Altered expression of p53, but not Rb, is involved in canine prostatic carcinogenesis

- The increased expression of p53 in prostate cancer corresponds to genetic defects in the p53 gene.
- Neoplastic cells maintain a similar expression of Rb as normal and hyperplastic cells.
- Rb expression if variable according to the cell-cycle status and differentiation.
- p53 and not Rb is involved in the development and growth of canine prostate cancer.

Abnormalities in the retinoblastoma (Rb) and p53 tumour suppressor gene have been frequently detected in human and canine cancers, but never investigated in canine prostate cancer, considered a good model for the advanced and aggressive androgen-resistant prostate cancer in men. Therefore, the aim of this study was to evaluate the immunohistochemical expression of Rb and p53 in 6 normal canine prostates, 15 canine prostates with benign prostatic hyperplasia (BPH) and 10 prostatic carcinomas (PCs). In all normal samples, p53 was expressed in low number of epithelial cells, while a greater number of positive cells were observed in BPH and PC. The mean number of positive cells was statistically significantly higher in PCs than normal and hyperplastic prostates. A cytoplasmic or nucleo-cytoplasmic staining was observed in 5 out of 10 PCs. Rb protein was expressed in high number of normal, hyperplastic and neoplastic cells without a statistically significant differences. Considering that Rb is frequently lost in human prostate cancer, we suggest that Rb is not involved in canine prostatic carcinogenesis. On the other hand, the increased expression of p53 that corresponds to genetic defects in the p53 gene may be associated with the malignant growth of canine prostate cancer, conferring an apoptosis-resistant phenotype.