Prostate cancer is the most common malignancy among men in Western industrialized countries. The molecular pathogenesis of the disease is poorly known. Over the past 10 years, chromosomal aberrations in prostate cancer have been studied with several techniques, such as loss of heterozygosity (LOH), classical cytogenetics, and molecular cytogenetics, namely with fluorescence in situ hybridization (FISH) and comparative genomic hybridization (CGH). These analyses, especially those performed by CGH, have enabled the distinction of the predominant chromosomal regions of involvement in prostate cancer. Studies have shown that the most common chromosomal alterations in prostate cancer are losses at 1p, 6q, 8p, 10q, 13q, 16q, and 18q and gains at 1q, 2p, 7, 8q, 18q, and Xq. Fluorescence in situ hybridization (FISH) has been used to identify the target genes for some of these chromosomal alterations. For example, amplifications of AR (at Xq12), MYC (8q24), and EIF3S3 (8q23) have been found in a large fraction of hormone-refractory prostate cancer by FISH. However, many of the critical oncogenes and tumor suppressor genes located in the altered chromosomal regions have not yet been identified.