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Radiation Biology Center, Kyoto University, Yoshida-Konoecho, Sakyo-ku, Kyoto 606 [N. N., I. S., M. I., K. I.]; and Second Department of Internal Medicine [N. N., Y. F., T. K., R. K., T. S., M. F., M. A., K. N.] and First Department of Surgery [I. S.], Kyoto University Faculty of Medicine, 54 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto 606, Japan
We analyzed the genetic alterations of the cyclin D1 and INT-2 genes in hepatocellular carcinomas (HCCs) from 45 patients. Among these, expression of the cyclin D1 mRNA was also analyzed in 18 of them by Northern blotting. The cyclin D1 gene was amplified 3–16 fold in five HCCs (11%); among these, the INT-2 gene was also amplified 2–10 fold in four HCCs. We analyzed the mRNA of cyclin D1 in four HCCs with gene amplifications, and 6–10 fold overexpressions were detected in all of them. Because the cyclin D1 gene was amplified in patients at an advanced stage of HCC with rapid tumor growth, it appeared to be associated with the aggressive behavior of tumors. Studies on loss of heterozygosity on chromosome 13q, where the retinoblastoma (RB) gene is located, indicated that all HCCs with an amplified cyclin D1 gene retained heterozygosity on chromosome 13q. These results suggest that amplification and overexpression of the cyclin D1 gene result in the rapid growth of a subset of HCC, even though the function of the RB gene is retained.
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.
Received 3/ 7/94. Accepted 5/ 4/94.
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