| Project/Area Number |
23710067
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Risk sciences of radiation/Chemicals
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| Research Institution | Nigata University of Phermacy and Applied Life Sciences (2012)
Niigata University (2011) |
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Principal Investigator |
GO Rieka 新潟薬科大学, 薬学部, 研究員 (40584769)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | 放射線発がん / 発がん母体細胞 / Bcl11b 遺伝子 / Bcl11b遺伝子 |
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| Research Abstract |
Cell of origin in γ-radiation induced mouse thymic lymphomas remains obscure. In this study, we generated mouse models in which loss of one Bcl11b allele occurs in thymocytes at different developmental stages and examined expansion and differentiation of premalignant thymocytes after irradiation. We showed that thymocytes at the immature stage were cells of origin and premalignant thymocytes retained the capacity to proliferate and differentiate. Also, loss of Bcl11b allele in thymocytes led to impaired cell cycle arrest at S phase after irradiation, suggesting that the impairment contributes to the development of the premalignant thymocytes.
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