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KMID : 0931320020020010080
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대한상부위장관.헬리코박터학회지
2002 Volume.2 No. 1 p.80 ~ p.88
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Novel Aspect of Gastric Carcinogenesis and Helicobacter pylori
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Hahm Ki-Baik
Han Sang-Uk
Cheong Jae-Youn
Park Hyun-Jin
Kim Young-Bae
Nam Ki-Taek
Kim Dae-Yong
Joo Hee-Jae
Choi Jun-Hyuk
Kim Jin-Hong
Lee Ki-Myung
Kim Myung-Wook
Cho Sung-Won
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Abstract
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Although many studies have found an association between Helicobacter pylori infection and the development of gastric cancer, many debates still exist and remain uncertain. Epidemiological and animal studies demonstrated a link between gastric cancer and chronic infection with H.pylori, but the exact mechanism responsible for the development of gastric cancer H.pylori-infected patients still remain obscure. In order to declare the clear association, definite evidences like that decrement in the incidence of gastric cancer after the eradication of H.pylori in designated area compared to non-eradicated region of the blockade of specific mechanism acting on the carcinogenesis by H.pylori infection. The other way is to identify the upregulating oncogenes or downregulating tumor suppressor genes specifically invovled in H.pylori-associated carcinogenesis. For that, we established the animal models using C57BL/6 mice strain. AL ready gastric carcinogenesis was developed in Mongolian gerbils infected with H.pylori, but there has been no development fo gastric cancer in mice model infected with H.pylori after long term evaluation. Significant changes such as atrophic gastritis were observed in mice model. However, we could observe the development of mucosal carcinoma in the stomach of transgenic featuring the loss of TGF-beta signaling by the expressions of dominant negative forms of type Ⅱ receptor specifically in the stomach. Moreover, the incidence of gastric adenocarcinoma was significantly increased in group administered with both MNU and H.pylori infection than MNU alone, signifying that H.pylori promoted the gastric carcinogenesis and there might be host susceptibility genes in H.pylori-associated gastric carcinogenesis. Based on assumption that chronic, uncontrolled inflammation might predispose to carcinogenesis, there have been several evidences showing chronic atrophic gastritis predisposed to gastric carcinogenesis in H.pylori infection. Although definite outcome of chemoprevention was not drawn after the long-term administration of anti-inflammatory durg in H.pylori infection, the actual incidence of atrophic gastritis and molecular evidence of chemoprevention could be obtained. Selective COX-2 inhibitor was effective in decreasing the development of gastric carcinogenesis provoked by H.pylori infection and carcinogen like in chemoprevention of colon carcinogenesis.
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KEYWORD
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Chemoprevention, Chronic atrophic gastritis, Gastric carcinogenesis, Helicobacter pylori
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