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Department of Urology, School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260 [T. I., N. N., H. S., J. S.]; Department of Molecular and Cell Genetics, School of Medicine, Tottori University, Yonago, Tottori 683 [M. O.]; Department of Biochemistry, Cancer Institute, Toshima, Tokyo 170 [M. E., Y. N.]; and Division of Radiation Hazards, National Institute of Radiological Sciences, Chiba 263 [I. H.], Japan; and the Johns Hopkins Oncology Center, and The James Buchanan Brady Urological Institute, Department of Urology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21231 [J. T. I.]
In previous allelotype analyses of human prostatic cancer specimens, allelic loss on the short arm of chromosome 8 is frequently observed. However, it is still unclear whether this allelic loss is an initial event or a later one in development of prostatic cancer. Our previous studies demonstrate that introduction of human chromosome 11 into highly metastatic rat prostatic cancer cells results in suppression of metastatic ability without suppression of the in vivo growth rate or tumorigenicity of the hybrid cells (T. Ichikawa et al. Cancer Res., 52: 34863490, 1992). To clarify the role of human chromosome 8 in prostatic cancer, this chromosome was introduced into highly metastatic rat prostatic cancer cells using microcell-mediated chromosome transfer. Introduction of human chromosome 8 resulted in suppression of metastatic ability of the microcell hybrids, whereas no suppression of the in vivo growth rate or tumorigenicity was observed. These results demonstrate that human chromosome 8 contains metastasls suppressor gene(s) for prostatic cancer derived from a rat. These also suggest that human chromosome 8 has an important role in development of prostatic cancer.
1 These studies were supported in part by Grants-in-Aid from The Japanese Urological Association (1992), the Ministry of Education, Science and Culture (05771175, 05151013, 05151032), and the Ministry of Health and Welfare (510).
2 To whom requests for reprints should be addressed.
Received 1/ 5/94. Accepted 3/18/94.
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