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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Isoelectric focusing in polyacrylamide gel combined with limited proteolysis is a simple and specific method for quantitation of estradiol receptors in breast cancer tissue. At least eight different samples can be analyzed simultaneously on one gel, and the whole procedure, including sample preparation, takes less than 7 hr. In comparison with sucrose gradient centrifugation, isoelectric focusing is more sensitive, possibly due to the short time (1.5 to 2 hr) needed for the analysis. Furthermore, only one incubation with tritium-labeled estradiol is needed for an analysis, which means that a smaller amount of tumor tissue is needed than for most other methods. This fact allows analysis of the estrogen receptor content in tumor material obtained from fine-needle biopsy.
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PMID:Estradiol receptor analysis in human breast cancer tissue by isoelectric focusing in polyacrylamide gel. 2 6

Concentrations of estrogen receptor (ER) and alpha-fetoprotein were determined by dextran-coated charcoal assay and analyzed with Scatchard plots and radioimmunoassay, respectively, in cytosols of 72 human breast cancers. The values for ER ranged from 0 to 340 fmoles/mg cytosol protein. The concentrations of alpha-fetoprotein, which were low in all tumor cytosols examined, ranged from less than 0.1 to 1.1 ng/mg cytosol protein. No positive relationship was found between ER and alpha-fetoprotein concentrations. These results show that ER, but not alpha-fetoprotein, usually accounts for most of the high estrogen-binding capacity in cytosols of human breast cancers.
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PMID:Estrogen receptor and alpha-fetoprotein in human breast cancer: brief communication. 7 14

A proportion of cancers in endocrine target tissues can show the presence of specific receptors for either steroid or polypetide hormones. Manipulation of the controlling hormones does not guarantee regression. A third of cancers in endocrine target organs (breast, uterine endometrium, and prostate) show a 50% reduction in size of lesions after hormonal therapy. If regression resulting from an aggressive form of therapy lasts a short while and the tumor reactivates by the time the unpleasant effects of the therapy wear off, the treatment is not palliative. Endocrine therapy in prostatic cancer is palliative but there is no evidence that is increases survival. 11 different progestational agents in endometrial cancer therapy in the past 25 years resulted in a 30-35% response. Response must be maintained by continual treatment and may last from 12 months to 7-8 years. In breast cancer, tumors with a significant level of estrogen receptor (ER+) have about a 60% chance of regression vs. tumors without estrogen receptors (ER-), 10%. Advanced cancers of the thyroid of the papillary or follicular type regress when the patient is treated by thyroxine, .3 mg daily. Leukemia and lymphoma are frequently treated, with varying degrees of success with corticosteroid therapy, which may also predispose the patient to intercurrent infection. Renal cancer has been often treated by medroxyprogesterone acetate or testosterone propionate, with little success.
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PMID:Endocrine therapy in cancer. 8 86

Steroid delta 4-5 alpha- and delta 4-5 beta-reductase activity was determined in 16 human mammary tumors and 8 DMBA-induced rat mammary tumors using a spectrophotometric assay. Steroid delta 4-5 alpha-reductase was present in all tumors investigated while delta 4-5 beta-reductase was detected in only 6 estrogen receptor negative human breast tumors and absent in all estrogen receptor positive human breast tumors as well as in all rat mammary tumors. Further support for the presence of delta 4-5 beta-reductase was established by using a dual-labelling technique consisting of incubating tumor slices with [14C] testosterone and adding [3H] etiocholanolone, [3H] testosterone and [3H]-5 alpha-dihydrotestosterone at the end of the reaction. Following extraction and chromic acid oxidation, 4-androstenedione, 5 beta-androstanedione and 5 alpha-androstanedione were isolated and purified, and the constancy of the 14C/3H ratio was used as proof of 5 alpha-reductase and 5 beta-reductase. These results were shown to be consistent with the data obtained using the spectrophotometric assay.
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PMID:Steroid delta 4-5 beta-reductase in human mammary tumors. 10 50

