2018 Fiscal Year Final Research Report
Progression of the gastric cancer using novel mouse spontaneously developed differentiated type adenocarcinoma
| Project/Area Number |
16K08708
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Experimental pathology
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| Research Institution | Shinshu University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
中山 淳 信州大学, 学術研究院医学系, 教授 (10221459)
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| Research Collaborator |
Arisaka Nobuhiko
Miyashita Masaki
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Keywords | A4gnt欠損マウス / 胃癌 / ピロリ菌 / エピジェネティック |
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| Outline of Final Research Achievements |
Infection with Helicobacter pylori is the major cause of gastric cancer. Mice deficient in αGlcNAc contained in gastric mucin, which has tumor suppressor function in differentiated type adenocarcinoma, were infected with H. pylori to investigate the molecular mechanism of tumorigenesis prior to gastric cancer development. We obtained new findings on epigenetic changes mainly in microRNA expression analysis related with the pathological findings depending on H. pylori infection.Although the progression of differentiated type adenocarcinoma on A4gnt KO mice was not fully clear by pathological or molecular processes related to H. pylori infection in the lack of αGlcNAc on gastric gland mucin, it was shown that severe gastric erosion occurred in A4gnt KO mice infected with H. pylori due to mucosal infiltration with neutrophils.
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| Free Research Field |
実験病理学，糖鎖生物学，感染症
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| Academic Significance and Societal Importance of the Research Achievements |
A4gnt KOマウスにピロリ菌感染を生じさせることは，胃癌発生の要因となり得るヒトの体質のような，癌化リスクを基本要素として持つ基盤に，胃癌の主因であるピロリ菌感染をモデル化できると期待される実験系であり，ピロリ菌初感染から胃粘膜上皮細胞の不可逆的な変成をきたす過程を解明し，より効果的に癌化リスクを減らすピロリ菌除菌のタイミングを見いだせるものと思われる．
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