There is a clear genetic component to prostate cancer susceptibility. Regio
ns reported to be linked to prostate cancer include 1q24-25 (HPC-1), 1q42.2
-43, and Xq27-28. There is limited genetic information on familial prostate
tumors. We used the Utah Population Database to identify familial prostate
cancer cases and selected 35 cases from high-risk families. Tissue blocks
containing discernable tumor were available from 19 cases; 13 of these yiel
ded adequate specimens for analysis. Six cases came from families with link
age to HPC-1, 3 were known to have linkage to Xq27-28, and 4 had no linkage
to a known locus; 7 cases were analyzed from patients who showed no known
linkage (sporadic tumors) as controls. These paraffin-embedded tumors were
laser microdissected, degenerate oligonucleotide (DOP)-amplified, and label
ed for fluorescence detection by comparative genomic hybridization (CGH). L
oss of 7q, 10q, and 16q and gain of Xq were common abnormalities present in
both familiar and sporadic tumors. Distinctive abnormalities included loss
of 3p12-3p22 in 3 of 6 HPC-1-linked cases and in 2 of 3 X-linked cases and
gain of 6q11-6q21 in 2 each of HPC-I and X-linked tumors. In conclusion, l
aser microdissection, DOP-PCR, and CGH is a feasible method for analysis of
paraffin-embedded prostate tumors. This study provides preliminary data su
ggesting that familial prostate cancer harbors some unique genetic changes
when compared with sporadic prostate tumors. (C) 2000 Elsevier Science Inc.
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