P-246 Comparison of microbiome diversity in gastric cancer patients and in non-cancerous patients

Abstract

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 Heliobacter pylori infection. H.pylori-induced gastritis reduces acid secretion from gastric mucosa and causes atrophic gastritis and intestinal metaplasia, which are known to be pre-cancerous lesions. According to previous studies, H.pylori is rarely detected in atrophic mucosa or in mucosa with intestinal metaplasia. This suggests that the hypochlorhydric conditions created by H.pylori provide a suitable environment for carcinogenesis, rather than H.pylori working as the direct carcinogen itself. This raises the possibility that bacteria other than H.pylori could contribute to carcinogenesis of gastric cancer. The aim of the present study was to compare the composition of the gastric microbiome of advanced gastric cancer patients and non-cancerous individuals. Gastric mucosa collected by biopsy during esophagogastroduodenoscopy (EGD) from seven patients with advanced gastric cancer (AGC) and six non-cancerous patients (control group) was evaluated. Gastric biopsies were obtained from the margin of cancer in cancer patients. In the control group, biopsies were done from antrum with normal mucosal morphology. DNA was extracted from the gastric mucosal tissues and 16s rRNA genes were amplified from the isolated DNA. Then they were analyzed using the molecular profiling approach terminal restriction fragment length polymorphism (T-RFLP). Cloning and sequencing of 16S rRNA genes was performed to discover the identities of bacteria residing in the gastric mucosa. A higher number of species were detected in the control group, with an average of 102 species, compared to the cancer group, with an average of 72 species. The gastric cancer microbiome was characterized by reduced microbial diversity compared to that of the control group. Many different bacterial species were found in both groups but distribution was quite different between the two groups. Fusobacteria was more dominant in the cancer group and Rhodobacterales was found more prominent in the control group. Gastric H.pylori was detected only in one patient from each group. A more diverse gastric microbiome was observed in non-cancerous patients and the composition of species was different between the two groups. These results suggest that microbial dysbiosis may be involved in gastric carcinogenesis, but it is not yet clear that microbial transition accelerates carcinogenesis. Further studies should include a more detailed analysis of the spatial and temporal composition of the gastric microbiome. A better understanding of microbial differences and changes in healthy and gastric cancer patients could verify the carcinogenesis of gastric cancer.