| Project/Area Number |
18590578
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Hygiene
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| Research Institution | Chubu University |
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Principal Investigator |
YAMANOSHITA Osamu Chubu University, College of Life and Health Sciences, Department of Biomedical Sciences, Lecturer (50424924)
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| Co-Investigator(Kenkyū-buntansha) |
NASU Tamie Nagoya University, graduate School of Medicine, Department of Occupational and Environmental Health, Professor (10020794)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥300,000)
Fiscal Year 2007: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2006: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | selenium / melanoma |
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| Research Abstract |
Selenium was thought that it had the chemopreventive effect for some cancer, and we confirmed by this effect's using model mouse of melanoma.
In this research, the selenium compound (Se-Selenometylselenosysteine) was administered to the melanoma model mouse for 37 weeks (The tumor generation is observed for about ten weeks). Though, the tumor incidence of the selenium administering group was higher than that of the control group at the beginning of this experiment, the results of tumor incidence were reversed 15 weeks. Moreover, the delay of an increase of the tumor volume was observed after 30 weeks between control group and selenium high dose group. These results suggested that the selenium compound used by this research has a chemopreventive effects against melanoma.
To explore the mechanism of this effect, we tested the hypothesis that the selenium compound cause the demethylation of tumor suppressor gene promoter and continuously re-express these genes.
When we analyzed the methylation status of tumor suppressor gene promoter and expression level of these genes, there was the difference between the tumors of control group and Se-administration group. Tumors of Se-administration group were a higher expression than that of control group in some tumor suppressor gene. At methylation status of these genes, tumors of Se-administration group were more demethylated than that of control group. These results suggested that Se caused the demethylation in tumor suppressor gene promoters and re-express these genes. It would be a mechanism of chemopreventive effect of Se against melanorma.
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