Mechanism of low dose(rate) radiation induced tumor development by using intestinal stem cell organoid system
Project/Area Number |
17K00553
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Risk sciences of radiation and chemicals
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Research Institution | Hiroshima University |
Principal Investigator |
Sasatani Megumi 広島大学, 原爆放射線医科学研究所, 准教授 (80423052)
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Co-Investigator(Kenkyū-buntansha) |
河合 秀彦 広島大学, 医系科学研究科(薬), 准教授 (30379846)
神谷 研二 広島大学, 医療政策室, 特任教授 (60116564)
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Project Period (FY) |
2017-04-01 – 2020-03-31
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Project Status |
Completed (Fiscal Year 2019)
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Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2019: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
|
Keywords | 放射線 / 発がん / 低線量(率) / 幹細胞 / 動物モデル / 低線量・低線量率 / 放射線発がん / 年齢依存性 / 低線量(率)放射線発がんリスク |
Outline of Final Research Achievements |
It is known that radiation-induced cancer risk in childhood is higher than in adulthood in human. Thus, age at exposure is a major effect modifier of radiation-induced cancer. Given that the Fukushima Daiichi Nuclear Power Plant accident in Japan is reviving concern about cancer risk at low radiation doses, especially in childhood, clarifying the mechanism of susceptibility for radiation-induced carcinogenesis in childhood needs to be investigated in each organ. The application of animal models might be useful for understanding the mechanism of age-dependent cancer risk. Here, we elucidated the age dependence of the exposure in model mice of intestinal tumors, and analyzed the effects of radiation response and age on irradiation on carcinogenesis, including cell competition of small intestinal stem cells. And our results suggest that there is the relationship between intestinal morphogenesis and radiation-induced cancer risk.
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Academic Significance and Societal Importance of the Research Achievements |
福島原発事故後、胎児期・小児期被ばくにおける発がんリスクの増加が懸念されている。しかしながら、放射線発がんにおける被ばく時年齢依存性の有無とその分子メカニズムについては未だ未解明の部分が多い。そのため、本研究成果は、動物モデルを用いて放射線発がんにおける被ばく時年齢依存性の機構解明に関する新規知見が得られており、学術的に重要といえる。また、各年齢における放射線発がんリスクとその分子機構が解明されれば、放射線発がんリスク評価のみならず放射線防護体系の基盤確立に貢献できることが期待される。
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Report
(4 results)
Research Products
(24 results)
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[Journal Article] A chemical modulator of p53 transactivation that acts as a radioprotective agonist.2018
Author(s)
Akinori Morita, Ippei Takahashi, Megumi Sasatani, Shin Aoki, Bing Wang, Shinya Ariyasu, Kaoru Tanaka, Tetsuji Yamaguchi, Akiko Sawa, Yurie Nishi, Tatsuro Teraoka, Shohei Ujita, Yosuke Kawate, Chihiro Yanagawa, Keiji Tanimoto, Atsushi Enomoto, Mitsuru Nenoi, Kenji Kamiya, Yasushi Nagata, Yoshio Hosoi and Toshiya Inaba
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Journal Title
Molecular Cancer Therapeutics
Volume: 17
Issue: 2
Pages: 432-442
DOI
NAID
Related Report
Peer Reviewed / Open Access
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[Journal Article] Overexpression of Rev1 promotes the development of carcinogen-induced intestinal adenomas via accumulation of point mutation and suppression of apoptosis proportionally to the Rev1 expression level.2017
Author(s)
Sasatani M, Xi Y, Kajimura J, Kawamura T, Piao J, Masuda Y, Honda H, Kubo K, Mikamoto T, Watanabe H, Xu Y, Kawai H, Shimura T, Noda A, Hamasaki K, Kusunoki Y, Zaharieva EK, Kamiya K.
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Journal Title
Carcinogenesis.
Volume: 38(5)
Issue: 5
Pages: 570-578
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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[Journal Article] Establishment of induced pluripotent stem cells from normal B cells and inducing AID expression in their differentiation into hematopoietic progenitor cells2017
Author(s)
Fumihiko Kawamura, Makoto Inaki, Atsushi Katafuchi, Yu Abe, Naohiro Tsuyama, Yumiko Kurosu, Aki Yanagi, Mitsunori Higuchi, Satoshi Muto, Takumi Yamaura, Hiroyuki Suzuki, Hideyoshi Noji, Shinichi Suzuki, Mitsuaki A. Yoshida, Megumi Sasatani, Kenji Kamiya, Masafumi Onodera & Akira Sakai
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Journal Title
Scientific Reports
Volume: -
Issue: 1
Pages: 1-11
DOI
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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