TESTOLACTONE IS A SYNTHETIC ANTINEOPLASTIC AGENT. ALTHOUGH THE PRECISE MECHANISM BY WHICH TESTOLACTONE PRODUCES ITS CLINICAL ANTINEOPLASTIC EFFECTS HAS NOT BEEN ESTABLISHED, ITS PRINCIPAL ACTION IS REPORTED TO BE INHIBITION OF STEROID AROMATASE ACTIVITY AND CONSEQUENT REDUCTION IN ESTRONE SYNTHESIS FROM ADRENAL ANDROSTENEDIONE, THE MAJOR SOURCE OF ESTROGEN IN POSTMENOPAUSAL WOMEN. BASED ON IN VITROSTUDIES, THE AROMATASE INHIBITION MAY BE NONCOMPETITIVE AND IRREVERSIBLE. THIS PHENOMENON MAY ACCOUNT FOR THE PERSISTENCE OF TESTOLACTONE'S EFFECT ON ESTROGEN SYNTHESIS AFTER DRUG WITHDRAWAL.