Experimental and Clinical Studied for process of gastric carcinogenesis

胃癌发生过程的实验与临床研究

• 批准号: 12671215
• 负责人: SUGIYAMA Atsushi
• 金额: $ 2.3万
• 依托单位: Shinshu University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2000
• 资助国家: 日本
• 起止时间: 2000 至 2001
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-12671215/
• 关键词: gastric cancer; Helicobacter pylori; Phenotype of cancer; promotor effect; duodenogastric reflux; gastric mucin; α-4GnT mRNA; Prostaglandini; α4-GnT遺伝子; スナネズミ; 発癌のプロモーター; 形質発現; 腸上皮化生; ピロリ菌陰性胃癌

The process of gastric carcinogenesis concerning Helicobacter pylori ( Hp ) was studied, and following results were obtained.1. In Mongolian gerbil ( MG ) model Hp and chemical carcinogen induce several phenotype of gastric cancer, but intestinal metaplasia may be a direct precursor only in a subset of the intestinal-type tumors.2. In the relationship between Hp and gastric carcinogenesis, Hp is a promoter rather than an initiator, and other environmental factors ( the timing of carcinogen administration ) play important roles.3. Hp infection plus duodenogastric reflux increase cell proliferation in the gastric mucosa in MG model.4. Hp eradication diminishes enhancing effect of Hp infection on glandular stomach carcinogenesis in MGs. Hp eradication may be useful as a prevention approach against stomach cancer.5. In the early stage of Hp infection, accentuation of intramucosal PGE2 and hypersecretion of mucin from gland mucus cells have a protective effect against gastric mucosal injury induced by necrotizing agents.6. As results, the expression level of a 4GnT mRNA tended to be increased in the pyloric mucosa with Hp infection, suggesting that Hp infection enhances the biosynthesis of gland mucous cell-type mucin.

本研究对幽门螺杆菌（Helicobacter pylori，Hp）在胃癌发生过程中的作用进行了研究，取得了以下结果.在蒙古沙鼠（MG）模型中，Hp和化学致癌物可诱发多种胃癌表型，但肠上皮化生可能仅是一个亚组的胃癌的直接前体.在Hp与胃癌发生的关系中，Hp是一种促进剂而非引发剂，其他环境因素（致癌剂给药时机）也起重要作用. Hp感染+胃反流可促进MG模型胃粘膜细胞增殖.根除Hp可降低Hp感染对MG腺胃癌发生的促进作用。根除Hp可能是预防胃癌的有效方法。在Hp感染早期，胃粘膜内PGE2的升高和腺粘液细胞粘蛋白的分泌增加对坏死因子引起的胃粘膜损伤具有保护作用.结果表明，幽门螺杆菌感染时幽门粘膜中α 4GnT mRNA的表达水平有增加的趋势，提示幽门螺杆菌感染促进了腺粘液细胞型粘蛋白的生物合成。

项目成果

Maruta F,Sugiyama A et al: "Role of nitrosourea in the induction of intestinal metaplasia and gastric carcinoma in Mongolian gerbils infected with Helicobacter pylori"Scandinavian Journal of gastroenterology. (In press). (2001)

Maruta F，Sugiyama A等人：“亚硝基脲在感染幽门螺杆菌的蒙古沙鼠中诱导肠上皮化生和胃癌中的作用”斯堪的纳维亚胃肠病学杂志。

Marta F, Sugiyama A et al.: "Timing of N-methyl-N-nitrosourea administration effects gastric carcinogenesis in Mongolian gerbils infected with Helicobacter pylori"Cancer Letter. 160. 99-105 (2000)

Marta F、Sugiyama A 等人：“N-甲基-N-亚硝基脲给药时机影响感染幽门螺杆菌的蒙古沙鼠的胃癌发生”《癌症信》。

丸田福門,杉山敦 ほか: "Helicobacter pylori感染スナネズミにおける胃発癌"消化器科. 30. 16-22 (2000)

Fukumon Maruta，Atsushi Sugiyama 等：“感染幽门螺杆菌的沙鼠的胃癌发生”，胃肠病学系，30. 16-22 (2000)。

Shimizu N, Sugiyama A et. al: "Eradication diminishes enhaucing effects of Helicobacter pylori infection on glandular stomach carcinogenesis in Mongolian gerbils"Cancer Research. 60. 1512-1514 (2000)

清水 N，杉山 A 等。

Maruta,F., Ota,H., Genta,M., Sugiyama,A., Tatematsu,M., Katsuyama,T., Kawasaki,S.: "Role of N-methyl-N-nitrosurea in the induction of intestinal metaplasia and gastric adenocarcinoma in Mongolian gerbils infected with Helicobacter pylori"Scand J Gastroent

Maruta，F.，Ota，H.，Genta，M.，Sugiyama，A.，Tatematsu，M.，Katsuyama，T.，川崎，S.：“N-甲基-N-亚硝基脲在诱导肠道中的作用