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Increased H. pylori stool shedding and EPIYA-D cagA alleles are associated with gastric cancer in an East Asian hospital

Sarah Talarico,Christina K. Leverich,B. Wei,Jie Ma,Xinguang Cao,Yongjun Guo,G. Han,Lena Yao,Steven G. Self,Yuzhou Zhao,N. Salama

Published 2018 in bioRxiv

ABSTRACT

Background Helicobacter pylori infection induces chronic inflammation and tissue damage in the stomach, increasing risk for gastric cancer. Paradoxically, these tissue alterations may promote loss of H. pylori infection during cancer progression. H. pylori’s role in cancer progression beyond initiation is unclear. Geographic variation in gastric cancer risk has been attributed to variation in carriage and type of the H. pylori oncogene cagA. Methods To investigate possible differences in H. pylori load in the stomach and shedding in stool, H. pylori load and cagA genotype were assessed using droplet digital PCR assays on gastric mucosa and stool samples from 49 urea breath test-positive individuals, including 25 gastric cancer and 24 non-cancer subjects at Henan Cancer Hospital, Henan, China. Results Quantitation of H. pylori DNA indicated similar gastric loads among cancer and non-cancer cases, but the gastric cancer group had a median H. pylori load in the stool that was six times higher than that of the non-cancer subjects. While the cagA gene was uniformly present among study subjects, only 70% had the East Asian cagA allele, which was significantly associated with gastric cancer (Fisher’s Exact Test, p = 0.03). Conclusion H. pylori persists in a subset of gastric cancer cases and thus may contribute to cancer progression. In this East Asian population with a high prevalence of the cagA gene, the East Asian allele could still provide a marker for gastric cancer risk. Impact This study contributes to our understanding of H. pylori dynamics in the context of pathological changes.

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