Comparative genomic hybridization reveals DNA copy number gains to frequently occur in human prostate cancer

BACKGROUND. Despite intensive studies over many years, there is only limite d knowledge on the genetic changes underlying the development and progressi on of prostate cancer. No specific prostate carcinoma-related genetic event has yet been identified. METHODS. In order to gain an overall view of regional chromosome gains and losses, comparative genomic hybridization (CGH) was used on a series of 16 prostate adenocarcinomas. Five benign prostate hyperplasia (BPH) samples we re also evaluated. RESULTS. Using CGH, chromosome alterations were observed in 81% of the pros tate carcinomas analyzed. Gains of DNA copy numbers were found as the predo minant imbalance, with chromosomes 3q (56%),:12q (56%), 8q (50%), Xq (50%), 4 (44%), 6q (44%), 5 (38%), 7q (38%), 9p (38%), and 13q (31%) being most f requently involved. Whereas DNA copy number gains comprised the whole chrom osome or almost a Mi hole arm of chromosomes 4, 5, 6, 9, and 13, the minima l overlapping regions on the other chromosomes were mapped to 3q25-q26, 8q2 1-q22, 12q13-q21, 7q31, and Xq22-q25. High-level amplifications were not fo und. Other chromosomes with nonrandom gains or losses of DNA sequences were discovered. The five BPH samples were found to be normal. CONCLUSIONS. Amplification events at different chromosomal sites seem impor tant in prostate cancer development. A new chromosome region with DNA copy number gains was identified on 12q, while other regions on 3q, 7q, 8q, and Xq were confirmed or narrowed down, indicating a possible role of known or putative protooncogenes in these regions for prostate cancer growth. Our lo w detection rate of DNA losses may to some part be explained by CGH immanen t technical Limitations. (C) 1999 Wiley-Liss, Inc.