Low dose aminoglutethimide without hydrocortisone for the treatment of advanced postmenopausal breast cancer. 1989

P F Bruning, and J M Bonfrer, and A A Hart, and E van der Linden, and M de Jong-Bakker, and A J Moolenaar, and W J Nooijen
Department of Clinical Oncology, The Netherlands Cancer Institute (Antoni van Leeuwenhoekhuis), Amsterdam.

One hundred and one postmenopausal patients with advanced breast cancer were enrolled in a randomized phase II clinical trial to investigate the clinical and hormonal response to aminoglutethimide administered at daily doses of 2 x 125 mg, 3 x 125 mg or 2 x 250 mg, with no addition of hydrocortisone. Among 71 evaluable patients 25% showed objective tumor response (three complete, 15 partial), at all three dose levels and irrespective of the major tumor site. Previous treatment with Tamoxifen had been successful in 75%. Out of the 18 responding patients 10 had estrogen receptor positive, four had estrogen receptor negative tumors; the receptor status was unknown in four other patients. Progression-free interval was more than 700 days in 50% of the responders. Drowsiness caused early drug withdrawal in one patient. Side-effects were very mild, comparing favorably with standard therapy of 250 mg aminoglutethimide q.i.d. plus hydrocortisone. Plasma estrogen levels were reduced by all doses to the same 50% or less as in patients on standard treatment. In nine out of 27 patients a further decrease of estrone levels could be monitored with clinically improved results in five. Plasma cortisol and mineralocorticoids remained normal throughout more than 6 months. The original role of hydrocortisone administration to suppress a reflex rise of ATH in 'medical adrenalectomy' with standard dose aminoglutethimide is no longer tenable. Further phase III comparative clinical results pending, low dose aminoglutethimide as an aromatase inhibitor may at present be considered as an appropriate second-line endocrine treatment with low toxicity and expense.

UI MeSH Term Description Entries
D008593 Menopause The last menstrual period. Permanent cessation of menses (MENSTRUATION) is usually defined after 6 to 12 months of AMENORRHEA in a woman over 45 years of age. In the United States, menopause generally occurs in women between 48 and 55 years of age. Change of Life, Female
D008875 Middle Aged An adult aged 45 - 64 years. Middle Age
D011960 Receptors, Estrogen Cytoplasmic proteins that bind estrogens and migrate to the nucleus where they regulate DNA transcription. Evaluation of the state of estrogen receptors in breast cancer patients has become clinically important. Estrogen Receptor,Estrogen Receptors,Estrogen Nuclear Receptor,Estrogen Receptor Type I,Estrogen Receptor Type II,Estrogen Receptors Type I,Estrogen Receptors Type II,Receptor, Estrogen Nuclear,Receptors, Estrogen, Type I,Receptors, Estrogen, Type II,Nuclear Receptor, Estrogen,Receptor, Estrogen
D001943 Breast Neoplasms Tumors or cancer of the human BREAST. Breast Cancer,Breast Tumors,Cancer of Breast,Breast Carcinoma,Cancer of the Breast,Human Mammary Carcinoma,Malignant Neoplasm of Breast,Malignant Tumor of Breast,Mammary Cancer,Mammary Carcinoma, Human,Mammary Neoplasm, Human,Mammary Neoplasms, Human,Neoplasms, Breast,Tumors, Breast,Breast Carcinomas,Breast Malignant Neoplasm,Breast Malignant Neoplasms,Breast Malignant Tumor,Breast Malignant Tumors,Breast Neoplasm,Breast Tumor,Cancer, Breast,Cancer, Mammary,Cancers, Mammary,Carcinoma, Breast,Carcinoma, Human Mammary,Carcinomas, Breast,Carcinomas, Human Mammary,Human Mammary Carcinomas,Human Mammary Neoplasm,Human Mammary Neoplasms,Mammary Cancers,Mammary Carcinomas, Human,Neoplasm, Breast,Neoplasm, Human Mammary,Neoplasms, Human Mammary,Tumor, Breast
D004341 Drug Evaluation Any process by which toxicity, metabolism, absorption, elimination, preferred route of administration, safe dosage range, etc., for a drug or group of drugs is determined through clinical assessment in humans or veterinary animals. Evaluation Studies, Drug,Drug Evaluation Studies,Drug Evaluation Study,Drug Evaluations,Evaluation Study, Drug,Evaluation, Drug,Evaluations, Drug,Studies, Drug Evaluation,Study, Drug Evaluation
D004958 Estradiol The 17-beta-isomer of estradiol, an aromatized C18 steroid with hydroxyl group at 3-beta- and 17-beta-position. Estradiol-17-beta is the most potent form of mammalian estrogenic steroids. 17 beta-Estradiol,Estradiol-17 beta,Oestradiol,17 beta-Oestradiol,Aerodiol,Delestrogen,Estrace,Estraderm TTS,Estradiol Anhydrous,Estradiol Hemihydrate,Estradiol Hemihydrate, (17 alpha)-Isomer,Estradiol Monohydrate,Estradiol Valerate,Estradiol Valeriante,Estradiol, (+-)-Isomer,Estradiol, (-)-Isomer,Estradiol, (16 alpha,17 alpha)-Isomer,Estradiol, (16 alpha,17 beta)-Isomer,Estradiol, (17-alpha)-Isomer,Estradiol, (8 alpha,17 beta)-(+-)-Isomer,Estradiol, (8 alpha,17 beta)-Isomer,Estradiol, (9 beta,17 alpha)-Isomer,Estradiol, (9 beta,17 beta)-Isomer,Estradiol, Monosodium Salt,Estradiol, Sodium Salt,Estradiol-17 alpha,Estradiol-17beta,Ovocyclin,Progynon-Depot,Progynova,Vivelle,17 beta Estradiol,17 beta Oestradiol,Estradiol 17 alpha,Estradiol 17 beta,Estradiol 17beta,Progynon Depot
D004970 Estrone An aromatized C18 steroid with a 3-hydroxyl group and a 17-ketone, a major mammalian estrogen. It is converted from ANDROSTENEDIONE directly, or from TESTOSTERONE via ESTRADIOL. In humans, it is produced primarily by the cyclic ovaries, PLACENTA, and the ADIPOSE TISSUE of men and postmenopausal women. Folliculin (Hormone),Estrone, (+-)-Isomer,Estrone, (8 alpha)-Isomer,Estrone, (9 beta)-Isomer,Estrovarin,Kestrone,Unigen,Wehgen
D005260 Female Females
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D006854 Hydrocortisone The main glucocorticoid secreted by the ADRENAL CORTEX. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Cortef,Cortisol,Pregn-4-ene-3,20-dione, 11,17,21-trihydroxy-, (11beta)-,11-Epicortisol,Cortifair,Cortril,Epicortisol,Hydrocortisone, (11 alpha)-Isomer,Hydrocortisone, (9 beta,10 alpha,11 alpha)-Isomer,11 Epicortisol

