| Project/Area Number |
20012037
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| Research Category |
Grant-in-Aid for Scientific Research on Priority Areas
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| Allocation Type | Single-year Grants |
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| Review Section |
Biological Sciences
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| Research Institution | Kyushu University |
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Principal Investigator |
TSUZUKI Teruhisa Kyushu University, 大学院・医学研究院, 教授 (40155429)
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| Co-Investigator(Kenkyū-buntansha) |
NAKATSU Yoshimichi 九州大学, 大学院・医学研究院, 准教授 (00207820)
OHNO Mizuki 九州大学, 大学院・医学研究院, 助教 (70380524)
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| Co-Investigator(Renkei-kenkyūsha) |
YAO Takashi 順天堂大学, 医学部, 教授 (20243933)
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| Project Period (FY) |
2008 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥18,000,000 (Direct Cost: ¥18,000,000)
Fiscal Year 2009: ¥9,000,000 (Direct Cost: ¥9,000,000)
Fiscal Year 2008: ¥9,000,000 (Direct Cost: ¥9,000,000)
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| Keywords | 遺伝子 / 核酸 / 癌 / ゲノム / 動物 / 活性酸素 / 突然変異 / 消化管 |
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| Research Abstract |
To elucidate the roles of DNA repair genes in the suppression of oxidative DNA damage-induced tumorigenesis, we performed KBrO3-induced tumorigenesis experiments using Ogg1-, Mth1-, Msh2- or Trp53-deficient mice. We observed an enhanced tumor-formation in the small intestines of Msh2- or Trp53-deficient mice, as compared with the wild type and heterozygous mice. These results indicate that in addition to Mutyh, Msh2 and p53 are involved in the suppression of oxidative stress-induced intestinal tumorigenesis in mice. The number of tumors was marginally increased in Ogg1- or Mth1-deficient mice, in comparison to the wild-type mice, suggesting that Ogg1 and Mth1 may play a limited role in the suppression of intestinal tumorigenesis caused by oxidative stress.
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