidemiology and Prevention Unit Fondazione IRCCS Istituto Nazionale dei Tumori Milan Italy
  • S. Panico
    Clinical Medicine and Surgery Department Università degli Studi di Napoli Federico II Naples Italy
  • R. Tumino
    Cancer Registry and Histopathology Department ASP "Civic ‐ M.P. Arezzo" Hospital Ragusa Italy
  • C. Sacerdote
    Unit of Cancer Epidemiology, Citta' della Salute e della Scienza Hospital, University of Turin and Centre for Cancer Prevention (CPO) Turin Italy
  • J.R. Quirós
    EPIC Asturias, Public Health Directorate Asturias Spain
  • E.J. Duell
    Unit of Nutrition and Cancer Catalan Institute of Oncology (ICO‐IDIBELL) Barcelona Spain
  • M. Porta
    Hospital del Mar Research Institute – IMIM CIBER Epidemiología y Salud Pública (CIBERESP) and Universitat Autònoma de Barcelona Barcelona Spain
  • M.J. Sánchez
    Escuela Andaluza de Salud Pública. Instituto de Investigación Biosanitaria ibs.GRANADA. Hospitales Universitarios de Granada/Universidad de Granada Granada Spain
  • M.D. Chirlaque
    CIBER in Epidemiology and Public Health (CIBERESP) Madrid Spain
  • A. Barricarte
    CIBER in Epidemiology and Public Health (CIBERESP) Madrid Spain
  • P. Amiano
    Public Health Division of Gipuzkoa BioDonostia Research institute San Sebastian Spain
  • W. Ye
    Department of Medical Epidemiology and Biostatistics Karolinska Institutet Stockholm Sweden
  • P.H. Peeters
    Department of Epidemiology, Julius Center for Health Sciences and Primary Care University Medical Center Utrecht Utrecht The Netherlands
  • K.T. Khaw
    University of Cambridge School of Clinical Medicine Cambridge United Kingdom
  • A. Perez‐Cornago
    Cancer Epidemiology Unit Nuffield Department of Population Health, University of Oxford Oxford United Kingdom
  • T.J. Key
    Cancer Epidemiology Unit Nuffield Department of Population Health, University of Oxford Oxford United Kingdom
  • H.B. Bueno‐de‐Mesquita
    Department of Epidemiology and Biostatistics School of Public Health Imperial College London United Kingdom
  • E. Riboli
    Department of Epidemiology and Biostatistics School of Public Health Imperial College London United Kingdom
  • P. Vineis
    MRC‐PHE Center for Environment and Health School of Public Health Imperial College London United Kingdom
  • I. Romieu
    International Agency for Research on Cancer Lyon France
  • M.J. Gunter
    International Agency for Research on Cancer Lyon France
  • V. Chajès
    International Agency for Research on Cancer Lyon France

抄録

<jats:p>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 (OR<jats:sub>T3‐T1</jats:sub>[odds ratio for highest versus lowest tertile] =0.63; 95%CI[confidence interval] = 0.41–0.98; <jats:italic>p</jats:italic><jats:sub>trend</jats:sub> = 0.036), n‐3 polyunsaturated α‐linolenic acid (OR<jats:sub>T3‐T1</jats:sub> = 0.60; 95%CI = 0.39–0.92; <jats:italic>p</jats:italic><jats:sub>trend</jats:sub> = 0.02) and docosapentaenoic acid (OR<jats:sub>T3‐T1</jats:sub> = 0.52; 95%CI = 0.32–0.85; <jats:italic>p</jats:italic><jats:sub>trend</jats:sub> = 0.008). Industrial trans‐fatty acids were positively associated with pancreatic cancer risk among men (OR<jats:sub>T3‐T1</jats:sub> = 3.00; 95%CI = 1.13–7.99; <jats:italic>p</jats:italic><jats:sub>trend</jats:sub> = 0.029), while conjugated linoleic acids were inversely related to pancreatic cancer among women only (OR<jats:sub>T3‐T1</jats:sub> = 0.37; 95%CI = 0.17–0.81; <jats:italic>p</jats:italic><jats:sub>trend</jats:sub> = 0.008). Among current smokers, the long‐chain n‐6/n‐3 polyunsaturated fatty acids ratio was positively associated with pancreatic cancer risk (OR<jats:sub>T3‐T1</jats:sub> = 3.40; 95%CI = 1.39–8.34; <jats:italic>p</jats:italic><jats:sub>trend</jats:sub> = 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.</jats:p>

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