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Category: Bacterial Pathogenesis
Gastric Cancer, Page 1 of 2
< Previous page | Next page > /docserver/preview/fulltext/10.1128/9781555818005/9781555812133_Chap40-1.gif /docserver/preview/fulltext/10.1128/9781555818005/9781555812133_Chap40-2.gifAbstract:
Gastric cancer is one of the most common malignancies in the world, although the incidence and mortality rate have been decreasing in recent decades. The association between Helicobacter pylori and gastric cancer may be explained by two possible mechanisms: one is based on a carcinogenesis-promoting effect of H. pylori itself and the other is based on the establishment of a carcinogenic environment due to long-term infection with H. pylori. In the second case, although H. pylori may have no carcinogenesis-promoting effect itself, infection causes inflammation of the gastric mucosa and chronic infection causes mucosal atrophy, resulting in intestinal metaplasia. Microsatellite instability (MSI) is a marker of mutations that develop subsequent to deficient DNA mismatch repair (MMR) activity. An accumulation of genetic alterations may result in development of gastric cancer, having an analogy with that of colon cancer. Genetic alterations occur in oncogenes, tumor suppressor genes, cell adhesion molecules, telomere and telomerase activity, and genetic instability. Different histological types of gastric cancer exhibit different patterns of genetic alterations. We need the genetic information associated with oncogenesis in Mongolian gerbils, such as the p53 gene, which might be an appropriate gene to investigate the oncogenic mechanisms of both types of gastric cancer induced by H. pylori infection.
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Association of H. pylori infection with development of gastric cancer. (Reprinted from reference 8 with permission.)
Association of H. pylori infection with development of gastric cancer. (Reprinted from reference 8 with permission.)
Molecular pathways linking H. pylori and gastric carcinogenesis.
Molecular pathways linking H. pylori and gastric carcinogenesis.
Status of the gastric mucosa in two populations with a high incidence of H. pylori infection. One population (A) experiences a rapid transition of superficial gastritis to atrophic pangastritis. Gastric cancer begins to be seen in patients in their 40s, and the incidence increases thereafter. This pattern is typical in Japan or Korea. The population represented in panel ? has a low rate of development of atrophic pangastritis, and gastric cancer is a rare disease. Such a pattern is typical in tropical countries such as Bangladesh.
Status of the gastric mucosa in two populations with a high incidence of H. pylori infection. One population (A) experiences a rapid transition of superficial gastritis to atrophic pangastritis. Gastric cancer begins to be seen in patients in their 40s, and the incidence increases thereafter. This pattern is typical in Japan or Korea. The population represented in panel ? has a low rate of development of atrophic pangastritis, and gastric cancer is a rare disease. Such a pattern is typical in tropical countries such as Bangladesh.
Comparison of gastric mucosal lesions and serum parameters between H. pylori IgG antibody-positive and -negative asymptomatic personsa
Comparison of gastric mucosal lesions and serum parameters between H. pylori IgG antibody-positive and -negative asymptomatic personsa
Development of gastric cancer in H. pylori-infectedMongolian gerbils
Development of gastric cancer in H. pylori-infectedMongolian gerbils
Genetic alterations in both types of human gastric cancera
Genetic alterations in both types of human gastric cancera