| Project/Area Number |
26461899
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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 |
Radiation science
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| Research Institution | Kochi University (2016-2017)
Kansai Medical University (2014-2015) |
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Principal Investigator |
Tsuno Takaya 高知大学, 医学部, 研究員 (60598259)
|
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| Co-Investigator(Kenkyū-buntansha) |
岩田 亮一 関西医科大学, 医学部, 助教 (60580446)
八幡 俊男 高知大学, 教育研究部医療学系臨床医学部門, 助教 (40380323)
|
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2017: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | IFN-α / BID / apotosis / BID遺伝子治療 / 幹細胞 / アポトーシス / IFN / 放射線治療 / 集学的治療 / BID遺伝子 / BID遺伝子集学的治療 / 癌幹細胞 |
|---|
| Outline of Final Research Achievements |
BID functions in the mitochondrial apoptotic pathway. We constructed the BID gene vector using a retro-viral vector, including a control one. The retro-viral vectors were transfected into a human glioblastoma stem cells, which are called as MD13. The MD13 cells were then inoculated into the brains of nude mice. The nude mice were treated with PEG-IFN-α or saline, which was subcutaneously and weekly injected 4 times. As a result, BID+IFN significantly prolonged overall survival. The immunohistochemistry using the brain specimens revealed underexpression of BCL2, which suppresses apoptosis, and overexpression of AIF in the nuclei, which are induced by apoptosis. These results suggest that BID+IFN demonstrated anti-tumor effects even against glioblastoma stem cells in vivo.
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