2017 Fiscal Year Final Research Report
Development of fundic gland type adenocarcinomas; mechanism of carcinogenesis and role of eradication of Helicobacter pylori
| Project/Area Number |
15K08960
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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 |
Gastroenterology
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| Research Institution | Fujita Health University |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Keywords | Stomach / Fundic gland / Pyloric gland / Helicobacter pylori / Intestinal metaplasia / Eradication / Development |
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| Outline of Final Research Achievements |
Helicobacter pylori (Hp) represents an important factor in the development of intestinal metaplasia (IM) and gastric cancer. Eradication of Hp could control gastric foveolar hyperplasia but not proliferation of IM glands, suggesting the IM could represent a histological irreversible point with eradication. Elimination of the bacteria induced regression of the gastric adenocarcinomas by the replacement with less atypical or normal epithelia at the surface and the bottom as early as 2 months after eradication both in fundic and pyloric mucosa. Microarray analyses using 4 and 49-day-old mice stomach revealed that H19 and insulin like growth factor 2 were overexpressed in the younger age, when fundic glands have not been fully developed. Higher expression of these two genes in gastric cancers revealed worse prognosis using The Cancer Genome Atlas data. Gastric cancer may take advantage of their own growth regulatory mechanisms especially in fundic mucosa.
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| Free Research Field |
病理学
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