| Project/Area Number |
20591497
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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 |
Radiation science
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| Research Institution | Ibaraki Prefectural University of Health Science |
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Principal Investigator |
KUBOTA Nobuo Ibaraki Prefectural University of Health Science, 保健医療学部, 教授 (20046139)
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| Research Collaborator |
OKAYASU Ryuuichi 放射線医学総合研究所, 粒子線生物, グループリーダー
OHARA Maki 茨城県立医療大学, 保健医療学部, 嘱託助手
TANAKA Aya 茨城県立医療大学, 保健医療学部, 嘱託助手
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2008: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | CDK阻害剤 / イソチオシアネート / 放射線増感 / sulforahane / Benthyl isothiocyanate / 膵臓癌細胞 / アポトーシス / XIAP / Apaf-1 / Cyclin-dependent kinase / ヒト腫瘍細胞 / sulforaphane / DNA二重鎖切断修復 / Sufforaphane / DNA修復阻害 |
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| Research Abstract |
Isothiocyanates (ITCs) exhibit tumor prevention acivity. ITCs induce the upregulation of tumor suppressors CKI (CDK inhibitor) such as p21 and p27, and provide a protective effect to normal cells against cancer. Here, we report that Sulforaphane (SFN) and Benzyl isothiocyanate (BITC), enhance radiosensitivity in human tumor cells by repair inhibition of radiation-induced DNA double strand breaks through the impairment of nonhomologous end joining (NHEJ) and homologous recombination repair (HRR) pathways. SFN and BITC also synergisitically increase the radiation-induced apoptosis in human tumor cells. Our data suggest the potential use of SFN and BITC as an adjuvant to radiation therapy in the near future.
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