NUMERICAL ABNORMALITIES OF CHROMOSOME-7 IN HUMAN PROSTATE-CANCER DETECTED BY FLUORESCENCE IN-SITU HYBRIDIZATION (FISH) ON PARAFFIN-EMBEDDEDTISSUE-SECTIONS WITH CENTROMERE-SPECIFIC DNA PROBES

Fluorescence in situ hybridization (FISH) using chromosome-specific al pha-satellite DNA probes for chromosomes 7, 8, and 12 was performed on paraffin-embedded tissue sections and touch imprint preparations of 5 3 cases of human prostate cancer. Subsequent haematoxylin and eosin (H & E) staining of the hybridized tissue sections allowed unambiguous a ssignment of hybridization signals either to tumour or to non-tumorous parenchyma. Fifty-three cases of human prostate cancer were evaluated for numerical aberrations of chromosome 7. Scoring 200 cells of tumou r and non-tumorous parenchyma in each case revealed abnormalities excl usively in tumour parenchyma in 41 cases (77 per cent). Ten of 41 case s (24 per cent) showed trisomy 7, and 15 cases (37 per cent) monosomy 7 or trisomy 7 in combination with monosomy 7, respectively. Sixteen c ases (39 per cent) exhibited polysomy 7 in cells of the tumour parench yma. In the tumour tissue in one case, different polyploid clones (tri ploid, tetraploid) and polysomy 7 could be identified by double hybrid ization with chromosome-specific DNA probes for chromosome 7, plus 8 o r 12. The indicated numerical aberrations of chromosome 7 were correla ted with 78 per cent of advanced pathological stages or poorly differe ntiated tumours (pT3/4 or G3) of prostate carcinomas. A statistical an alysis of the data revealed significant relationships of particular nu merical abnormalities of chromosome 7 to different pathological catego ries (pT, G, pN) of tumour classification. For the T-classification, t he frequency of cells carrying polysomy 7 and polysomy 7/+7 increases significantly from pT1 to pT3/4 (P=0.022). A significant increase from G1 to G3 also became apparent for the total frequencies of numerical abnormal cells (P=0.05).