Association of helicobacter pylori infection and chronic atrophic gastritis with risk of colonic, pancreatic and gastric cancer: A ten-year follow-up of the ESTHER cohort study

// Xin-Zu Chen 1, 2, * , Ben Schöttker 2, * , Felipe Andres Castro 2 , Hongda Chen 2 , Yan Zhang 2 , Bernd Holleczek 2, 3 , Hermann Brenner 2, 4 1 Department of Gastrointestinal Surgery, West China Hospital, Sichuan University, Chengdu, China 2 Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany 3 Saarland Cancer Registry, Saarbrücken, Germany 4 German Cancer Consortium (DKTK), Heidelberg, Germany * These authors contributed equally to this work Correspondence to: Hermann Brenner, e-mail: h.brenner@dkfz.de Keywords: helicobacter pylori, chronic atrophic gastritis, colon cancer, pancreatic cancer, gastric cancer Received: November 21, 2015 Accepted: February 09, 2016 Published: March 06, 2016 ABSTRACT Objectives: To assess the association of H. pylori and chronic atrophic gastritis (AG) with colonic, pancreatic and gastric cancer in a population-based prospective cohort. Methods: Serum antibodies against H. pylori in general and specific to cytotoxin-associated gene A (CagA), as well as serum pepsinogen I and II were analyzed in 9,506 men and women, aged 50–75 years in a cohort study from Saarland, Germany. Incident cases of colonic, pancreatic and gastric cancer were ascertained by record linkage with data from the Saarland Cancer Registry. Results: During an average follow-up of 10.6 years, 108 colonic, 46 pancreatic and 27 gastric incident cancers were recorded. There was no association between H. pylori infection and colonic cancer (HR = 1.07; 95% CI 0.73–1.56) or pancreatic cancer (HR = 1.32; 0.73–2.39), regardless of either CagA seropositivity or AG status. In contrast, CagA+ infection was associated with a strongly increased risk of gastric cancer, especially non-cardia gastric cancer, and this association was particularly pronounced in the presence of AG. Compared to people without AG and without CagA+ infection, people with both risk factors had a significantly increased risk of non-cardia gastric cancer (HR = 32.4; 7.6–137.6). Conclusions: This large cohort study did not observe an association of H. pylori infection or AG with colonic or pancreatic cancer, but underlines that the vast majority of non-cardia gastric cancers arise from AG and infection with CagA+ H. pylori strains.