| Project/Area Number |
63570747
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Urology
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| Research Institution | Osaka University Medical School |
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Principal Investigator |
FUJITA Jun Osaka University Medical School Associate Professor, 医学部, 助教授 (50173430)
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| Co-Investigator(Kenkyū-buntansha) |
KITAMURA Yukihiko Osaka University Medical School Professor, 医学部, 教授 (70028520)
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| Project Period (FY) |
1988 – 1989
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| Project Status |
Completed (Fiscal Year 1989)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1989: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1988: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Oncogene / Kidney tumor / Chimeric mouse / Anti-oncogene / carcinogenesis / Ras oncogene / 多段階発癌 / 点突然変異 / DNAトランスフェクション / 染色体欠失 / 体細胞変異 |
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| Research Abstract |
Two H-ras oncogenes were detected bY NIH/3T3 transfection assay out of 16 primary kidney tumors, 15 renal cell carcinomas (RCC), and one transitional cell carcinoma in 16 patients. Analysis of ras M_r 21,000 protein suggested single point mutations within codon 12 and 61 in each case. The restriction endonuclease analysis of H-ras gene at codon 12 confirmed this in one of them, and the remaining 15 tumors did not have a mutation at this site. DNAs from the noncancerous portions of the kidney with codon 12 mutated tumor, but not leukocytes from the same patient, showed an abnormal resistance to the endonucleases MspI and HpaII, suggesting a presence of codon 12 mutated H-ras gene in the noncancerous cells. No amplification of ras genes was detected in the 16 tumors analyzed. In one of eight tumors from patients heterozygous for H-ras related BamHI restriction fragments, one allele was lost in the tumor but not in the noncancerous portion of the same kidney. Although cytogenetic studies have previously suggested nonrandom involvement of c-raf-1 gene in RCC, no abnormality in the size nor amount of raf transcript was detected in the 15 RCCs. Our results thus indicated that the genetic lesions affecting ras genes do occur in human RCC, and probably serve as one of multisteps in the carcinogenic process.
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