Research Papers:

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, Ben Schöttker, Felipe Andres Castro, Hongda Chen, Yan Zhang, Bernd Holleczek and Hermann Brenner _

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Oncotarget. 2016; 7:17182-17193. https://doi.org/10.18632/oncotarget.7946

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Xin-Zu Chen1,2,*, Ben Schöttker2,*, Felipe Andres Castro2, Hongda Chen2, Yan Zhang2, Bernd Holleczek2,3, Hermann Brenner2,4

1Department of Gastrointestinal Surgery, West China Hospital, Sichuan University, Chengdu, China

2Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany

3Saarland Cancer Registry, Saarbrücken, Germany

4German 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


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.

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