VIRULENCE GENES OF H. PYLORI IN GASTRIC CANCER

摘要

Gastric intestinal metaplasia and gastric cancer are associated with Helicobacter pylori, but the bacterium often is undetectable in these lesions. To unravel this apparent paradox, intestinal metaplasia, H. pylori presence and the expression of H. pylori virulence genes were quantified concurrently using histology, in situ hybridization and immunohistochemistry. H. pylori was detected inside metaplastic, dysplastic, and neoplastic epithelial cells, and cagA and babA2 expression was co-localized. Expression of cagA was significantly higher in patients with IM and adenocarcinoma than in controls. The preneoplastic "acidic" MUC2 mucin was detected only in the presence of H. pylori, and MUC2 expression was higher in 1M, dysplasia and cancer. These findings are compatible with the view that all stages of gastric carcinogenesis are fostered by persistent intracellular expression of H. pylori virulence genes, and especially cagA, inside MUC2-producing precancerous gastric cells and pleomorphic cancer cells. The invention further relates to virulence genes of H. pylori such as, but not limited to, an invA or invE gene, portions thereof, and sequences that hybridize or 15 are complementary with, the invA or invE gene. The gene may be isolated or produced recombinantly and used to create expressed product for the treatment and/or prevention of H. pylori infection.