Rectifying the Epigenetic Field Defect in Gastric Carcinogenesis
Journal Title: Journal of Cancer Sciences - Year 2015, Vol 2, Issue 2
Abstract
Gastric cancer is undoubtedly a fatal malignancy worldwide with high incidence and dismal prognosis. Its formation and development can be driven by genetic defects, dietary factors, alcohol consumption, viral infection, etc. Despite the multifactorial nature, more than 80% of gastric cancers are closely related to Helicobacter pylori (H. pylori) infection [1]. It is believed that H. pylori triggers chronic gastritis that results in gastric atrophy, intestinal metaplasia and dysplasia, and then finally to adenocarcinoma. Such microbial infection is associated with strong host response such as cytokine stimulation and neutrophil activation which play an important driver role in gastric carcinogenesis. The stimulated cytokines include pro-inflammatory interleukin-1β (IL-1β), IL-2, IL-6, IL-8 and tumor necrosis factor alpha (TNF-α), of which the IL-8 action in stimulating neutrophils is significantly enhanced upon infection by CagA-positive H. pylori [2].
Authors and Affiliations
Alfred S. L. Cheng
Keywords
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- EP ID EP209347
- DOI 10.13188/2377-9292.1000010
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