Genetic chances in clinically organ-confined prostate cancer by comparative genomic hybridization

Objectives. The genetic basis underlying prostate cancer development and pr ogression is poorly understood. The primary aim of this study was to identi fy chromosomal regions important for progression in clinically localized pr ostate cancer removed by radical prostatectomy. Methods. Comparative genomic hybridization was used for whole genome screen ing of DNA sequence copy number alterations in 28 pathologically organ-conf ined tumors (pT2) and 28 tumors with infiltration of the seminal vesicles ( pT3b). Results. Comparative genomic hybridization analysis showed on average 2.0 /- 2.4 chromosomal alterations per tumor with move frequent losses (mean 1. 3 +/- 1.8) than gains (mean 0.7 +/- 1.0). The percentage of tumors without alterations was higher in Stage pT2 (21%) than in Stage pT3b (50%). Losses of 8p (21%), 13q (21%), 5q (14%), 16q (14%), and 18q (13%) and gains of Xq (21%) and 8q (9%) were the most prevalent changes. Distinct regional altera tions included minimal overlapping regions of loss at 5q13-q21, 6q14-q21, a nd 18q21-qter. There was only a small increase in the number of alterations from Stage pT2 to Stage pT3b (mean 1.6 +/- 2.3 versus 2.5 +/- 2.4). Howeve r, two individual alterations-gain of 8q and loss of 18q-were significantly more frequent in Stage pT3b than in Stage pT2 prostate cancer (P = 0.02 an d P = 0.04, respectively), suggesting that genes in these regions may be im portant for prostate cancer progression. Conclusions. The detection of chromosome 8q gains and 18q losses and the id entification of the corresponding target genes could become a molecular too l for better characterization of clinically localized prostate cancer. UROL OGY 56: 880-885, 2000. (C) 2000, Elsevier Science Inc.