| Project/Area Number |
20591585
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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 |
Digestive surgery
|
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| Research Institution | Chiba Cancer Center (Research Institute) |
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Principal Investigator |
TAGAWA Masatoshi Chiba Cancer Center (Research Institute), がん治療開発グループ, 部長 (20171572)
|
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| Co-Investigator(Kenkyū-buntansha) |
SHIMADA Hideaki 東邦大学, 医学部, 教授 (20292691)
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| Project Period (FY) |
2008 – 2010
|
| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2009: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2008: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 食道がん / がん治療 / 遺伝子 / アデノウイルス / キャリアー細胞 / 遺伝子治療 / 制限増殖型ウイルス / 間葉系幹細胞 / アポトーシス / 細胞傷害活性 / 遺伝子医薬 / コクサキーアデノウイルス受容体 / CD46分子 / p53遺伝子 / 初期応答遺伝子 / ウイルス受容体 |
|---|
| Research Abstract |
Majority of human solid tumors, when clinically in an advanced stage, is resistant to most of conventional therapies and consequently improved prognosis with a novel strategy is a crucial target in clinical settings. We developed type 5 adenoviruses which replicated preferentially within tumors and then examined the anti-tumor effects. We also modified the adenoviruses of which the receptor-binding site was replaced with that of type 35 adenoviruses, which subsequently increased the infectivity to human tumors due to a high receptor expression in the tumors. We examined a possible advantage to use carrier cells which were infected with such adenoviruses.
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