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Journal of Cancer Prevention

Review

Journal of Korean Association of Cancer prevention 2003; 8(4): 223-235

Published online December 30, 2003

© Korean Society of Cancer Prevention

Helicobacter pylori and Gastric Cancer

Weon-Seon Hong

Abstract

Gastric cancer is the most common cause of cancer death in Korea and is the second most common cause in the world. Gastric carcinogenesis is closely associated with environmental factors in 70∼80% of gastric cancer and hereditary factors in the remaining 20∼30%. Environmental carcinogens such as high intake of salt, N-nitroso compounds and heterocyclic amines and Helicobacter pylori (H. pylori) infection are proven to be responsible for the development of gastric cancer, while many vegetables and fruits have the significant protective effect on gastric carcinogenesis. There are two hypotheses on the gastric carcinogenesis, multi-step gene mutation hypothesis and aneuploidy-cancer hypothesis. The multi-step hypothesis is more popular type, in which cancer develops as a result of accumulation of gene mutations, usually involving in 4∼7 genes. In aneuploidy-cancer hypothesis, an unbalanced set of chromosomes produces the carcinogenesis process. Gastric cancer has been divided histologically into two types, intestinal type and diffuse type. Intestinal type cancer usually initiates from gastric atrophy, intestinal metaplasia and dysplasia in sequence through the gastritis-cancer pathway, while diffuse type cancer develops directly from gastritis without intervening pathologies by aneuploidy-cancer pathway. There is considerable convincing evidence that both histological types are strongly associated with H. pylori infection. H. pylori, is now classified as group 1 carcinogen for human gastric cancer, because epidemiological and animal studies have demonstrated a significant link between gastric cancer and H. pylori infection. The inflammation caused by H. pylori is mediated by a variety of inflammatory cells infiltrated in gastric mucosa and cytokines. In susceptible persons, the inflammation leads to atrophy, intestinal metaplasia and finally gastric cancer. Previous studies have demonstrated that H. pylori infection leads to approximately 2-fold risk for gastric cancer in persons infected for less than 10 years. In persons infected for 10∼14 years and morethan 15 years, the infection increases in the risk four to five times- and eight to nine times-fold, respectively. Several mechanisms of gastric carcinogenesis by H. pylori infection have been reported; increased cell turnover due to persistent inflammation, increased reactive oxygen metabolites, increased apoptosis, increased microsatellite DNA instability (MSI), increased telomerase activity, increased certain cytokines, such as interleukin-8 (IL-8), interleukin-1β (IL-1β), cyclooxygenase-2 (COX-2), decreased ascorbic acid in gastric juice, decreased transforming growth factor-β (TGF-β) signalling, hypochlorhydria, increased bile reflux and damaged gastric mucus, etc. Although the exact pathogenesis of gastric carcinogenesis is nor clear, it appears to be strongly associated with persistent, severe and extensive inflammation of gastric mucosa. In addition, a lot of evidences have been accumulated so far that the eradication reduces the overall risk for gastric cancer, suggesting that H. pylori is the single most important risk factor for gastric cancer. This article addresses the predisposing factors and underlying mechanisms for gastric cancer, with a special emphasis on the effect of H. pylori on the gastric carcinogenesis.

Keywords: Gastric cancer, Helicobacter pylori, Carcinogenesis

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