Genetic alterations in microdissected prostate cancer cells by comparative genomic hybridization

Prostate Cancer Prostatic Dis. 2000 Aug;3(2):110-114. doi: 10.1038/sj.pcan.4500401.

Abstract

Molecular genetic abnormalities were assessed on 23 cases of prostate adenocarcinoma by performing microdissection on archived tumor tissue sections followed by degenerate oligonucleotide primed PCR (DOP-PCR) on extracted DNA, providing sufficient product to carry out comparative genomic hybridization (CGH). The results of CGH show a significant regional DNA copy number alteration in 100% of the cases. Copy number gains were detected most frequently in chromosome 8q (91.3%), followed by chromosome X (43.5%), and chromosomes 20, 7, 4, and 3 (8.7%). DNA copy number losses occurred most frequently 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 microdissection and DOP-PCR yields product for analysis that represents DNA from pure tumor cells. CGH shows high sensitivity in detecting copy number alterations. This method indicates regions of the genome that are likely to be driven to amplification or deletion by the presence of oncogenes or tumor suppressor genes, respectively. The most common alteration detected was a regional gain in copy number in chromosome 8 near 8q21, indicating an oncogene in this region may be key to development of prostate adenocarcinoma. Prostate Cancer and Prostatic Diseases (2000) 3, 110-114