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Genetic Factors and Suppression of Metastatic Ability of Prostatic Cancer¹

The Johns Hopkins Oncology Center [T. I., Y. I., J. T. I.] and Department of Urology [J. T. I.], The Johns Hopkins University School of Medicine, Baltimore, Maryland 21231

Progression of prostatic cancer from nonmetastatic to high metastatic ability may involve the loss of a metastasis suppressor gene. To test this possibility, nonmetastatic and highly metastatic Dunning rat prostatic cancer cells were fused. Hybrid clones were isolated which conserved the chromosomes from their parental cells. When these hybrids were injected into animals, none developed distant metastases. When these nonmetastatic primary tumors were passaged in vivo, occasional animals developed distant metastases. Cytogenetic analysis of eight of these metastatic revertants demonstrated a consistent loss of a copy of a normal chromosome 2. Although previous studies have demonstrated that specific chromosomes can inhibit tumorigenicity in cell fusion experiments, this is the first study to show that prostatic cancer metastasis is associated with the loss of a specific chromosome. Furthermore, these studies suggest that a metastasis suppressor gene for rat prostatic cancer is located on chromosome 2.

¹ These studies were supported by Department of Health and Human Services Grant CA 50601.

² To whom requests for reprints should be addressed, at Breast Cancer Laboratories, The Johns Hopkins Oncology Center, Room 201, 422 N. Bond Street, Baltimore, MD 21231.

Received 3/19/91. Accepted 5/ 1/91.

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