Key points are not available for this paper at this time.
Gastric adenocarcinoma is the third leading cause of cancer-related death worldwide, accounting for more than 720,000 deaths annually 1. The strongest known risk factor for this devastating disease is infection with Helicobacter pylori, which drives the development of premalignant lesions (such as gastric atrophy, intestinal metaplasia, and dysplasia) that can lead to gastric cancer (Fig 1). However, although H. pylori is the most common bacterial infection worldwide and colonizes greater than 50% of the global population, only 1%–3% of infected individuals ever develop gastric cancer. Open in a separate window Fig 1 Alterations in the gastric microbiota following Helicobacter pylori infection and gastric disease progression. (A) Schematic representation of the predominant phyla of the gastric microbiota based on H. pylori infection status. H. pylori-negative individuals harbor a microbiota that is more complex and highly diverse compared to H. pylori-positive individuals. (B) Schematic representation of the predominant genera at different stages within the gastric carcinogenesis cascade. Following infection with H. pylori, Proteobacteria and specifically H. pylori dominate the gastric microbiota. This leads to the development of chronic gastritis. In the later stages of the disease, ranging from intestinal metaplasia to gastric adenocarcinoma, a number of genera are enriched. These include Escherichia-Shigella and Burkholderia within the Proteobacteria phylum; Lactobacillus, Lachnospiraceae, Streptococcus, and Veillonella within the Firmicutes phylum; and Prevotella within the Bacteroidetes phylum.
Noto et al. (Thu,) studied this question.