Risk Factors

Helicobacter pylori infection Helicobacter pylori infection can cause inflammatory responses that induce atrophic gastritis and intestinal metaplasia of gastric mucosa, resulting in reduced gastric acidity, which in turn facilitates in vivo formation of carcinogenic N-nitroso compounds and leads to the intestinal type of stomach cancer. In addition, H. pylori infection can trigger a cascade of inflammatory responses and oxidative damage to induce cell proliferation and malignant transformation, leading to the diffuse type of stomach cancer. It was estimated that H. pylori infection accounted for approximately 50-60% of stomach cancer cases and was associated with an approximately sixfold increased risk at least 10 years prior to diagnosis. These may have been underestimated because of the possibility of loss of the infection or antibody due to extensive replacement of gastric mucosa with intestinal metaplasia in people with stomach cancer.

Infection of H. pylori is common—50% worldwide and 90% in developing countries. However, only a small percentage develops into stomach cancer, suggesting that factors such as diet and genetic susceptibility modify risk.

Dietary factors Pickled vegetables and smoked, cured, salted, or dried fish or meat contain nitrite or N-nitroso compounds. These preserved foods, as well as grilled or charcoal flame-broiled food that contains polycyclic aromatic hydrocarbons, have been shown to be associated with increased risk of stomach cancer in most studies. Despite the fact that vegetables are a major source of nitrate, evidence suggests an inverse association between fresh fruits and vegetables and stomach cancer risk; the associations for yellow- or green-colored vegetables and citrus fruits are particularly strong. A few studies have reported a lower risk for stomach cancer among people consuming more allium vegetables, onions, and garlic. Some, but not all, studies have found a positive association between starchy food consumption and stomach cancer risk.

Vitamin C intake is consistently found to be inversely associated with stomach cancer risk in observational studies. Vitamin C can act as a powerful water-soluble antioxidant as well as an effective scavenger of nitrite. Protective roles of a-tocopherol and ft-carotene are suggestive but less strong. These micronutrients may also be surrogate markers of healthy dietary pattern or lifestyle.

Evidence is inconsistent regarding the role of alcohol, coffee, or black tea consumption in the development of stomach cancer. However, green tea consumption was associated with a lower risk in several studies, presumably because of its polyphenol content.

High intake of salt is associated with a higher risk of stomach cancer. Animal studies have demonstrated that salt per se can damage gastric mucosa and induce gastritis. However, in humans, high salt intake correlates positively with intake of processed meat or fish that contains nitrosamines. Hence, it is unclear whether salt evokes stomach cancer or is merely a marker of other exposures.

Cigarette smoking Tobacco use is associated with a 1.5- to 2.0-fold increased risk for stomach cancer, and it has been estimated to account for 10-17% of stomach cancer cases. These estimates may have been confounded by other factors such as poor diet.

Familial factors Familial aggregation of stomach cancer derives mostly from common environmental exposures and lifestyle factors. Hereditary stomach cancer is rare. Germline mutations in the gene coding for cell adhesion protein E-cadherin (CDH1) were found to be associated with stomach cancer of the diffuse type. Germline mutation of p53 has also been reported. People with hereditary nonpoly-posis colorectal cancer are also at higher risk for stomach cancer.

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