Chromosome Deletion Patterns in Prostate Cancer

Various nonrandom chromosomal aberrations have been identified in prostate carcinoma. These aberrations include deletions of several chromosome regions, particularly the chromosome 8 short arm. Large-scale numerical aberrations, reflected in aberrant DNA ploidy, are also found in a minority of cases. However, it is unclear whetherprostate carcinomas contain aberrations of certain chromosome regions that are deletedfrequently in other common types ofcancer. In this study, we performed dual-colorfluorescence in situ hybridization on intact nuclei from touch preparations of 16prostate cancers. Chromosome copy number was determined using pericentromeric probes, whereas potential chromosome arm deletions were evaluated using yeast artificial chomosome (YAC) and Pl probes. Two YAC probes targeted chromosome 8 short arm regions known to be deleted frequently in prostate cancer. Other YACs and Pls were for chromosome regions, including 1p22, 3p14, 6q21, 9p21, and 22q12, that are deletion targets in a variety of cancers although not extensively studied in prostate cancer. Hybridization efficiencies and signal intensities were exceUentfor both repeat sequence (a-satellite) and singlecopy (YAC and P1) fluorescence in situ hybridization probes. Of 16 prostate cancers, 11 had clonal aberrations of I or more of the 13 chromosome regions evaluated, and 10 cases (62.5%) had 8p deletions, including 4 cases with 8p deletion in virtually all cells and aneuploidy in only a subset of those deleted ceUs. Deletions at 3p14, 6q21, and 22q12 were identified in 2, 1, and I case, respectively, and each ofthose cases had a similarly sized cell population with 8p deletion. These studies confirm 8p deletion in the majority ofprostate carcinomas. 8p deletions appear to be early events in prostate tumortigenesis, often antedating aneuploidy. Fluorescence in situ hybridization strategies incorporating pericentromeric and single-copy regional chromosome probes offer a powerful and efficient meansfor determiningfrequency andprogression ofoncogenetic events in prostate cancer. (AmJ Pathol 1996, 149:1565-1573)