LOSS OF HETEROZYGOSITY AND OVEREXPRESSION OF P53 GENE IN HUMAN PRIMARY PROSTATIC ADENOCARCINOMA

We have examined the loss of heterozygosity (LOH) of codon 72 and evaluated the overexpression of the tumor suppressor gene p53 in 43 primary human prostatic adenocarcinomas (PC). DNA from tumors and normal tissues were extracted from radical prostatectomy specimens. LOH was determined by restriction fragment length polymorphism analysis (RFLP) of the codon-specific endonuclease-digested polymerase chain reaction (PCR) products. Results showed 17 heterozygous cases (39%) among this patient group. Seven of the heterozygous cases displayed LOH. Six of the seven LOH cases were high-grade PCs with Gleason's combined score of greater than or equal to 7 and showed capsular invasion. One of the LOH cases, however, displayed an intermediate morphological score of 6 but also with evidence of capsular invasion. The 43 primary PCs were also examined for overexpression of p53 by a monoclonal antibody-mediated immunofluorescence reaction. Overexpression of nuclear p53 as detected by antibody was demonstrable only in tumors with combined morphological Grade greater than or equal to 7. No significant overexpression of p53 was noted in lower-grade tumors. In addition, 10 cases of benign prostatic hyperplasia (BPH) were evaluated for p53 expression. All 10 cases showed no detectable p53 overexpression.