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Updated: Sep 27, 2026

Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer
Published on: September 18, 2020
Gastric Microbiota from Populations with High Risk of Gastric Cancer in Nariño, Colombia
Siomy Portilla1,2, Alvaro Pazos1,2, Vanessa Pabón2,3
1Department of Biology, Faculty of Exact and Natural Sciences, University of Nariño, Pasto 520002, Colombia.
Abstract:
Gastric cancer is a major cause of cancer mortality in Colombia, particularly in the Andean region of Nariño. Helicobacter pylori is the main etiological factor, but its oncogenic potential depends on bacterial variability, host susceptibility, and interactions with the gastric microbiota. This study evaluated the composition and diversity of the gastric microbiota in patients with preneoplastic lesions. Gastric biopsies from 30 patients (24 with non-atrophic gastritis (NAG); 6 with atrophic gastritis and intestinal metaplasia (AGIM)) were analyzed by full-length 16S rRNA gene sequencing using Oxford Nanopore MinION. Taxonomic classification was performed with Kraken and SILVA v132. Alpha and beta diversity were analyzed in R, and differential abundance was assessed using ANCOM-BC2 and DESeq2. Sequencing generated 532,734 high-quality reads, from which 912 genera across 46 phyla were identified. Proteobacteria, Campylobacterota, and Actinobacteriota predominated, with Helicobacter, Pseudomonas, and Cutibacterium as the most abundant genera. Helicobacter abundance, rather than lesion type, significantly influenced community structure. High Helicobacter abundance was associated with greater alpha diversity and distinct beta diversity. No significant differences were observed between NAG and AGIM. Prevotella and Alteromonas were enriched in AGIM, whereas Pseudomonas increased approximately 64-fold in samples with low Helicobacter abundance. These findings indicate that Helicobacter abundance was significantly associated with differences in gastric microbial community structure, suggesting that microbial interactions may contribute to early gastric carcinogenesis.
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