2016 Fiscal Year Final Research Report
Roles of DNA damage and repair pathway in gastric carcinogenesis after eradication of Helicobacter pylori
Project/Area Number |
26430132
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Tumor biology
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Research Institution | National Institute of Health Sciences |
Principal Investigator |
Toyoda Takeshi 国立医薬品食品衛生研究所, 病理部, 室長 (50443453)
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Project Period (FY) |
2014-04-01 – 2017-03-31
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Keywords | 胃がん / 除菌 / 慢性胃炎 / ヘリコバクター・ピロリ / スナネズミ |
Outline of Final Research Achievements |
In this study, we investigated the possible mechanisms in gastric carcinogenesis after eradication of Helicobacter pylori using a Mongolian gerbil model. The incidences of gastric adenocarcinoma in MNU-treated gerbils at week 52 were 0% in early eradication, 14% in late eradication, and 71% in non-eradication group. Although the degree of chronic gastritis was attenuated, inflammatory findings were still observed in the gastric mucosa after eradication. mRNA expression of Il-1β and Tnf-α in the antrum and corpus rapidly reduced by eradication, while Il-6 and Ifn-γ expression tended to decrease gradually. At week 52, Il-6 expressions in MNU-treated and eradicated groups were higher than those in MNU-untreated and eradicated groups. These results suggest that chronic gastritis with expression of inflammatory cytokines such as Il-6 can persist for a long period even after eradication and may be involved in the development of stomach cancer after eradication.
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Free Research Field |
総合生物
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