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Query: UMLS:C0006142 (breast cancer)
 160,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A simple procedure for the assay of specific estrogen receptors in breast cancer tissue is described. Estrogen receptors were detected in 74% of primary tumors, 71% of skin metastases and 63% of lymph node metastases. Postmenopausal patients and younger oophorectomized women had estrogen receptor-containing tumors more frequently, and at higher levels, than uncastrated, premenopausal, patients. The stability of estrogen receptors was not affected by the transportation of samples from distant hospitals, providing that they were kept frozen in Tris buffer, pH 8.0, at all times.
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PMID:Experience with a simple method for estrogen receptor assay in breast cancer. 0 1

Breast cancer is the result of a multistage carcinogenic process. Initiation, promotion, dependency and autonomy make up a sequence of experimentally distinguishable phases of this process. Progression--the transition from dependency on hormonal support to autonomy--is demonstrable clinically. High-affinity saturatable estrogen binding by breast cancer cytosols distinguishes endocrine-responsive mammary neoplasms from autonomous breast cancers. Approximately 70% of neoplasms containing estrogen-recepor protein at a level of 2.5 femtomoles per mg. protein or higher regress after endocrine ablation (ovariectomy in premenopausal women; adrenalectomy or hypophysectomy in postmenopausal women). Only about 5% of neoplasms lacking the receptor will respond to these maneuvers. Estrogen-receptor content also predicts clinically for estrogen and androgen responsiveness, and experimentally for prolactin dependency. Fifty per cent of primary breast cancers in women are receptor-positive. Normal breast tissue and benign breast lesions characteristically lack receptor protein. The receptor proteins appear to be induced in neoplastic cells during mammary carcinogenesis in endocrinologic settings where non-cancerous breast cells do not contain free receptor in large amounts and fail to manifest endocrinologic growth stimulation. Implications of these findings for endocrinologic management of disseminated mammary cancer, adjuvant therapy, and breast cancer prevention are discussed.
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PMID:Endocrinology in cancer of the breast. Status and prospects. 17 80

Using evidences of estrogen receptors in mammary tumor tissues it was tried 1. to find substances which inhibit the tumor growth by their binding to the estrogen receptors; 2. to predict responsiveness to endocrine therapy; and 3. to find a definition of an improved therapeutic strategy in breast cancer. There is a continuously increasing rate of receptor positive tumors, caused by an improved technique of determination and tissue handling. Estrogen receptors were detected in 73 per cent of all primary mammary tumors and 58 per cent of metastatic tumors respectively. As new therapeutic substances nafoxidine and Estracyt were tested in controlled clinical trials. To get exact data about hormonal sensitivity further quantitative investigations of receptor activities of mammary tumors and their therapeutical responsiveness have to be done. As a new step in the strategy of breast cancer therapy based on receptor determinations a combined therapy with hormones and cytotoxic chemotherapeutics has to be checked in clinical trials in uture.
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PMID:Significance of tissue estrogen receptors in the strategy of breast cancer treatment. 17 15

A relationship between exposure to exogenous estrogens and endometrial carcinoma has been reported in numerous studies. The incidence among those so exposed has been estimated to have been increased from 7.5 to 8 times that of those not exposed. Long-term therapy with estrogens for menopausal symptoms has been the usual history. Breast cancer patients treated with estrogens and young women taking sequential oral contraceptives have had increased risks. In this study, the records of Olmsted County, Minnesota, residents with endometrial uterine cancer diagnosed between 1945-1974 at the Mayo Clinic or at other medical facilities were reviewed. There were 122 adenocarcinomas and 23 adenoacanthomas. In 3 instances, adenocarcinomas contained zones of uterine sarcoma. For each of the 146 patients there were 4 age-matched controls. Estrogen use for 6 months or more was recorded for 39 (27%) of the 145 cases and for 163 (28%) of the 580 controls. The controls had more frequent histories of short-term estrogen therapy. Cancer patients had relatively more estrogen use for menopausal symptoms. The relative risk of endometrial cancer tended to increase with the duration of exposure to conjugated estrogens from 2.0 with any exposure to 4.9 (p less than .01) after 6 months or more and to 7.9 after 3 years or more. The risk increased with larger doses (1.25 mg or more) and with continuous administration of conjugated estrogen. Myometrial invasion was superficial in 77 cases and deep in 44 cases. Long-term use of conjugated estrogen was frequently associated with low-stage low-grade superficially invasive endometrial malignancy. The 5-year survival rate of the 145 patients was 85%. Patients with Stage 1 had a 95% relative 5-year survival rate. Those with Stages 2, 3, or 4 had 50% survival rates. Of other risk factors, obesity and nulliparity were noted. Patients had more frequent records of benign cystic adenoma and of adenomatous hyperplasia than controls. The corrected age-specific rate for endometiral cancer increased to a maximum of about 90/100,000 population per year in the group aged 55-64 and then diminished with age. An increase in endometrial cancer among those at risk may have been nullified by an increase in those who have had a hysterectomy. In this study the incidence of endometrial carcinoma in Olmsted County does not show an increase in the last 3 decades. It is noted that the long-term use of conjugated estrogens in this area has been relatively low.
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PMID:Exogenous estrogen and endometrial carcinoma: case-control and incidence study. 19 Aug 87

