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. 2016 Mar 29;7(13):17182-93.
doi: 10.18632/oncotarget.7946.

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
Affiliations

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 et al. Oncotarget. .

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.

Keywords: chronic atrophic gastritis; colon cancer; gastric cancer; helicobacter pylori; pancreatic cancer.

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Conflict of interest statement

CONFLICTS OF INTEREST

None declared.

Figures

Figure 1
Figure 1. Crude incidence rate (per 100,000 person-years) of gastric, colonic and pancreatic cancer by H. pylori infection and CagA serostatus at baseline
Figure 2
Figure 2. Incidence of cancer by H. pylori IgG and CagA serostatus
Kaplan-Meier curves and Log-rank test of the incidence of (A) gastric, (B) colonic and (C) pancreatic cancer. Significant differences were observed for gastric cancer incidence in comparisons of virulent strains to non-infected (p < 0.0001), and virulent strains to non-virulent strains (p = 0.003), but not in non-virulent strains to non-infected (p = 0.686). No significant differences were observed for colonic and pancreatic cancer incidence (p > 0.05).
Figure 3
Figure 3. Flow chart for selection of the study population
See this image and copyright information in PMC

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