Hormonal therapy in endometrial carcinoma. 1990

K C Podratz
Department of Obstetrics and Gynecology, Mayo Clinic, Rochester, MN 55905.

Although hormonal agents have been used to treat endometrial cancer for nearly 30 years, response rates have remained essentially unchanged. Furthermore, objective response rates vary considerably from institution to institution, presumably because of differences in accepted response criteria and patient selection. The latter is particularly influenced by the distribution within the treated population of well-differentiated and poorly differentiated tumor histologic types. Nevertheless, the rapid attrition after hormonal therapy begins and the limited long-term salvage in nonselected patients with advanced primary or recurrent disease suggest primary nonresponsiveness or acquired tumor refractoriness to hormonal therapy. The determination of tumor progesterone receptor levels has made it easier to identify patients with sensitivity to such therapy. Recent investigations have shown favourable response rates (72%) after administration of progestational agents in patients with progesterone receptor-rich tumors. Similarly, responses have been reported with antiestrogens and combination progestin-antiestrogen therapy, recent laboratory observations having suggested potential benefit from sequential administration. Although these clinical and laboratory findings are encouraging, the limited duration of objective responses and the poor long-term survival rates continue to temper enthusiasm for routine hormonal therapy. Properly stratified (according to pathologic, biochemical, and clinical criteria), prospective, randomized, double-blind studies with more definitive end points, such as progression-free survival and overall survival, are mandatory to further evaluate the merits of various therapeutic regimens using gonadal hormones.

UI MeSH Term Description Entries
D011372 Progestins Compounds that interact with PROGESTERONE RECEPTORS in target tissues to bring about the effects similar to those of PROGESTERONE. Primary actions of progestins, including natural and synthetic steroids, are on the UTERUS and the MAMMARY GLAND in preparation for and in maintenance of PREGNANCY. Gestagenic Agent,Progestagen,Progestagenic Agent,Progestational Agent,Progestational Compound,Progestational Hormone,Progestogen,Progestogens,Gestagen,Gestagen Effect,Gestagen Effects,Gestagenic Agents,Gestagenic Effect,Gestagenic Effects,Gestagens,Progestagenic Agents,Progestagens,Progestational Agents,Progestational Compounds,Progestational Hormones,Progestin,Progestin Effect,Progestin Effects,Progestogen Effect,Progestogen Effects,Agent, Gestagenic,Agent, Progestagenic,Agent, Progestational,Compound, Progestational,Effect, Gestagen,Effect, Gestagenic,Effect, Progestin,Effect, Progestogen,Effects, Gestagen,Effects, Gestagenic,Effects, Progestin,Effects, Progestogen,Hormone, Progestational
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
D011980 Receptors, Progesterone Specific proteins found in or on cells of progesterone target tissues that specifically combine with progesterone. The cytosol progesterone-receptor complex then associates with the nucleic acids to initiate protein synthesis. There are two kinds of progesterone receptors, A and B. Both are induced by estrogen and have short half-lives. Progesterone Receptors,Progestin Receptor,Progestin Receptors,Receptor, Progesterone,Receptors, Progestin,Progesterone Receptor,Receptor, Progestin
D002277 Carcinoma A malignant neoplasm made up of epithelial cells tending to infiltrate the surrounding tissues and give rise to metastases. It is a histological type of neoplasm and not a synonym for "cancer." Carcinoma, Anaplastic,Carcinoma, Spindle-Cell,Carcinoma, Undifferentiated,Carcinomatosis,Epithelial Neoplasms, Malignant,Epithelioma,Epithelial Tumors, Malignant,Malignant Epithelial Neoplasms,Neoplasms, Malignant Epithelial,Anaplastic Carcinoma,Anaplastic Carcinomas,Carcinoma, Spindle Cell,Carcinomas,Carcinomatoses,Epithelial Neoplasm, Malignant,Epithelial Tumor, Malignant,Epitheliomas,Malignant Epithelial Neoplasm,Malignant Epithelial Tumor,Malignant Epithelial Tumors,Neoplasm, Malignant Epithelial,Spindle-Cell Carcinoma,Spindle-Cell Carcinomas,Tumor, Malignant Epithelial,Undifferentiated Carcinoma,Undifferentiated Carcinomas
D004965 Estrogen Antagonists Compounds which inhibit or antagonize the action or biosynthesis of estrogenic compounds. Estradiol Antagonists,Antagonists, Estradiol,Antagonists, Estrogen
D005260 Female Females
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D014594 Uterine Neoplasms Tumors or cancer of the UTERUS. Cancer of Uterus,Uterine Cancer,Cancer of the Uterus,Neoplasms, Uterine,Neoplasms, Uterus,Uterus Cancer,Uterus Neoplasms,Cancer, Uterine,Cancer, Uterus,Cancers, Uterine,Cancers, Uterus,Neoplasm, Uterine,Neoplasm, Uterus,Uterine Cancers,Uterine Neoplasm,Uterus Cancers,Uterus Neoplasm
D015996 Survival Rate The proportion of survivors in a group, e.g., of patients, studied and followed over a period, or the proportion of persons in a specified group alive at the beginning of a time interval who survive to the end of the interval. It is often studied using life table methods. Cumulative Survival Rate,Mean Survival Time,Cumulative Survival Rates,Mean Survival Times,Rate, Cumulative Survival,Rate, Survival,Rates, Cumulative Survival,Rates, Survival,Survival Rate, Cumulative,Survival Rates,Survival Rates, Cumulative,Survival Time, Mean,Survival Times, Mean,Time, Mean Survival,Times, Mean Survival

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