Affiliations 

  • 1 Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden
  • 2 Department of Public Health and Clinical Nutrition, Umeå University, Umeå, Sweden
  • 3 Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden
  • 4 Metabolic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD
  • 5 Unit of Nutrition and Cancer, Cancer Epidemiology Research Program, Catalan Institute of Oncology (ICO-IDIBELL), Barcelona, Spain
  • 6 Department of Public Health, Section for Epidemiology, Aarhus University, Aarhus, Denmark
  • 7 Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany
  • 8 Prevention and Implementation Group, Section of Early Detection and Prevention, Section of Nutrition and Metabolism, International Agency for Research on Cancer, Lyon, France
  • 9 Hellenic Health Foundation, Athens, Greece
  • 10 Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom
  • 11 Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, United Kingdom
  • 12 Translational Research Laboratory, IDIBELL-Catalan Institute of Oncology, Barcelona, Spain
  • 13 Unit of Nutrition and Cancer. Cancer Epidemiology Research Program. Catalan Institute of Oncology-IDIBELL. L'Hospitalet de Llobregat, Barcelona, Spain
  • 14 Epidemiology and Prevention Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Milano, Italy
  • 15 Cancer Risk Factors and Life-Style Epidemiology Unit, Cancer Research and Prevention Institute - ISPO, Florence, Italy
  • 16 Dipartimento di medicina clinica e chirurgia Federico II, Naples, Italy
  • 17 Danish Cancer Society Research Center, Copenhagen, Denmark
  • 18 Andalusian School of Public Health, Instituto De Investigación Biosanitaria Ibs, Granada, Spain
  • 19 Department of Epidemiology, Regional Health Council, IMIB-Arrixaca, Murcia, Spain
  • 20 Department of Epidemiology, Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands
  • 21 Department of Surgery, Institution of Clinical Sciences Malmö, Lund University, Malmö, Sweden
  • 22 Department of Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden
  • 23 Molecular and Genetic Epidemiology Unit, Human Genetics Foundation, Turin, Italy
  • 24 CIBER of Epidemiology and Public Health (CIBERESP), Madrid, Spain
  • 25 Hormones and Women's Health Team, INSERM, Centre for Research in Epidemiology and Population Health (CESP), U1018, Nutrition, Villejuif, F-94805, France
  • 26 Department of Gastroenterology and Pancreatology, Beaujon Hospital, University Paris 7, Clichy, France
  • 27 Université Paris Sud and Gastroenterology Unit, Hôpitaux Universitaires Paris Sud, CHU de Bicêtre, AP-HP, Le Kremlin Bicêtre, France
  • 28 Department for Determinants of Chronic Diseases (DCD), National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands
Int J Cancer, 2017 Apr 15;140(8):1727-1735.
PMID: 28032715 DOI: 10.1002/ijc.30590

Abstract

The association between H. pylori infection and pancreatic cancer risk remains controversial. We conducted a nested case-control study with 448 pancreatic cancer cases and their individually matched control subjects, based on the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, to determine whether there was an altered pancreatic cancer risk associated with H. pylori infection and chronic corpus atrophic gastritis. Conditional logistic regression models were applied to calculate odds ratios (ORs) and corresponding 95% confidence intervals (CIs), adjusted for matching factors and other potential confounders. Our results showed that pancreatic cancer risk was neither associated with H. pylori seropositivity (OR = 0.96; 95% CI: 0.70, 1.31) nor CagA seropositivity (OR = 1.07; 95% CI: 0.77, 1.48). We also did not find any excess risk among individuals seropositive for H. pylori but seronegative for CagA, compared with the group seronegative for both antibodies (OR = 0.94; 95% CI: 0.63, 1.38). However, we found that chronic corpus atrophic gastritis was non-significantly associated with an increased pancreatic cancer risk (OR = 1.35; 95% CI: 0.77, 2.37), and although based on small numbers, the excess risk was particularly marked among individuals seronegative for both H. pylori and CagA (OR = 5.66; 95% CI: 1.59, 20.19, p value for interaction 

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.