Helicobacter pylori: gastric cancer and beyond

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Abstract
Infection with Helicobacter pylori is the strongest known risk factor for gastric adenocarcinoma, but only a minority of colonized individuals develop cancer of the stomach. H. pylori strains exhibit extensive genetic diversity and strain-specific proteins augment the risk for malignancy. β-catenin signalling has an important role in conjunction with other oncogenic pathways in the regulation of host responses to H. pylori that have carcinogenic potential. Transactivation of epidermal growth factor receptor may help us understand the epithelial signalling pathways that mediate H. pylori-induced carcinogenesis. Chronic inflammation can induce aberrant β-catenin activation in the context of H. pylori infection. A mechanistic understanding of H. pylori activation of oncogenic signalling may lead to key insights into malignancies that arise from inflammatory foci in other organ systems.