Roles of DNA damage and repair pathway in gastric carcinogenesis after eradication of Helicobacter pylori

2016 Fiscal Year Final Research Report

• Project/Area Number: 26430132
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Tumor biology
• 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)
• Project Period (FY): 2014-04-01 – 2017-03-31
• 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.

Free Research Field

総合生物