Related Publications

P F Bruning, and J M Bonfrer, and A A Hart, and E van der Linden, and M de Jong-Bakker, and A J Moolenaar, and W J Nooijen
January 1986, Breast cancer research and treatment,
P F Bruning, and J M Bonfrer, and A A Hart, and E van der Linden, and M de Jong-Bakker, and A J Moolenaar, and W J Nooijen
October 1986, Cancer treatment reports,
P F Bruning, and J M Bonfrer, and A A Hart, and E van der Linden, and M de Jong-Bakker, and A J Moolenaar, and W J Nooijen
January 1985, European journal of cancer & clinical oncology,
P F Bruning, and J M Bonfrer, and A A Hart, and E van der Linden, and M de Jong-Bakker, and A J Moolenaar, and W J Nooijen
July 1989, European journal of cancer & clinical oncology,
P F Bruning, and J M Bonfrer, and A A Hart, and E van der Linden, and M de Jong-Bakker, and A J Moolenaar, and W J Nooijen
January 1983, European journal of cancer & clinical oncology,
P F Bruning, and J M Bonfrer, and A A Hart, and E van der Linden, and M de Jong-Bakker, and A J Moolenaar, and W J Nooijen
September 1984, Lancet (London, England),
P F Bruning, and J M Bonfrer, and A A Hart, and E van der Linden, and M de Jong-Bakker, and A J Moolenaar, and W J Nooijen
October 1985, British journal of cancer,
P F Bruning, and J M Bonfrer, and A A Hart, and E van der Linden, and M de Jong-Bakker, and A J Moolenaar, and W J Nooijen
May 1983, British journal of cancer,
P F Bruning, and J M Bonfrer, and A A Hart, and E van der Linden, and M de Jong-Bakker, and A J Moolenaar, and W J Nooijen
August 1982, Cancer research,
P F Bruning, and J M Bonfrer, and A A Hart, and E van der Linden, and M de Jong-Bakker, and A J Moolenaar, and W J Nooijen
January 1987, Bulletin du cancer,
Copied contents to your clipboard!