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Chapter 40 : Gastric Cancer

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Abstract:

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 and gastric cancer may be explained by two possible mechanisms: one is based on a carcinogenesis-promoting effect of itself and the other is based on the establishment of a carcinogenic environment due to long-term infection with . In the second case, although 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 infection.

Citation: Asaka M, Sugiyama T, Sepulveda A, Graham D. 2001. Gastric Cancer, p 481-498. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch40
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Figure 1

Association of infection with development of gastric cancer. (Reprinted from reference with permission.)

Citation: Asaka M, Sugiyama T, Sepulveda A, Graham D. 2001. Gastric Cancer, p 481-498. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch40
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Figure 2

Molecular pathways linking and gastric carcinogenesis.

Citation: Asaka M, Sugiyama T, Sepulveda A, Graham D. 2001. Gastric Cancer, p 481-498. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch40
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Figure 3

Status of the gastric mucosa in two populations with a high incidence of 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.

Citation: Asaka M, Sugiyama T, Sepulveda A, Graham D. 2001. Gastric Cancer, p 481-498. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch40
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Tables

Generic image for table
Table 1

Comparison of gastric mucosal lesions and serum parameters between IgG antibody-positive and -negative asymptomatic persons

Citation: Asaka M, Sugiyama T, Sepulveda A, Graham D. 2001. Gastric Cancer, p 481-498. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch40
Generic image for table
Table 2

Development of gastric cancer in -infectedMongolian gerbils

Citation: Asaka M, Sugiyama T, Sepulveda A, Graham D. 2001. Gastric Cancer, p 481-498. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch40
Generic image for table
Table 3

Genetic alterations in both types of human gastric cancera

Citation: Asaka M, Sugiyama T, Sepulveda A, Graham D. 2001. Gastric Cancer, p 481-498. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch40

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