Immunolocalization of oestrogen and progesterone receptors in prostatic hyperplasia and carcinoma

Oestrogen receptors and progesterone receptors were immunolocalized in 19 patients with benign prostatic hyperplasia and in 26 patients with prostatic carcinoma. Immunohistochemistry was performed on tissue that had been fixed in 8% paraformaldehyde and then paraffin-embedded, using microwave irradiation for antigen retrieval. Oestrogen receptor expression was observed exclusively in the stromal cells of six out of 26 (23%) patients with prostatic carcinoma, but in none of the cells of patients with benign prostatic hyperplasia. Progesterone receptor expression was detected in 16 of 19 (84%) and 17 of 19 (89%) of the epithelial cells and stromal cells of patients with benign prostatic hyperplasia, respectively. In patients with prostatic carcinoma, progesterone receptor immunoreactivity was observed in 12 of 20 (46%) and 20 of 26 (77%) of the carcinoma and stromal cells of prostatic carcinoma, respectively. The ratio of epithelial cells with progesterone receptor immunoreactivity corresponded well with that of stromal cells with immunoreactivity in patients with benign prostatic hyperplasia. However, the ratio of stromal cells with progesterone receptor immunoreactivity was much higher than that in carcinoma cells in patients with prostatic carcinoma. Immunolocalization patterns or the ratio of the cells with progesterone receptor immunoreactivity did not significantly correlate with histological differentiation or patient's age in carcinoma cases. However, patients with advanced surgical stages of disease demonstrated a significantly smaller number of carcinoma and stromal cells with progesterone immunoreactivity in patients with prostatic carcinoma. These results suggest that oestrogens do not have a direct effect on the biological behaviour of benign prostatic hyperplasia and prostatic carcinoma, but that progesterone appears to play a role in the pathogenesis of benign prostatic hyperplasia and prostatic carcinoma.