Common precancerous lesions of gastric cancer

Common precancerous lesions of gastric cancer

The lesion of gastric cancer is first of all a histological concept, which refers to certain pathological changes in the gastric mucosa. These lesions are more likely to become cancerous than normal or other gastric mucosal lesions, such as atypical hyperplasia of gastric mucosal epithelium and intestinal metaplasia of gastric mucosa. Whether it is the precancerous disease of gastric cancer or precancerous lesions, there are a few cases of canceration, but it does not mean that they will develop into cancer in the future. Most cases will have the possibility of stopping development or reversing after treatment. The precancerous disease of gastric cancer is also a clinical concept, which means that certain diseases have a higher chance of developing gastric cancer, such as gastric polyps, gastric ulcers, and chronic atrophic gastritis.

Gastric precancerous lesions are divided into two aspects: precancerous state and precancerous lesions. Gastric precancerous state refers to precancerous diseases of the stomach, such as CAG, ulcer disease, gastric polyps, residual gastritis and hypertrophic gastritis. These benign gastric diseases have a higher chance of developing gastric cancer. Among them, CAG is the most common gastric precancerous state.

In the national gastric cancer epidemiological study, the survey results of various gastric cancer high-incidence areas showed that there was a parallel relationship between the prevalence of CAG and the mortality rate of gastric cancer. Many scholars at home and abroad have conducted follow-up observations on CAG for varying periods of time, and up to 10% of them have lesions. The main pathological characteristics of CAG are chronic inflammation of the mucosa and glandular atrophy, often accompanied by intestinal metaplasia (IM) and atypical hyperplasia of the gastric mucosa. Some statistics show that CAG is accompanied by intestinal metaplasia in 65.5%, and it increases with age. As the atrophic area expands, the proportion of intestinal metaplasia also increases.

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