Endocrine Abstracts

Androgen, a key endocrine factor that drives normal prostate gland growth, is implicated in the progression of prostate cancer and benign prostate hyperplasia. However, failure to adapt androgen ablation therapy for the treatment of prostatic diseases cast doubts on our understanding of androgen role in the regulation of normal and abnormal prostate gland growth. This study was conducted to gain further insight into the role of androgen in maintaining a balanced prostatic cell proliferation, differentiation and death. The effect of androgen ablation on the prostate gland growth was compared in normal and castrated dogs. Mature dogs were castrated under general anesthesia and euthainized after one and two weeks. Normal prostate gland structure is characterized by the presence of differentiated columnar secretary epithelial cells and progenitor basal cells that are located within acini embedded in a thin fibromuscular tissue. Histological evaluation of prostate gland from castrated dogs revealed that different prostatic cells experienced variable changes ranged from cellular atrophy to death or hyperplasia. The secretory epithelial cells became atrophied within one week of castration and underwent a massive death after two weeks. These changes were accompanied by basal cell hyperplasia with no signs of differentiation into secretory epithelial cells. In addition, androgen ablation allowed for a progressive mesynchymal cell proliferation, leading to a prominent increase in the inter-acinar fibromuscular tissue. Based on these findings it appears that androgen presence is a prerequisite for secretory cell survival, cell proliferation and to drive differentiation of proliferating cells into viable secretory epithelial cells.