| Project/Area Number |
15H01834
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Childhood science (childhood environment science)
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| Research Institution | National Institutes for Quantum and Radiological Science and Technology |
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Principal Investigator |
Kakinuma Shizuko 国立研究開発法人量子科学技術研究開発機構, 放射線医学総合研究所 放射線影響研究部, 部長(任常) (20392219)
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| Co-Investigator(Kenkyū-buntansha) |
尚 奕 国立研究開発法人量子科学技術研究開発機構, 放射線医学総合研究所 放射線影響研究部, 研究員(任常) (50533189)
森岡 孝満 国立研究開発法人量子科学技術研究開発機構, 放射線医学総合研究所 放射線影響研究部, 主幹研究員(定常) (70253961)
臺野 和広 国立研究開発法人量子科学技術研究開発機構, 放射線医学総合研究所 放射線影響研究部, 主任研究員(定常) (90543299)
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| Co-Investigator(Renkei-kenkyūsha) |
SHIMADA YOHSIYA 国立研究開発法人量子科学技術研究開発機構, 理事 (10201550)
NISHIMURA MAYUMI 国立研究開発法人量子科学技術研究開発機構, 放射線医学総合研究所・放射線影響研究部, 主任研究員 (70218204)
AMASAKI YOSHIKO 国立研究開発法人量子科学技術研究開発機構, 放射線医学総合研究所・放射線影響研究部, 研究員 (80435700)
IMAOKA TATSUHIKO 国立研究開発法人量子科学技術研究開発機構, 放射線医学総合研究所・放射線影響研究部, チームリーダー (40356134)
BLYTH BENJAMIN 国立研究開発法人量子科学技術研究開発機構, 放射線医学総合研究所・放射線影響研究部, 主任研究員 (70642289)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥40,430,000 (Direct Cost: ¥31,100,000、Indirect Cost: ¥9,330,000)
Fiscal Year 2017: ¥9,620,000 (Direct Cost: ¥7,400,000、Indirect Cost: ¥2,220,000)
Fiscal Year 2016: ¥13,130,000 (Direct Cost: ¥10,100,000、Indirect Cost: ¥3,030,000)
Fiscal Year 2015: ¥17,680,000 (Direct Cost: ¥13,600,000、Indirect Cost: ¥4,080,000)
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| Keywords | 子ども被ばく / 放射線 / 発がん / ゲノム変異 / 放射線発がん / 子ども |
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| Outline of Final Research Achievements |
Since the Fukushima nuclear power plant accident, carcinogenesis induced by radiation has been a matter of concern. On the other hand, proton and heavy particle radiotherapies of childhood cancer have begun and the risk of second cancer due to neutron beams and carbon ions is concerned. To reduce the risk of childhood radiation exposure, it is urgent to clarify the mechanism of carcinogenesis. In this study, carcinogenic mechanisms were investigated with focuses on the age at radiation exposure, radiation type, and organ dependence. Analyses were performed on pathology and genomic mutations of cancers obtained from carcinogenesis experiments using mice and rats. As a result, in blood cancers, causal genes and mutation mechanisms were specific to childhood exposure. For solid cancers, high LET radiation was related with accelerated development and tumors at more advanced stages, but no difference in genomic mutations. Thus, study of epigenetic alterations is warranted in the future.
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