1999 Fiscal Year Final Research Report Summary
Alteration and cell biological characterization of cell cycle-associated genes in human renal cell carcinomas.
| Project/Area Number |
10671463
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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 | Tokyo Medical and Dental University |
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Principal Investigator |
YOSHIDA Mitsuaki a. Tokyo Medical and Dental University, Medical Research Institute, Department of Molecular Cytogenetics, Research Associate, 難治疾患研究所, 助手 (60182789)
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| Co-Investigator(Kenkyū-buntansha) |
大島 博幸 東京医科歯科大学, 医学部, 教授 (60013934)
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| Project Period (FY) |
1998 – 1999
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| Keywords | human renal cell carcinoma / mitotic spindle check point / G1 / S border / p21 / p33 / MAD2 / BUB1 |
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| Research Abstract |
In recent years, it has been suggested that the alteration of genes, which are associated with the regulation of cell cycle, may be involved in the course of human carcinogenesis. Therefore, in the present study, we investigated the expression of these genes, p21, p33, BUB1 and MAD2 in both primary tissues and established cell lines from human renal cell carcinomas by RT-PCR technique. The expression of p21 gene was detected in 15 out of 17 cancer tissues involving 3 cases of metsttic tissue and p33 was also expressed in all of tissues analyzed. These results indicate that at least these genes regulating G1/S border may not be associated with the development of renal cell carcinoma. On the other hand, MAD2 gene was analyzed in 19 cases of primary tissue and 3 cases of metastatic tissue and the expression was not observed nine cases of primary and 1 case of metastasis. BUB1 was also analyzed in 22 cases with one primer and in 16 cases with two kinds of primer and the expression of this gene was not detected in 81〜95% of cases analyzed. These results suggest that loss of the expression of spindle check point components leading to chromosomal instability may be one of mechanism associated with the renal cell carcinogenesis.
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