| Project/Area Number |
06671587
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Urology
|
|---|
| Research Institution | KYOTO UNIVERSITY |
|---|
Principal Investigator |
TERACHI Toshiro Faculty of Medicine, Kyoto University Assistant Professor, 医学研究科, 講師 (50207487)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
TOYOKUNI Shinya Faculty of Medicine, Kyoto University Lecturer, 医学研究科, 講師 (90252460)
MIZUTANI Youichi Faculty of Medicine, Kyoto University Lecturer, 医学研究科, 助手 (10243031)
OGAWA Osamu Faculty of Medicine, Kyoto University Lecturer, 医学研究科, 助手 (90260611)
KAKEHI Yoshiyuki Faculty of Medicine, Kyoto University Assistant Professor, 医学研究科, 講師 (20214273)
|
|---|
| Project Period (FY) |
1994 – 1995
|
| Project Status |
Completed (Fiscal Year 1995)
|
| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1995: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1994: ¥1,600,000 (Direct Cost: ¥1,600,000)
|
|---|
| Keywords | Renal Cell Carcinoma / mdr 1 / MRP / E-Cadherin / MAP Kinase / chromosome 9P21-22 / P53 / HLA type / 腎細胞癌 / HLA class II抗原 / MAP kinase / MEK / Raf-1 / 染色体9p21-22 / p16 / 腎癌 / HLA-typing / p53遺伝子コドン72 / 8-hydroxydeoxyguanosine(8-OHdg) / proto-oncogene発現 / c-met / p16遺伝子異常 |
|---|
| Research Abstract |
Our results in the studies supported by Grants-in Aid from Ministry of Education, Science, and Culture of Japan are the followings :
1, The biological characteristics of renal cell carcinoma (RCC). 1) 'Persistent oxidative stress' was correlated with the carcinogenesis in RCCs. 2) The expression levels of the mdr1, MRP,and topoisomerase II were different among histopathologic subtypes of RCCs. In papillary subtype, MRP gene was much less expressed compared with other subtypes. 3) RCC cells which resisted to CDDP showed the increase of the sensitivity to CDDP,when these cells were treated with the antibody of Interleukin 6, or its receptor. 4) The expression levels of the E-cadherin were different among histopathologic subtypes of RCCs. In papillary and chromophobe subtypes, the expression of the E-cadherin was maintained. 5) Approximately 80% of the RCCs showed enhanced-expression of the c-met gene. 6) Constitutive Activation of Mitogen-Activated Protein (MAP) Kinases was demonstrated in almost half of Human RCCs. 7) The LOH on chromosome 9P21-22 was strongly correlated with the progression and metastasis of Human RCCs.
2, The factors contributed to the tumorigenesis or tumor development of renal cell carcinomas : In the aspects of the affected patients. 8) Allelic Frequency of p53 Gene Codon 72 Polymorphism was correlated with the carcinogenesis in Human RCCs. In the patients, the frequency of the Arg/Arg was lower, and that of the Pro/Pro was higher than the normal Japanese population. 9) In the patients affected RCCs, the frequency of the 0404 or the 0120 allele on the HLA class II DRB 1 was significantly low when compared with the normal Japanese population.
We could obtain so many systemic data of the tumorigenesis and development of human renal call carcinoma.
|
