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Loss of Heterozygosity of the BRCA1 and Other Loci on Chromosome 17q in Human Prostate Cancer¹

Departments of Radiation Oncology (Cancer Biology Division) [X. G., A. Z., A. S., A. T. P., K. V. H.] and Pathology [D. J. G., W. S., K. V. H.], Wayne State University School of Medicine, Detroit, Michigan 48202

A putative tumor suppressor gene, the BRCA1 gene, on chromosome 17q21 has recently been identified and shown to be mutated in breast and ovarian cancers. We have undertaken the present study to explore the possible involvement of the BRCA1 and/or other potential genes on chromosome 17q in prostate cancer. Twenty-three patients were screened by PCR for loss of heterozygosity at five microsatellite loci spanning the region of 17q12–21. One of the loci (i.e., D17S855) studied is intragenic to the BRCA1. Forty-four and 40% of the informative cases showed loss of heterozygosity at the BRCA1 (D17S855) and D17S856 loci, respectively, whereas 10%, 10%, and 11% of the informative cases were positive for loss of heterozygosity at the D17S250, D17S579, and D17S588 loci, respectively. Overall, 52% (11/21) of the informative cases have allelic loss of at least one locus on chromosome 17q. Our data suggest that the BRCA1 and/or other genes within the interval between BRCA1 and D17S856 on 17q21 may be important in the pathogenesis of prostate cancer.

¹ Supported by Harper Hospital Development Fund (A. T. P., K. V. H.).

² To whom requests for reprints should be addressed, at Division of Cancer Biology, Department of Radiation Oncology, Wayne State University, 431 Chemistry Building, Detroit, MI 48202.

Received 12/ 1/94. Accepted 1/20/95.

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