Introduction Prostate cancer constitutes a major health issue in Western countries where it is now the most frequently diagnosed invasive tumour and second leading cause of cancer deaths (Wingo et al. 1995). Androgen action in prostate cancers, as in the normal prostate gland and other target organs, is mediated by the androgen receptor (AR), a ligand-activated nuclear transcription factor that is a member of the steroid/thyroid hormone receptor gene superfamily (O'Malley 1990, Truss & Beato 1993). Although the human AR has only recently been cloned (Chang et al. 1988, Lubahn et al. 1988, Trapman et al. 1988, Tilley et al. 1989), specific actions of androgens on the growth, differentiation and function of the prostate gland were elucidated early this century. In 1941, Huggins and Hodges demonstrated that, similar to non-malignant prostate, prostate cancers were androgen-responsive and that tumour regression was evident following removal of testicular androgens by castration. More than