| Project/Area Number |
15K15697
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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 |
Pathobiological dentistry/Dental radiology
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| Research Institution | Kanagawa Dental College |
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Principal Investigator |
Hata Ryu-Ichiro 神奈川歯科大学, 大学院歯学研究科, 特任教授 (10014276)
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| Co-Investigator(Kenkyū-buntansha) |
前畑 洋次郎 神奈川歯科大学, 大学院歯学研究科, 講師 (80410009)
陽 暁艶 神奈川歯科大学, 大学院歯学研究科, 特別研究員 (90744954)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | がん抑制法 / 癌抑制性ケモカイン / 分子標的予防医学 / がん抑制分子 / 多段階癌抑制分子 / 癌の分子標的予防法 / ケモカインBRAK / がん抑制性ケモカイン / がん予防法 |
|---|
| Outline of Final Research Achievements |
The main cause of Japanese death by cancer is due to the recurrence and metastasis. We have previously reported that the rate of carcinogenesis, the growth of tumor transplants and metastasis in CXCL14 over-expressed transgenic (Tg) mouse were significantly lower compared with that for isogenic wild type C57BL/6 (Wt) mice. Here we investigated suppression mechanisms of metastasis by CXCL14 using the pulmonary metastasis system of the malignant melanoma cell and the cell culture system. It was confirmed that anticancer drugs such as cetuximab and gefitinib stimulated expression of BRAK and this is essential for tumor growth suppression.
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