| Project/Area Number |
17591708
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Urology
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| Research Institution | National Institute for Radiological Sciences |
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Principal Investigator |
YOSHIDA Mitsuaki National Institute of Radiological Sciences, Research Center for Radiation Emergency Medicine, Department of Radiation Dosimetry, Biodosimetry Section, Section Head, 緊急被ばく医療研究センター, 室長 (60182789)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 2006: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2005: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | renal cell carcinoma / chromosome abnormality / chromosome 5 / partial trisomy / amplification / prognosis / ヒト腎細胞癌 / 第5染色体長腕増幅 / 微小核細胞融合法 |
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| Research Abstract |
In order to investigate the relationship between amplification of a long arm of chromosome 5 (5q) and prognosis in human renal cell carcinoma (RCC), the frequency of partial trisomy for 5q was determined in an increased number of RCC specimen by both conventional banding and interphase FISH analyses. An amplification of 5q was found in 53 (44%) out of 121 cases. These RCC samples were grossly classified into three groups by the copy number of 5q: tumors with 2 copies of 5q, with 3 copies, with 4 or more copies and the correlation between numerical changes of 5q and clinical outcome of the RCC patients was analyzed by Kaplan-Meier methods. The results revealed that RCC patients with tumors carrying four or more copies of the 5q segments had significantly worse outcomes than those with tumors that harbor three copies (P=0.007). Patients with three appear to show a better prognosis than those with two copies. In particular, when the observation period was interrupted at 60 months, this tendency is more evident.
In the present study, one of chromosome 5 derived from normal cell was introduced into RCC cells from both non-papillary and papillary cell lines in order to clarify the role of amplification of chromosome 5 in RCC. However, the clones with three of whole chromosome 5 were not obtained by micro-cell fusion. On the other hand, the clones from papillary RCC cell lines indicated three copies of chromosome 5 and the growth suppression in vitro was characteristically observed, suggesting that the putative tumor suppressor gene(s) may be associated with the development and /or progression of papillary renal cell carcinoma. It will be necessary to search the candidate gene on a long arm of chromosome 5 which may be involved in the course of RCC development and progression.
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