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Allelotype Study of Primary Hepatocellular Carcinoma¹

Departments of Biochemistry [M. F., T. T., Y. N.] and Pathology [O. H., T. K.], Cancer Institute, 1-37-1, Kami-Ikebukuro, Toshima-ku, Tokyo 170; The Second Department of Surgery, Shinshu University, School of Medicine, 3-1-1, Asahi, Matsumoto, 390 [M. F.]; Institute for Molecular and Cellular Biology, Osaka University, Suita, Osaka 565 [T. Im., K. M.]; The First Department of Surgery, Hyogo College of Medicine, 1-1, Mukogawa, Nishinomiya, 663 [E. O., M. M.]; The Third Department of Internal Medicine, University of Tokyo, Faculty of Medicine, Hongo, Bunkyo-ku, Tokyo 113 [T. Is., H. N.]; and Department of Gastroenterology, National Tokyo Sanatorium Hospital, 3-1-1, Takeoka, Kiyose, Tokyo 204 [H. H., M. Y.], Japan

Accumulation of mutations in oncogenes and tumor suppressor genes transforms a normal cell to a malignant cell by allowing it to escape from normal control of growth. In order to learn (a) how many tumor suppressor genes are involved in the tumor progression of hepatocellular carcinoma, (b) whether there is any association among allelic losses of chromosomes, or (c) whether integration of hepatitis B virus into host DNA influences any particular chromosomal losses, we have examined loss of heterozygosity with 44 restriction fragment length polymorphism markers in 46 cases of hepatocellular carcinoma. The markers represented all chromosomal arms except 5p, 8p, 9p, 18p, and acrocentric chromosomes. Allelic losses in tumors indicated that five tumor suppressor genes, located on chromosomes 5q, 10q, 11p, 16q, and 17p, may be involved in this cancer. However, no significant associations were observed among the various allelic losses or between the integration of hepatitis B virus and chromosomal losses. Furthermore, a deletion map for chromosome 16q indicated the localization of a tumor suppressor gene between q22 and q24 and that for chromosome 17p suggested the existence of a second tumor suppressor gene in addition to the p53 gene.

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

² To whom requests for reprints should be addressed.

Received 8/20/90. Accepted 10/22/90.

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