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Activated H-ras Oncogenes in Human Kidney Tumors¹

Institute for Cancer Research, Osaka University Medical School, Nakanoshima, Kita-ku, Osaka 530, Japan [J. F., H. O., Y. E., Y. K.], and Laboratory of Cellular and Molecular Biology, National Cancer Institute, NIH, Bethesda, Maryland 20892 [M. H. K., S. K. S., J. S. R.]

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.

¹ Supported in part by Grants-in-Aid from the Ministry of Education, Science and Culture and the Ministry of Health and Welfare of Japan.

² To whom requests for reprints should be addressed.

Received 1/21/88. Revised 5/13/88. Accepted 6/17/88.

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