| Project/Area Number |
26640087
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Tumor biology
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| Research Institution | Gunma Institute of Public Health and Environmental Sciences |
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Principal Investigator |
Murata Naoya 群馬県衛生環境研究所, その他部局等, 研究企画係研究員 (00533473)
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| Co-Investigator(Renkei-kenkyūsha) |
OKAJIMA Fumikazu 群馬大学, 生体調節研究所, 教授 (30142748)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 発癌 / pH感知性受容体 / TDAG8 / 発がん / ｐＨ感知性受容体 / ＴDAG8 |
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| Outline of Final Research Achievements |
We analyzed a role of the host immunity in the tumor formation using TDAG8-receptor-deficiency mice. As a result, the tumor formation was induced with a single subcutaneous dosage of chemical carcinogen 3-methylcholanthrene(3-MCA) in more than 90% of the wild type, but was reduced to its half in the TDAG8-deficiency type. However, immunohistological examination show no significant difference in the degree of immune cells( e.g. CD3-positive T cell)infiltration to the tumor tissues between both types. In addition, no significant difference was found between both types not only in the tumor formation with inoculation of 3-MCA-induced mouse fibrosarcoma cell strain (MC57G) but also in MC57G-induced cytotoxic activity. Thus, it was supposed that the suppressive effect on the tumor formation found in TDAG8-deficiency type is induced by indirect cellular or humoral regulation mechanisms of the host immunity, but not by direct cytotoxic activity by the immune cells, such as T cells.
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