Analysis of the gastric microbiome in gastric cancer patients and in non-tumorous patients

Abstract

Background: Gastric cancer is the fifth most common cancer worldwide and it is the most commonly diagnosed cancer in Korea. The most clearly known microbiologic risk factor is Helicobacter pylori infection. Chronic inflammation of gastric mucosa accelerates a cascade of chronic active gastritis, multifocal atrophy intestinal metaplasia, gastric dysplasia and gastric adenocarcinoma. Studies proved H. pylori reduces microbial diversity, but it is reversible with H. pylori eradication. Thus, we could assume gastric carcinogenesis may not solely depend on H. pylori. In this study, we analyzed and compared gastric microbiome in gastric cancer patients and non-cancer patients to find changes between the two groups. Additionally, we analyzed microbial diversity of cancerous lesions and para-cancerous lesions in the cancer group in an effort to reveal the role of microbiome in carcinogenesis.

Methods: Gastric mucosa collected by biopsy during esophagogastroduodenoscopy (EGD) from 10 patients with gastric cancer and 18 non-cancer patients. Gastric biopsies were obtained from the margin of cancer and para-cancerous lesions in cancer patients. In control group, samples were obtained from antrum with normal mucosal morphology. DNA was extracted from the gastric mucosal tissues and 16s rRNA genes were amplified. Then they were analyzed by microbiome analysis program.

Results: Higher number of species was detected in the control group (average of 97.75 species) compared to the cancer group (average of 73.4 species). The gastric cancer microbiome was showed reduced microbial diversity compared to that of control group. Fusobacteria was more dominant in cancer group and Rhodobacterales was found more prominent in control group. We compared microbial diversity of the cancer lesion and the para-cancerous lesion within the cancer group and higher number of species was detected in non-tumorous lesion.

Conclusions: Gastric microbiome of non-tumorous patients was more diverse and the composition of species was different between the two groups. These results suggest that microbial dysbiosis may be involved in gastric carcinogenesis. Further studies should include more detailed analysis of spatial and temporal composition and the comparison between different pathologic types and tumor location are necessary. Better understanding of microbial differences and changes in healthy and gastric cancer patients could verify the carcinogenesis of gastric cancer.