| Project/Area Number |
08671801
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Urology
|
|---|
| Research Institution | Tokyo Medical and Dental University |
|---|
Principal Investigator |
YOSHIDA Mitsuaki A. Tokyo Medical and Dental University, Medical Research Institute, Department of Cytogenetics, Research Associate, 難治疾患研究所, 助手 (60182789)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
OSHIMA Hiroyuki Tokyo Medical and Dental University, Faculty of Medicine, Department of Urology,, 医学部, 教授 (60013934)
|
|---|
| Project Period (FY) |
1996 – 1997
|
| Project Status |
Completed (Fiscal Year 1997)
|
| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1997: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1996: ¥1,700,000 (Direct Cost: ¥1,700,000)
|
|---|
| Keywords | Renal cell carcinoma / Chromosome abnormality / Chromosome 9p / p16 / Chromosome 1p / Progression / Tumor suppressor gene / P16遺伝子 |
|---|
| Research Abstract |
In order to investigate the genetic changes involved in the progression of human renal cell carcinoma (RCC), chromosome analysis was performed on a total of 81 RCC primary tumors (72 non-metstatic and 9 metastatic tumors). We found deletion of a short arm of chromosome 1 in 8 out of 9 metastatic cases and in 2 of 72 non-metastatic tumors and also identified loss of a short arm of chromosome 9 in 6 cases of metastatic and 2 cases of non-metastatic tumors, respectively. These results suggest the possibilities that the abnormalities of these chromosomes 1 and 9 may be associated with the progression of human RCC.CDKN2 (p16/CDKN2^<INK4>/MTS1) which encodes p16 protein maps to 9p21 region and was frequently inactivated in a various type of human tumor cell lines and primary tumors, suggesting that p16^<INK4> might be one of tumor suppressor genes associated with the development or progression of human tumors. LOH (loss of heterozygosity) of 9p region was observed in approximately 40 % of RCC primary tumors (Cairns et al., 1995). On the basis of these data reported previously and our data from chromosome analyzes, to observe the potential role of p16 gene inactivation in RCC progression, we analyzed the structure and expression of this gene by using both PCR and RT-PCR techniques in a total of 13 RCC cell lines ( 8 non-metastatic and 5 metastatic lines). The abnormalities of this gene were detected in 11 cell lines (7 non-metastatic and 4 metastatic lines). Our data in the present study suggest that the abnormalities of p16 gene may be involved in the process of progression of RCC.However, p16 abnormalities were not detected in original primary cancer tissues of cell lines. Another explanation for these results is the possibility that p16 abnormalities may be contributed to the in vitro immortalization of RCC cells.
|
