Molecular mechanism of radiation induced-leukemia using the animal model
| Project/Area Number |
25340032
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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 |
Risk sciences of radiation and chemicals
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| Research Institution | Hiroshima University |
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Principal Investigator |
Sasatani Megumi 広島大学, 原爆放射線医科学研究所, 助教 (80423052)
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| Co-Investigator(Kenkyū-buntansha) |
神谷 研二 広島大学, 医療政策室, 特任教授 (60116564)
飯塚 大輔 広島大学, 原爆放射線医科学研究所, 助教 (00455388)
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| Project Period (FY) |
2013-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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| Keywords | ゲノム障害 / ゲノム修復 / 放射線 / 発がん / 白血病 / 突然変異 / 放射線発がん / 線量率効果 / 低線量（率） / 動物モデル |
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| Outline of Final Research Achievements |
Ionizing radiation increases the risks of leukemia and certain types of solid tumors. The relative risk of radiation-induced leukemia is much higher than those of solid tumors. Recently, Dr. Nakamura has hypothesized about the mechanism of radiation induced leukemia where the radiation-related acute lymphoid leukemia (ALL) risk for a population is almost entirely attributable to a small number of predisposed individuals in whom relatively large numbers of translocation-carrying pre-ALL cells have accumulated. To prove this hypothesis, we focused on BCR/ABL fusion gene which is a one of common chromosomal translocations known as Philadelphia chromosome and explored radiation induced tumorigenesis study by using BCR/ABL transgenic mice (BCR/ABLTg/- mice). Our data showed that BCR/ABLTg/- mice are susceptible to radiation-induced thymic lymphoma development.
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Report
(5 results)
Research Products
(54 results)
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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 level2017
Author(s)
Sasatani M, Xi Y, Kajimura J, Kawamura T, Piao J, Masuda Yuji, Honda H, Kubo K, Mikamoto T, Watanabe H, Xu Y, Kawai H, Shimura T, Noda A, Hamasaki K, Kusunoki Y, Zaharieva K E, and Kamiya K
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Journal Title
Carcinogenesis
Volume: 印刷中
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Peer Reviewed / Open Access / Acknowledgement Compliant
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[Journal Article] RAD18 Activates the G2/M Checkpoint through DNA Damage Signaling to Maintain Genome Integrity after Ionizing Radiation Exposure.2015
Author(s)
Sasatani M, Xu Y, Kawai H, Cao L, Tateishi S, Shimura T, Li J, Iizuka D, Noda A, Hamasaki K, Kusunoki Y, Kamiya K.
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Journal Title
PLoS One
Volume: 10
Issue: 2
Pages: 1-16
DOI
Related Report
Peer Reviewed / Open Access
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[Journal Article] A novel ATM/TP53/p21-mediated checkpoint only activated by chronic γ-irradiation2014
Author(s)
CAO Lili, KAWAI Hidehiko, SASATANI Megumi, IIZUKA Daisuke, MASUDA Yuji, INABA Toshiya, SUZUKI Keiji, OOTSUYAMA Akira, UMATA Toshiyuki, KAMIYA Kenji, SUZUKI Fumio
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Journal Title
PLoS One
Volume: 9
Issue: 8
Pages: e104279-e104279
DOI
NAID
Related Report
Peer Reviewed / Open Access
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[Presentation] KH-3, a Novel Chemical Modulator of p53, Enhances p21 Induction and Protects Mice from Gastrointestinal Death by Abdominal Irradiation2015
Author(s)
Morita A, Takahashi I, Aoki S, Bing Wang, Ariyasu S, Sasatani M, Tanaka K, Yamaguchi T, Tanimoto K, Kamiya K, Hosoi Y, Nagata Y, Inaba T
Organizer
15th International Congress of Radiation Research
Place of Presentation
Kyoto
Year and Date
2015-05-27
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