Focus is on the current concepts of hormone receptors in breast cancer and their significance to the practicing physician. Hormone receptor assays have proven to be valuable to physicians treating patients with breast cancer. About 2/3 of patients with estrogen receptor (ER+) tumors experience palliation of their symptoms after some type of hormonal manipulation. At this time it is believed that estrogen exerts the most powerful effect on the cancer. There are several methods of testing for estrogen receptors. The 1st method involves injection of tritiated hexesterol prior to surgery and subsequent checking for radioactive estrogens in the mammary tissue. More recently, methods are used in which the receptors can be quantified. 1 method uses a sucrose density gradient. Another and less expensive method is the Dextran-coated charcoal test (DCC). Estrogen receptors have been found in 73% of primary and 58% of metastatic breast cancers using the DCC test. The treatment of choice is always dependent on the patient involved. If the lesion is ER+, some type of hormone manipulation may be considered, which type depending on the menopausal status of the women.
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PMID:Clinical considerations of hormonal receptors in breast cancer. 22 75

Aldehyde-resistant, diaminobenzidine-stained endogenous peroxidases form ideal markers for the biochemical endpoints of hormone stimulation and differentiation of certain mammalian cells and tissues. The lactoperoxidase (LPO)-type of endogenous peroxidases are synthesized by the acinar cells of the salivary, Harderian, lacrimal and mammary glands and are present in their secretions. These LPO-type enzymes, that are inhibited by cyanide and aminotriazole, appear to operate extracellularly as bactericidal agents in milk and in other biological fluids. In the mammary gland, lactoperoxidase is a consistent marker enzyme for differentiated acinar cells engaged in lactogenesis. Myeloperoxidase (MPO)-type endogenous peroxidases are prominent markers for the GERL endomembrane system and differentiated lysosomes in certain cells of the reticuloendothelial system and phagocytes. MPO is prominent within eosinophils, peritoneal macrophages and in Kupffer cells. The MPO-type endogenous peroxidases function primarily within lysosomes as bactericidal agents. Thyroid peroxidase (TPO) is relegated to the cisternae of the granular endoplasmic reticulum and Golgi apparatus, to apical cytoplasmic vesicles and to the luminar cell membrane surface of acinar cells. The enzyme is probably activated at release and functions both in the organification reaction (T leads to To) and in the biosynthesis of thyroxine. Thyroid stimulating hormone (TSH) appears to play a key role in the regulation of TPO levels and activity in the thyroid gland. Certain tissues displaying growth-dependency on estrogen (i.e., uterus, cervix, vagina and the DMBA-induced rat mammary tumor) synthesize and secrete endogenous peroxidase into their lumina. These enzymes serve as important marker proteins of estrogen action, in that they occur distal to the binding of estrogen to its receptor protein. Estrogen antagonists, particularly CI-628 (Parke-Davis) and Nafoxidine (Upjohn) that appear to function through the estrogen receptor mechanism, also induce synthesis of the reproductive tract endogenous peroxidase but inhibit growth of these tissues. Progesterone antagonizes the synthesis of the reproductive tract peroxidases and inhibits growth of the tissues as well, in part, through the reduction of the cytosol estrogen receptor protein. Endogenous peroxidase activity appears to represent a reliable marker for rodent breast cancer tissues displaying dependency for estrogen and is of potential interest as a diagnostic marker protein in human breast cancer. Rat uterine peroxidase (UP) has been investigated by microelectrophoretic techniques. The molecular weight of UP has been determined in the range of 100,000 by using polyacrylamide gradient gels in the absence and presence of nonionic and anionic detergents. The isoelectric point of UP is located between pH 4.5 and 5.9. Employing the two-dimensional combination of isoelectric focusing and gel gradient electrophoresis, UP was separated into two subunits, one having a molecular weight of 70,000, the other less than 20,000.
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PMID:Mammalian endogenous peroxidases as cellular markers and as biosynthetic endpoints of hormone-mediated activity: viewpoint from cytochemistry. 22 20

