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Allelotype of Renal Cell Carcinoma¹

Department of Biochemistry, Cancer Institute [R. M., Y. N.], Department of Genetic Research Laboratory, SRL Incorporation [R. M., M. T., K. H., Y. T.], Department of Urology, Kobe National Hospital [J. I.], Department of Urology [S. K.], Department of Pathology [S. M.], Kobe University, School of Medicine, Tokyo, Japan

Several recent studies based on restriction fragment length polymorphism analysis have supported the concept that the accumulation of multiple genetic alterations converts a normal cell to a malignant cell. Activation of oncogenes and/or inactivation of tumor suppressor genes have been observed during tumor progression in colorectal cancer, lung cancer, and breast cancer. To investigate the possibility that multiple genes are altered during the progression of renal cell carcinoma, we have used restriction fragment length polymorphism markers throughout the genome to test for loss of heterozygosity in 38 renal cell carcinomas. Nearly 64% of the tumors had lost heterozygosity on the short arm of chromosome 3. We also observed loss of heterozygosity averaging about 30% at informative loci on six other chromosomal arms (chromosomes 5q, 6q, 10q, 11q, 17p, and 19p). These results lead us to suspect the existence of several tumor suppressor genes associated with carcinogenesis of renal cell carcinoma.

¹ This work was supported in part by a Grant-in-Aid from the Ministry of Education, Science and Culture, Japan.

² To whom requests for reprints should be addressed, at Department of Biochemistry, Cancer Institute, 1-37-1, Kami-Ikebukuro, Toshima-ku, Tokyo 170, Japan.

Received 8/31/90. Accepted 11/12/90.

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