Incubation of estradiol in vitro at 25 degrees C with homogenates of carcinogen-induced mammary tumors of ovariectomized rats stimulated the magnesium-dependent RNA polymerase activity of nuclei of the hormone-dependent (HD) (regressing) tumors, but had no effect on this activity in nuclei of hormone-independent (HI) (growing) tumors. Furthermore, recombination of the nuclei and cytosol fractions of HD and HI tumors indicated that the in vitro effect of estradiol on subsequent tumor nuclear RNA synthesis required the estrogen receptor-containing cytosol but was specific to nuclei of the HD tumor. This constituted the first direct in vitro effect of estrogen on a specific biochemical process in an HD mammary tumor.
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PMID:Estrogen-dependent in vitro stimulation of RNA synthesis in hormone-dependent mammary tumors of the rat. 16 35

Rodent and human mammary tumor systems were investigated to relate the steroid alcohol and estrogen sulfotransferase activities to the hormoanl dependency of the tumor as determined by estrogen receptor content. Unlike the normal mammary gland or the hyperplastic alveolar nodule, rodent mammary neoplasms displayed significant levels of these two sulfotransferases. In the hormone-independent mouse tumors produced from out-growth lines D1, D2, and D8, high dehydroepiandrosterone sulfotransferase activity was characteristic of the rapidity with which hyperplastic alveolar nodules developed into a neoplasms (V-max = 52.8 versus 1.8 fmoles/min/mg protein) while estrone sulfotransferase activity was either not detectable or low (V-max = 5.5 fmoles). After oophorectomy of mice bearing slowly developing tumors, both sulfotransferases in the nonregressing neoplasms showed marked increases in activity (V-max dehydroepiandrosterone = 30.0 fmoles; V-max estrone = 18.5 fmoles). Strain differences not the estrogen receptor content of hormone-dependent rat mammary tumors. In Wistar-Lewis rats the steroid alcohol sulfotransferase activity was at least 35 times higher than in the Sprague-Dawley strain. As was observed in the mouse mammary tumor, Sprague-Dawley rat neoplasms that grew in the absence of ovarian hormones contained significantly greater levels of the steroid alcohol sulfotransferase. Possible correlaion between presence of the steroid alcohol sulfotransferase and the estrogen receptor protein was observed in a limited number of human breast carcinomas.
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PMID:The steroid alcohol and estrogen sulfotransferases in rodent and human mammary tumors. 16 83

Preneoplastic mammary nodule outgrowth lines were examined for their ability to grow and produce tumors in ovariectomized BALB/c mice. In addition, these nodule outgrowth lines and tumors derived from them were investigated for cytoplasmic estrogen receptor proteins by qualitative and quantitative techniques. Early ovariectomy, performed within 4 weeks after transplantation, slightly delayed but did not permanently block the ability of three different nodule lines to completely fill the fat pad with nodule tissue. Ovariectomy performed later than 4 weeks after transplantation or adrenalectomy performed early or late had no effect on nodule growth. Neither early nor late ovariectomy or adrenalectomy had an effect on the maintenance of the nodule alveolar phenotype. Ovariectomy performed 3 weeks after transplantation had little effect on the tumor potential of the low oncogenic line D1 or the high oncogenic line D2. Samples of nodule outgrowths transplanted from ovariectomized mice responded to a chemical carcinogen in a similar manner, as did nodule outgrowths transplanted from control experiments. Thus, the altered hormonal environmenment in ovariectomized mice apparently did not select for subpopulations of nodule cells with altered tumorigenic potentials. The ovarian independence of the nodule lines and tumors derived from them was correlated with a very low level of cytoplasmic estrogen receptor. These results, along with other data, illustrate the nature of the independence on ovarian hormonal control for tumorigenesis in these mammary tumor virus-free nodule lines.
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PMID:Hormone dependence and estradiol receptors in the D series of mammary nodule outgrowth lines and tumors. 16 55

