Molecular genetic abnormalities were assessed on 23 cases of prostate adeno
carcinoma by performing microdissection on archived tumor tissue sections f
ollowed by degenerate oligonucleotide primed PCR (DOP-PCR) on extracted DNA
, providing sufficient product to carry out comparative genomic hybridizati
on (CCH). The results of CGH show a significant regional DNA copy number al
teration in 100% of the cases. Copy number gains were detected most frequen
tly in chromosome 8q (91.3%), followed by chromosome X (43.5%), and chromos
omes 20, 7, 4, and 3 (8.7%). DNA copy number losses occurred most frequentl
y in chromosome 18 (34.8%), followed by chromosome 20 (21.7%), chromosomes
16 and 22 (17.4%) and chromosomes 12, 17, and 19 (8.7%). Since tissue micro
dissection and DOP-PCR yields product for analysis that represents DNA from
pure tumor cells. CGH shows high sensitivity in detecting copy number alte
rations. This method indicates regions of the genome that are likely to be
driven to amplification or deletion by the presence of oncogenes or tumor s
uppressor genes, respectively. The most common alteration detected was a re
gional gain in copy number in chromosome 8 near 8q21, indicating an oncogen
e in this region may be key to development of prostate adenocarcinoma.