Stomach cancer enters through the mouth
Ninety-five percent of malignant tumors of the stomach are adenocarcinomas, and the term gastric cancer generally refers to adenocarcinoma of the stomach, with other malignant tumors of the stomach being rare. In 1965 Lauren described two histological types of gastric adenocarcinoma: the intestinal type and the infiltrative type, explaining the etiological and epidemiological features of gastric cancer.
The intestinal type originates from precancerous areas, such as atrophy of the gastric mucosa or gastrointestinal epithelial metaplasia. This type is more common in men and is the predominant tissue type in areas with a high incidence of gastric cancer, suggesting the role of environmental factors in the development of gastric cancer. The infiltrative type has no typical recognizable precancerous lesions and has a slightly higher incidence in women and young adults, with a higher tendency of familial incidence (type A blood), suggesting a genetic link. The changes in the incidence of gastric cancer in different populations in the same region or in different geographic areas over time reflect the differences and variations in the incidence of intestinal type gastric cancer, e.g. Napoleon went to die in St. Helena due to gastric cancer, his grandfather and father both died of gastric cancer, but for the analysis of Napoleon’s medical history data, he had a combination of H. pylori infection at the same time. The common factors known to cause gastric cancer are: gender (more common in men), genetic factors, chronic gastritis and H. pylori infection.
Most studies have found that food plays an important role in the development of gastric cancer. Consumption of raw vegetables, fruits, especially citrus fruits, and fiber-rich foods can reduce the risk of gastric cancer, as can the consumption of foods rich in vitamins A and C. By the same token, the risk of gastric cancer can be reduced after treatment. By the same token, to prevent recurrence and reoccurrence of gastric cancer after treatment, the corresponding dietary principles should be followed. The following is a list of risk factors related to the development of gastric cancer, which should be avoided by patients after treatment.
Risk factors related to the development of gastric cancer
1.Nutritional aspects
Low fat or low protein diet
Cured meat or cured fish
High nitrate diet
Low dietary vitamins A and C
2.Environmental aspects
Improper food disposal (smoking)
Lack of refrigerator
Bad drinking water (well water)
Occupational pollution
3.Medical aspects
Previous gastric surgery
H. pylori infection
Gastric atrophic gastritis, gastrointestinal epithelial metaplasia.
The exact factors of gastric cancer development are not very clear yet, and may be the interaction of environmental and genetic factors. A large number of basic and clinical studies suggest that Hp infection is one of the important factors inducing gastric cancer, and it may be a synergistic carcinogenic factor of gastric cancer.
Since 1983, when Mashall and Warren successfully isolated Hp from patients with gastritis and peptic ulcer, it has attracted the attention of scholars and gradually recognized that Hp is the main cause of chronic gastritis and peptic ulcer and is closely related to the occurrence of gastric cancer. 1994, WHO International Agency for Research on Cancer listed Hp as a class I carcinogenic risk factor. Recently, Chinese scholars have reached some consensus on the relationship between Hp and gastric cancer, and concluded that Hp can increase the risk of gastric cancer, and Hp is related to both intestinal and diffuse gastric cancer.
Regarding the mechanism of Hp infection causing gastric cancer, it is generally believed that in the course of chronic active inflammation caused by long-term Hp infection, the direct or interrogative attack of a series of pathogenic factors (such as urease, vacuolar toxin, toxin-related gene protein, inflammatory mediators, reactive oxygen metabolites, etc.) causes excessive proliferation of gastric mucosal epithelial cells, abnormal apoptosis and a series of histopathological changes, which ultimately lead to the development of gastric cancer.