In estrogen target tissues and hormone-dependent tumors, the steroid enters the cells and binds to a cytoplasmic protein called the estrogen receptor (ER). The steroid-receptor complex then migrates to the nuclei, where it initiates the biochemicial events characteristic of estrogen stimulation. Since ER is absent in tissues not responsive to estrogen, recent studies have asked whether ER assays in human breast cancer tissue might be used to identify those patients likely to respond to endocrine therapy. Data on 436 clinical trials contributed from a dozen centers around the world now clearly indicate that if a patient's tumor does not contain ER, there is virtually no chance of tumor regression following endocrine therapy. A large number of patients can be thus spared unrewarding major endocrine ablative therapy if ER assays are performed routinely. Of tumors with positiev ER, 55-60% respond to endocrine therapy. This single piece of data, when coupled with available clinical prognostic factors such as menopausal status, disease free interval, site of the dominant lesion, and especially response to previous hormonal therapies, should be practicing oncologist to select or reject endocrine therapy with considerable confidence.
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PMID:Current status of estrogen receptors in human breast cancer. 16 60

Less than half of premenopausal patients with mammary cancer and even fewer postmenopausal patients have tumors that respond to endocrine ablation. The level of estrogen receptor protein (estrophilin) in the mammary cancer tissue provides an indication of the hormone dependency of the tumor and may be sued to predict the response to endocrine treatment when recurrent disease appears. Metastatic growths usually have a similar content. This is a report of an investigation of the estrophilin content of specimens of tumors from patients with metastatic and recurrent mammary cancer for correlation with their response to endocrine changes. Primary tumors were also studied for future clinical use if needed. The estrophilin was determined in specimens from 214 metastatic growths and 359 primary breast cancers. The uptake of estradiol in an in vitro system and the blocking effect of specific inhibitors provided a means of distinguishing between estrogen responsive tissues which contained receptor proteins and non-estrogen-responsive tissues which did not contain these receptors. Some form of endocrine manipulation was used in 82 patients. Of these, 69 had ablative therapy. Of the 69, significant receptor levels were present in 27 and 2/3 of them had remissions. Of the 42 with negative e strophilin determinations, none had a remission after ablation. Therefore, the absence of significant amounts of estrophilin in breast cancer tissue indicates that the patient has little chance of responding to endocrine manipulation and should be spared this method. In 16 others, hormonal additive treatment was used. Only 1 of 6 patients with negative determinations benefited temporarily from the additive hormone therapy. Discussion and questions by others followed presentation of this paper. Other hormones as possibly important were suggested. Combining chemotherapy with adrenalectomy was suggested. It was stated that some noncancerous breast tissues also contain estrogen binding proteins. Dr. Block answered questions and added comments. He stated that estrophilin is present in many tissues but in very low amounts. It is a quantitative difference that is important.
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PMID:The prediction of hormonal dependency of mammary cancer. 16 54

In order to test the in vivo effect of prolactin on estrogen receptor (ER) binding capacity in tumors induced by 7,12 dimethylbenz(a)anthrancene (DMBA-tumor), growth of the tumors from changes in prolactin and estrogen levels was compared retrospectively with cytoplasmic ER levels. It was demonstrated that some tumors required prolactin, some needed prolactin-estrogen during their growth period anda small number were not influenced by hormonal milieu. ER was present in hormonally dependent tumors but was low or absent in hormonaly-independent tumors. Deletion of hormones by endocrine ablation in the host rat resulted in tumor regression loss of ER. Replenishment of ER and subsequent tumor growth were accomplished by injection of prolactin or prolactin-estrogen in endocrine ablated rats but were not achieved in rats bearing tumors exposed to prolactin-nafoxidine. Our results demonstrate that both estrogen and prolactin were essential for growth of hormonally dependent DMBA-tumors. Tumor growth was also prevented when cytoplasmic ER was not replenished , indicating that ER may be an indispensable prerequisite for growth. Prolactin, independently of or cooperatively with estrogen, stimulated ER binding capacity. These results support the hypothesis that there may exist a prolactin regulatory mechanism of estrogen action at the tumor site. The interactions of estrogen and prolactin in situ in modulating hormonal receptor binding capacities may contribute to the overall stimulatory effect of these two hormones on DMBA-tumors.
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PMID:On the mechanism of prolactin and estrogen action in 7,12 dimethylbenz(A)anthracene-induced mammary carcinoma in the rat. II. In vivo tumor responses and estrogen receptor. 17 65


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