| Project/Area Number |
23591398
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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 |
Hematology
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| Research Institution | Kagoshima University |
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Principal Investigator |
SUZUKI Shinsuke 鹿児島大学, 医歯(薬)学総合研究科, 助教 (20437974)
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| Co-Investigator(Renkei-kenkyūsha) |
KOSAI Kenichirou 鹿児島大学大学院医歯学総合研究科先進治療科学専攻運動機能修復学講座遺伝子治療, 再生医学分野, 教授 (90258418)
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| Project Period (FY) |
2011-04-28 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 癌特異的増殖型アデノウイルス / 成人T細胞白血病 / サービビン / HTLV-1 bZIP factor / 成人T細胞白血病幹細胞 / 癌特異的増殖型デノウイルス / ウイルス由来遺伝子 / 癌特異的増殖型アデノウイ ルス / 白血病幹細胞 / 成人Ｔ細胞白血病 |
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| Outline of Final Research Achievements |
Adult T-cell leukemia (ATL) develops after long-term infection with the human T-cell leukemia virus type I (HTLV-1). Survivin-responsive conditionally replicating adenoviruses (Surv.CRAs) in which expression of the adenoviral early region 1A (E1A) gene is regulated by the survivin promoter, has been demonstrated to treat a variety of cancers. Six ATL cell lines were infected with Surv.CRAs at a various multiplicity of infection. The survivin promoter was strongly activated in 6 cell lines. Moreover, the expression of the coxsackie and adenovirus receptor (CAR), important for cell infection by adenoviruses, was highly upregulated in these cell lines. In contrast, weak activation of the survivin promoter and low expression of CAR were observed in peripheral blood lymphocytes (PBLs) of healthy subjects. Surv.CRAs efficiently replicated and induced cell death in 5 out of 6 cell lines compared to minimal viral replication in normal PBLs, in which there was no significant cytotoxicity.
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