Optimization of cytokine gene therapy based on the regulation of transcription/translation, pharmacokinetics, and cellular response.
| Project/Area Number |
24390008
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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 |
Physical pharmacy
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| Research Institution | Kyoto University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
NISHIKAWA Makiya 京都大学, 大学院薬学研究科, 准教授 (40273437)
TAKAHASHI Yuki 京都大学, 大学院薬学研究科, 助教 (00547870)
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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 |
¥18,590,000 (Direct Cost: ¥14,300,000、Indirect Cost: ¥4,290,000)
Fiscal Year 2014: ¥5,850,000 (Direct Cost: ¥4,500,000、Indirect Cost: ¥1,350,000)
Fiscal Year 2013: ¥6,240,000 (Direct Cost: ¥4,800,000、Indirect Cost: ¥1,440,000)
Fiscal Year 2012: ¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
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| Keywords | ドラッグデリバリー / 遺伝子治療 / インターフェロン / IDO-1 / 腫瘍組織関連マクロファージ / 抗原特異的免疫応答 / サイトカイン / プラスミドDNA / 融合タンパク質 / RNA干渉 |
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| Outline of Final Research Achievements |
The goal of the present study was the development of effective cancer therapy by gene transfer of interferon -γ(IFN-γ). For this goal, it was hypothesized that IDO-1, an IFN-γ-induced immunosuppressive molecule, and tumor-associated macrophage (TAM) might hinder anti-tumor effect of IFN-γ. Base on this hypothesis, the role of these factors in the IFN-γ cancer gene therapy was investigated. We found that TAM reduced the anti-tumor effect of IFN-γ and depletion of TAM restored it. On the other hand, IDO-1 hardly affected the anti-tumor effect of IFN-γ. In the process of these investigations, we also found that persistent transgene expression of antigenic protein induced the transgene-specific immune response, which removed the transgene-expressing cells.
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Report
(4 results)
Research Products
(17 results)
