| Project/Area Number |
08457268
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
内分泌・代謝学
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| Research Institution | Nagasaki University |
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Principal Investigator |
YAMASITA Shunichi Nagasaki University, School of Medicine, Professor, 医学部, 教授 (30200679)
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| Co-Investigator(Kenkyū-buntansha) |
OHTSURU Akira Nagasaki University, School of Medicine, Assistant, 医学部, 助手 (00233198)
NAMBA Hiroyuki Nagasaki University, School of Medicine, Associate Professor, 医学部, 助教授 (80237635)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥7,600,000 (Direct Cost: ¥7,600,000)
Fiscal Year 1997: ¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1996: ¥4,500,000 (Direct Cost: ¥4,500,000)
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| Keywords | thyroid cancer / p53 / apoptosis / DNA repair / 甲状腺癌 / 放射線 / TSH変容体 |
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| Research Abstract |
To elucidate the mechanism of thyroid tumorigenesis, we analyzed apoptosis and radiation sensitivity in thyroid cells. We confirmed thyroid cell is resistant for apoptosis following irradiation in vitro and in vivo. To further analyze the resistance of apoptosis, intracellular signal transduction molecules such as Bcl2, Fas, Bax, GADD45 and Waf1, which are p53 dependent, were examined. As a result GADD45 and Waf1 were increased by the p53 induction. On the contrary, Bcl, Fas and Bax were not regulated by p53 protein induction.
To investigate DNA repair, we performed DNA end-joining analysis. The activity of DNA end-joining was promoted by the increase of wild type p53. According to the results, once DNA damages are occurred in thyroid cells, the cells are survived, and might have DNA rearrangements. This result indicates one of the reasons of ret rearrangement which is frequently found in the thyroid cancers after Chernobyl accident.
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