| Project/Area Number |
24591781
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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 |
Radiation science
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| Research Institution | Oita University |
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Principal Investigator |
HIROMU Mori 大分大学, 医学部, 教授 (20128226)
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| Co-Investigator(Kenkyū-buntansha) |
KASHINO Genro 大分大学, 医学部, 准教授 (00437287)
MATSUMOTO Shunoro 大分大学, 医学部, 准教授 (80219500)
YAMADA Yasunari 大分大学, 医学部, 講師 (60244183)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2014: ¥130,000 (Direct Cost: ¥100,000、Indirect Cost: ¥30,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | PET / FDG / ワーブルグ効果 / フルオロデオキシグルコース / PET検査 / p53 / 18F-FDG |
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| Outline of Final Research Achievements |
FDG PET has been widely used in tumor diagnosis. In FDG PET, incorporations of FDG drug in tumor cells are more than normal tissue. It is suggested that deficiency of p53 function are related in FDG incorporation. However the details are unknown. Here we examined the relationship between p53 status and the levels of FDG incorporation into cells. In normal human fibroblast cells and breast cancer cell line MCF7, they contain wild type p53, and the expression of p53 was suppressed by knockdown method. The results showed that the knockdown of p53 gene was not affected in incorporation of FDG in these cells. In H1299 cells, which delete p53 expression, expression vector of wild type p53 was introduced and FDG incorporation was examined. However the levels of FDG incorporations in the cells are not different from that in parent H1299 cells. These results suggest that it is difficult to predict the p53 status by the incorporation levels of FDG.
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