Receptor stabilization, activation, dimerization, and binding to cogna
te sequences on DNA are possible with antagonists. Tissue-, steroid-,
and species-dependent differences in all these parameters, despite ide
ntical structure of the receptor from various sources for any one ster
oid hormone class, suggest posttranslational modifications of a primar
y gene product. Clinically, it is now possible to visualize receptor-s
pecific antihormone therapy of various steroid-dependent maladies (can
cer of the breast, uterus, or prostate, Cushing's disease, hypertensiv
e disorders, etc.) where surgical resection has been hitherto most eff
ective. Amelioration of adverse side effects, associated with currentl
y available semispecific derivatives, should permit wider applications
in a variety of other situations in the near future.