Is there still a role for intermittent androgen-deprivation therapy for prostate cancer? No.
In the 1990s, Bruchovsky et al1 and Sato et al2 reported that in the androgen-dependent mammary carcinoma and LNCaP (androgen-sensitive human prostate adenocarcinoma cells) prostate cancer models the proportion of residual “androgen-independent” stem cells, surviving androgen withdrawal, could adapt to androgen-depleted environment and that intermittent reexposure to androgens reduces the proportion of surviving cells and delay emergence of androgen independence, thus providing the basis for the intermittent androgen deprivation (IAD) hypothesis. Clinically it was proposed that IAD allows recovery of gonadal function and consequently reexposes the disease to intrinsic testosterone during off-treatment period. The objective was to delay emergence of androgen independence (as defined 26 years ago) and thus improve outcomes, including progression-free and overall survival (OS) and quality of life (QOL) compared with continuous androgen deprivation (CAD).