Despite many years of extensive investigation, there has been neither a clear-cut pattern of hormonal production nor milieu found in women with breast cancer. Estrogen replacement therapy for menopause does not significantly increase the risk of breast cancer and one study indicated that estrogen users have a lower incidence of breast cancer than that observed in untreated women. Some studies have shown that the mortality rate from breast cancer is lower in estrogen-treated postmenopausal women. Only one investigator has found any significantly increased risk of breast cancer in oral contraceptive users. In that report, increased duration of birth control pill use decreased the risk of breast carcinoma. Several studies were unable to find an increased risk of breast cancer from oral contraceptives while one investigation observed a lower incidence in birth control pill users than that expected. The mortality from carcinoma of the breast in oral contraceptive users was lower than in non-users, most likely due to earlier detection. Although some retrospective studies have indicated that estrogen use increases the risk of endometrial cancer, a prospective investigation found only an insignificant increase. Progestogens afford some protection from cancer in estrogen-treated postmenopausal women. The incidence of endometrial adenocarcinoma is lower than that observed in untreated postmenopausal women. Combination oral contraceptives are protective against developing adenocarcinoma of the endometrium but sequential birth control pills may afford less protection.
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PMID:The role of hormones in the etiology of breast and endometrial cancer. 29 15

Breast cancer is often hormone responsive, since growth or regression of tumors can often be modulated by appropriate endocrine manipulations. Estrogen and progesterone appear to be major hormones involved in regulation of breast tumor growth. It has been recently argued that a more accurate marker of hormonal responsiveness might result if an end product of an intact estrogen response system were measured instead of the initial hormone binding step. Progesterone receptor (PgR) has been investigated in this regard since it can be readily measured in human breast tumors and there is clear evidence in experimental breast tumor model systems that PgR is under acute estrogen control. PgR is rarely found in ER- metastatic breast tumors but is present in approximately 59% of ER+ metastatic tumors, especially in those tumors with high levels of ER. Preliminary clinical correlation of ER, PgR and response to endocrine therapy is encouraging. The response rate is significantly higher if the tumor contains both ER and PgR than if the tumor contains ER alone.
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PMID:Current status of estrogen and progesterone receptors in breast cancer. 32 86

The antiestrogens represent a group of compounds, not necessarily steroidal, which are able to decrease the specific uptake of estrogens in vitro and in vivo by various target tissues in the rat and in man. This action is explained either by competitive binding to estrogen receptor sites or, more probably, by failure of the antiestrogen complex, translocated into the nucleus, to stimulate neoformation of receptors in the cytoplasm. This explains the transient estrogenic effect of antiestrogen. Antiestrogens used in humans are hormone specific and antagonize also non-steroidal estrogens, like stilbestrol. Three compounds have been used in advanced breast cancer with the same indications as the older hormonal treatments. They are clomiphene citrate, nafoxidine and tamoxifen. Nafoxidine and tamoxifen are probably equally active. The response rate is between 28 and 35%, with a median duration of nine months. Nafoxidine is toxic for the skin and tamoxifen is the preferred compound. A randomized trial comparing ethinyl estradiol and an antiestrogen showed similar rates of response with the two compounds in advanced breast cancer. The uniformity of results of treatment of advanced breast cancer by hormonal agents including antiestrogens and their limitations, probably justifies the present-day concept which assigns hormonal treatment a secondary role, either as a supplement to cytotoxic chemotherapy or for old and debilitated patients. However, as a supplemented to chemotherapy, hormonal agents are probably important since recent studies have shown that apparently all breast cancers have positive receptor sites, albeit in variable amounts. Because of their lack of toxicity, antiestrogens are probably the best hormonal agents available at present.
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PMID:Antiestrogens in treatment of breast cancer. 32 87

Estrogen replacement in menopause should be used for specific symptoms such as ovarian failure, hot flushes, vaginal atrophy, atrophy of the vulva, and atrophic urethritis. The dose should be as low as possible to be effective and perscribed for as short as time as possible, since there are possible risks of uterine cancer, breast cancer, increased blood pressure, gallstones, deep vein thrombosis, and thromboembolism. Estrogens should be administered to provide the maximum benefit with the minimum risk involved. Estrogens should not be given to patients with known contraindications such as: suspected breast or uterine cancer; undiagnosed genital bleeding; Dubin-Johnson syndrome; acute hepatic disease; previous or present thromboembolism; or severe thrombophlebitis. Careful evaluation should be made before administering estrogen to women with uterine myomata, hyperlipidemia, hypercholesterolemia, sevare varicose veins, chronic hepatic dysfunction, diabetes mellitus, porphyria, or severe hypertension.
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PMID:Estrogen replacement in the menopause. 39 Apr 56


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