Food Science and Technology Department

 

Authors

Dominique S. Michaud, Brown University & Imperial CollegeFollow
Jacques Izard, The Forsyth Institute & Harvard School of Dental MedicineFollow
Charlotte S. Wilhelm-Benartzi, Imperial College
Doo-Ho You, The Forsyth Institute
Verena A. Grote, German Cancer Research Center (DKFZ)
Anne Tjønneland, Danish Cancer Society
Christina C. Dahm, Aarhus University & Aarhus University Hospital
Kim Overvad, Aarhus University
Mazda Jenab, International Agency for Research on Cancer (IARC-WHO)
Veronika Fedirko, International Agency for Research on Cancer (IARC-WHO)
Marie Christine Boutron-Ruault, Centre for Research in Epidemiology and Population Health & Paris South University
Françoise Clavel- Chapelon, Centre for Research in Epidemiology and Population Health & Paris South University
Antoine Racine, Centre for Research in Epidemiology and Population Health & Paris South University
Rudolf Kaaks, German Cancer Research Center (DKFZ)
Heiner Boeing, German Institute of Human Nutrition Potsdam-Rehbruecke
Jana Foerster, German Institute of Human Nutrition Potsdam-Rehbruecke
Antonia Trichopoulou, University of Athens Medical School & Hellenic Health Foundation
Pagona Lagiou, University of Athens Medical School & Harvard School of Public Health & Academy of Athens
Dimitrios Trichopoulos, Harvard School of Public Health & Academy of Athens
Carlotta Sacerdote, Center for Cancer Prevention (CPO-Piemonte) and Human Genetic Foundation (HuGeF)
Sabina Sieri, Fondazione IRCCS Istituto Nazionale dei Tumori
Domenico Palli, ISPO- Cancer Research and Prevention Institute
Rosario Tumino, "Civile - M.P.Arezzo" Hospital
Salvatore Panico, University Medical Centre Utrecht (UMCU)
Peter Siersema, University Medical Centre Utrecht (UMCU)
Petra HM Peeters, University Medical Center Utrecht
Eiliv Lund, University of Tromsø
Aurelio Barricarte, Public Health Institute of Navarra & CIBER Epidemiología y Salud Pública (CIBERESP)
José-María Huerta, CIBER Epidemiología y Salud Pública (CIBERESP) & Murcia Regional Health Authority
Esther Molina-Montes, CIBER Epidemiología y Salud Pública (CIBERESP) & Andalusian School of Public Health
Miren Dorronsoro, Basque Regional Health Department
J. Ramón Quirós, Health and Health Care Services Council
Eric J. Duell, Catalan Institute of Oncology (ICO-IDIBELL)
Weimin Ye, Karolinska Institutet & The Medical Biobank at Umeå University
Malin Sund, Umeå University
Björn Lindkvist, University of Gothenburg
Dorthe Johansen, Skåne University Hospital
Kay-Tee Khaw, University of Cambridge
Nick Wareham, MRC Epidemiology Unit,
Ruth C. Travis, University of Oxford
Paolo Vineis, Imperial College London
H. Bas Bueno-de-Mesquita, University Medical Centre Utrecht (UMCU) & National Institute for Public Health and the Environment (RIVM)
Elio Riboli, Imperial College London

Date of this Version

12-1-2014

Citation

Gut. 2013 December ; 62(12): . doi:10.1136/gutjnl-2012-303006.

Abstract

Objective—Examine the relationship between antibodies to 25 oral bacteria and pancreatic cancer risk in a prospective cohort study.

Design—We measured antibodies to oral bacteria in prediagnosis blood samples from 405 pancreatic cancer cases and 416 matched controls, nested within the European Prospective Investigation into Cancer and Nutrition study (EPIC). Analyses were conducted using conditional logistic regression and additionally adjusted for smoking status and body mass index.

Results—Individuals with high levels of antibodies against Porphyromonas gingivalis ATTC 53978, a pathogenic periodontal bacteria, had a 2-fold higher risk of pancreatic cancer than individuals lower levels of these antibodies (odds ratio [OR], 2.14; 95% confidence interval [CI], 1.05–4.36; >200 ng/ml vs ≤200 ng/ml). To explore the association with commensal (nonpathogenic) oral bacteria, we performed a cluster analysis and identified 2 groups of individuals, based on their antibody profiles. A cluster with overall higher levels of antibodies had a 45% lower risk of pancreatic cancer than a cluster with overall lower levels of antibodies (OR, 0.55; 95% CI, 0.36–0.83).

Conclusion—Periodontal disease might increase the risk for pancreatic cancer. Moreover, increased levels of antibodies against specific commensal oral bacteria, which can inhibit growth of pathogenic bacteria, might reduce the risk of pancreatic cancer. Studies are needed to determine whether oral bacteria have direct effects on pancreatic cancer pathogenesis or serve as markers of the immune response.

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