Helicobacter pylori Cytotoxin-Associated Genotype and Gastric Precancerous Lesions (original) (raw)

Helicobacter pylori is a bacterium that colonizes the human stomach and can establish a long-term infection of the gastric mucosa (1). The seroprevalence of H. pylori antibodies is 80%-90% in developing countries (2) but lower in developed countries, especially among later birth cohorts (3). Persistent H. pylori infection often induces gastritis and is associated with the development of peptic ulcer disease, atrophic gastritis, and gastric adenocarcinoma (4). Although gastric adenocarcinoma is one of the most common cancers worldwide, with 930 000 cases per year (5), the absolute risk for this disease is small in comparison to the prevalence of H. pylori infection. Thus, gastric adenocarcinoma can only be a rare outcome of H. pylori infection. This may be due to several factors, such as age at fi rst infection, environmental factors (e.g., diet), and genetic variation in both humans and H. pylori. There is evidence to support the existence of distinct genetic lineages of H. pylori (6), and this genetic variation may play a role in its pathogenicity. Among genes related to pathogenicity, the cytotoxin-associated (cagA) gene and the vacuolating cytotoxin (vacA) genes of H. pylori have been studied most extensively. The cagA gene, which is not present in all strains, is considered to be a marker for the presence of a pathogenicity island of approximately 35 000 bp that encodes a type IV secretion system that transfers the