| Project/Area Number |
24300325
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Carcinogenesis
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| Research Institution | Kanazawa University |
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Principal Investigator |
OSHIMA Masanobu 金沢大学, がん進展制御研究所, 教授 (40324610)
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| Co-Investigator(Renkei-kenkyūsha) |
OSHIMA Hiroko 金沢大学, がん進展制御研究所, 助教 (80362515)
ISHIKAWA Tomoo 金沢大学, がん進展制御研究所, 助教 (70322162)
NAKAYAMA Mizuho 金沢大学, がん進展制御研究所, 助教 (20398225)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥19,370,000 (Direct Cost: ¥14,900,000、Indirect Cost: ¥4,470,000)
Fiscal Year 2014: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2013: ¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
Fiscal Year 2012: ¥7,280,000 (Direct Cost: ¥5,600,000、Indirect Cost: ¥1,680,000)
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| Keywords | 胃がん / 炎症 / 微小環境 / 腫瘍免疫 / マウスモデル / TGF-beta / 自然免疫 |
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| Outline of Final Research Achievements |
It has been shown that inflammatory responses promote tumorigenesis. On the other hand, tumor immunity suppresses cancer development. In this project, we have examined characteristics of inflammatory microenvironment that was generated in gastric tumors of genetically engineered mouse model. Notably, infiltrated macrophages are polarized to M2 type, and CD4-positive T cells are infiltrated, which promotes tumorigenesis. Moreover, TGF-β signaling is enhanced and regulatory T cells are also infiltrated, suggesting that tumor immunity is suppressed in the inflammatory microenvironment. Importantly, depletion of Treg cells in tumor mouse model induced autoimmune gastritis by inhibition of immune suppression system, and such inflammatory responses further accelerated gastric tumorigenesis. Accordingly, these results suggest that regulation of the balance between inflammation and tumor immunity is important for direction of tumor promotion or suppression.
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