| Project/Area Number |
13470332
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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 |
Urology
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| Research Institution | Shiga University of Medical Science |
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Principal Investigator |
OKAMOTO Keisei Shiga University of Medical Science, Department of Urology, Research Assistant, 医学部, 助手 (50303780)
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| Co-Investigator(Kenkyū-buntansha) |
OKADA Osamu Shiga University of Medical Science, Department of Pathology, Professor, 医学部, 教授 (20127062)
OGAWA Osamu Kyoto University, Department of Urology, Graduate School of Medicine, Professor, 医学部, 教授 (90260611)
吉貴 達寛 滋賀医科大学, 医学部, 助教授 (80230704)
金 哲将 滋賀医科大学, 医学部, 講師 (10204968)
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| Project Period (FY) |
2001 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥10,100,000 (Direct Cost: ¥10,100,000)
Fiscal Year 2003: ¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 2002: ¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 2001: ¥4,500,000 (Direct Cost: ¥4,500,000)
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| Keywords | Renal cell carcinoma / tumor suppressor gen / chromosome 14q / rapid type / paraneoplastic syndrome / 不明熱 / 急速進行症例 |
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| Research Abstract |
Renal cell carcinomas (RCCs) are the most common kidney cancer in adults. So far nephrectomy is a single established treatment modality for RCCs. Loss of chromosome 14q has been frequently observed in RCCs. The 14q LOH is associated with poor prognosis of RCCs. However responsible genes or tumor suppressor genes on chromosome 14q arm have not been identified. We aimed identification of putative tumor suppressor gene for RCCs located on chromosome arm 14q. First we investigated candidate tumor suppressor gene on 14q: we analyzed IkB (14q13), CDKN3 (14q22), TNFAIP2 (14q32), FOS (14q24). The reduced expression was not observed in RCCs tissues and cell lines at these genes. We found SNPs. (single nucleotide polymorphisms) in exons 4, 5 and 6 of IkB. However we could not find any mutation in RCCs. Thus, we conclude IkB is not a major target of candidate tumor suppressor genes on chromosome 14q in RCCs. Similarly there was no mutation at CDKN3, TNSAIP2, FOS in RCCs. Putative RCC tumor suppressor gene on 14q is still under investigation. Now we are studying one candidate gene on 14q31. Additionally we have examined epigenetic profiles of E-cadherin gene in RCCs. We found biallelic methylation is a major pathway for silencing E-cadherin gene in RCCs.
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