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- Helicobacter pylori infection
- matrix metalloproteinase
- helicobacter pylori - pathogenesis
- bacterial pathogenesis
- gastric cancer
The attributable risk of gastric cancer conferred by Helicobacter pylori ranges from 75% to more than 90% depending on H pylori prevalence; however, only a fraction of colonised persons ever develop neoplasia.1 2 Disease risk involves well-choreographed interactions between pathogen and host, which are dependent upon strain-specific bacterial factors as well as host genotypic traits, each of which can be amplified by the environment. In their paper published in Gut, Kwon et al provide fresh insights into the role of a tumour suppressor, vitamin D3 upregulated protein 1 (VDUP1), in H pylori-associated gastric carcinogenesis (in press).3 Importantly, these investigators used multiple model systems to demonstrate that VDUP1 negatively regulates carcinogenesis induced by the combination of H pylori and N-methyl-N-nitrosourea (MNU) via dissociating proliferation from apoptosis and suppression of tumour necrosis factor α (TNFα)-dependent nuclear factor κB (NF-κB) activation and subsequent cyclooxygenase-2 (COX-2) expression.
Using a genetic model of VDUP1 deficiency, Kwon and colleagues observed that the incidence and severity of gastric premalignant and malignant lesions was increased in vdup1−/− mice compared with wild-type mice.3 This was accompanied by hyperproliferation that was not balanced by a corresponding increase in apoptosis. Contact between H pylori and epithelial cells in vitro dysregulates signalling pathways that influence oncogenesis, which mirrors interactions between H pylori and epithelial cells that occur within infected tissue. Kwon et al therefore also used an in vitro …