Loss and gain of chromosomes 1, 18, and Y in prostate cancer.

Nuclear suspensions of 42 prostate carcinoma specimens obtained at surgery were used to investigate loss and gain chromosomes 1, 18, and Y by fluorescence in situ hybridization (FISH) with centromere-specific probes. The outcome of FISH analysis was correlated with clinical parameters and the relationship between DNA-FCM (ploidy at cellular level) and FISH (ploidy of individual chromosomes) was assessed. Significant loss of chromosomes 1 and 18 was infrequent (respectively, three and five cases), but 53% of the tested specimens showed loss of Y. Loss was not correlated with DNA ploidy. Significant gain occurred in 36% (chromosome 1), 63% (chromosome 18), and 28% (Y) of the specimens. Gain of chromosome 18 was shown in DNA diploid (7/14) and aneuploid tumors (18/26), while gain of chromosomes 1 and Y was nearly restricted to DNA aneuploid specimens. Significant unbalance between these chromosomes occurred in 11 cases. Most cases which had significant gain of chromosome 1 or 18 showed trisomic as well as tetrasomic cells. Simultaneous loss of some and gain of other investigated chromosomes is suggestive of clonal heterogeneity and/or multiclonality. This was observed in eight tumors. Correlation between DNA-FCM and FISH was best for the Y chromosome. DNA-FCM showed more aberrant histograms with increasing stage and grade of tumors. The presence of numerical aberrations of the investigated chromosomes however, seemed independent of clinical grade or stage.