Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0006142 (breast cancer)
160,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estrogen receptor determinations have been performed on 241 cytosols from 160 breast cancer tumors using both radioactive ligands ([3H])-estradiol, [3H]R2858) and monoclonal antibodies (Abbott ER-EIA Kit) in order to compare the two methods and to evaluate the clinical usefulness of the new immunological, simplified assay. Intra- and interassay reproducibility of the enzyme immunoassay (EIA) method was studied during a 6-month period on 35 standard curves with 4 different batches of monoclonal antibodies. Intraassay coefficients of variation studied on duplicates were smaller than 5% in most cases. Interassay reproducibility of the curves showed coefficients of variation lower than 10% except for standard 0 and 5 fmol/ml. Seven different control specimens provided by Abbott Laboratories were assayed with the EIA method, with interassay coefficients of variation from 1.7% [233.4 +/- 4 (SD) fmol/ml] to 18.2% [18.5 +/- 3.3 fmol/ml]. Pooled cytosols used as control for the dextran coated charcoal method had interassay variation coefficients between 3.8 and 11.4%. Reproducibility has been studied on clinical specimens assayed twice at two different periods with either EIA or dextran coated charcoal methods. Slopes obtained were 1.05 and 0.96, respectively. A good stability of EIA results was obtained with protein concentrations in the range 4-0.15 mg/ml cytosol. No significant effects of dithiothreitol or monothioglycerol (1 mM) on EIA and dextran coated charcoal assay were observed. Eighty breast cancer cytosols were assayed with both EIA and Scatchard analysis. The slope of the regression curve obtained was 1.04 (r = 0.963). Cytosols were assayed by EIA and by a saturating concentration of tritiated ligand (5 nM). With 153 cytosols the EIA/5 nM slope was 1.34 (r = 0.978). This slope can be compared with the slope Scatchard/5 nM obtained with 90 cytosols: 1.29 (r = 0.985). Absence of cross-reactivity of monoclonal ER antibodies with progesterone receptor was observed.
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PMID:Comparison of monoclonal antibodies and tritiated ligands for estrogen receptor assays in 241 breast cancer cytosols. 242 45

Estrogen receptor determination was performed on 120 breast cancer cytosols, using the dextran-coated charcoal method (DCC) and an enzyme immunoassay (EIA) to compare the efficiency of the two techniques. A strong correlation was noted between ER concentrations determined by DCC and EIA (P less than 0.001). The mean ER-EIA value was significantly higher than the mean ER-DCC value in premenopausal (P less than 0.001) as well in postmenopausal (P less than 0.001) patients.
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PMID:Determination of estrogen receptors in human breast cancer: comparison between enzyme immunoassay and dextran-coated charcoal method. 243 12

Estrogen receptor (ER) concentrations have been determined in 191 freshly prepared cytosols from breast cancer biopsies using both the monoclonal enzyme immunoassay (ER-EIA) and the dextran-coated charcoal (ER-DCC) methods in a single laboratory. The concentrations of the ER detected using the two methods are highly and significantly correlated (linear regression curve: ER-EIA = 15.5 + 0.82 ER-DCC; r = 0.97). Nevertheless, it may be most correct to interpret the data by resolving the correlation into two lines, one describing the fit for cytosols with low and intermediate concentrations (the first 75% of the distribution of ER values for all primary breast cancers; less than 217 fmol ER/mg cytosol protein) and one describing the fit for cytosols with the highest ER concentrations (i.e., greater than or equal to 217 fmol ER/mg cytosol protein). Using a cutoff limit of 10 fmol/mg cytosol protein to distinguish between ER positive and ER negative biopsies, discrepancies in the classification of ER status were found in only 6% (12 of 191) of the cases using the two different methods. In all 12 cases, the ER concentrations as determined by both methods were in the lower range of receptor concentrations (0-53 fmol/mg cytosol protein). Of the 12 discrepancies, 10 biopsies were classified as ER negative using the ER-DCC method but ER positive using the ER-EIA method. Additional available data for these 10 patients indicate that the ER-EIA assay yielded the more biologically "correct" result. All 10 of these biopsies were either progesterone receptor positive or had nuclear ER. By identifying the outliers of the linear regression curves (points exceeding the 80% confidence interval) of the logarithmically transformed ER concentrations, 9 of the 12 biopsies were identified. Thus, it is unlikely that the observed discrepancies are due to random events in most cases here. Since most of the few deviations observed appear to represent true differences in the sensitivities of the two methods, the ER-EIA method appears to be superior to the ER-DCC method in our hands. The concentration of ER in 47 cytosols stored at -70 degrees C for 3-6 yr was analyzed using the ER-EIA method, and results were compared to the concentration of ER found using the ER-DCC method on freshly prepared cytosols when the biopsies had been received at the laboratory. The linear regression curve of the correlation between ER concentrations determined using the two methods did not differ significantly from that found for the 191 freshly prepared cytosols.
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PMID:Monoclonal antibody technique for detection of estrogen receptors in human breast cancer: greater sensitivity and more accurate classification of receptor status than the dextran-coated charcoal method. 244 74

Estrogen receptor (ER) expression was investigated by ER-immunocytochemical assay (ICA) and the dextran coated charcoal (DCC) method in 10 recurrent or primary-advanced breast cancer patients treated with endocrine or chemo-endocrine therapy. In 6 of these 10 patients, ER was examined both before and after treatments by the 2 methods. ER contents measured by the DCC method were found to be decreased after treatments, however, no change in the immunoreactivities of ER-ICA was observed. In the remaining 4 patients, the ER of new lesions refractory to endocrine or chemo-endocrine therapy was examined. ER status was determined as negative in 3 of the 4 patients by the DCC method, whereas by ER-ICA, the proportion of ER stained cells was about 70 per cent, those cells being diffusely distributed in the section. A discrepancy between ER-ICA and the DCC method was thus demonstrated in breast cancer patients treated by endocrine therapy.
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PMID:The discrepancy between immunocytochemical and biochemical assay of estrogen receptor in breast cancer patients treated by endocrine therapy. 251 9

Besides undergoing O-demethylation in vivo, the triarylethylene antiestrogen nitromifene [1-(4-(2-pyrrolidinylethoxy)phenyl)-1-(4-methoxy)-phenyl-2-phenyl- 2- nitroethene, 1] undergoes biotransformation via nitroreduction, ethene bond cleavage, and pyrrolidine ring oxidation affording ketone metabolites 2 and 3 and a lactam metabolite 4. Estrogen receptor (ER) affinities of 1, 2, and 4 were, in turn, 1.7, 0.1, and 3.8% that of estradiol in MCF 7 human breast cancer cells, and these compounds inhibited by 50% the proliferation of MCF 7 cells at respective concentrations of 1.1, 5.6, and 2.0 microM. The inhibitory effect of 4 was fully reversible by estradiol, but that of 2 was only partially reversible. Also 3, which did not interact with ER, inhibited proliferation by 44% at a concentration of 10 microM. These results suggested that in contrast to 4, the effects of 2 and 3 were due in part to interaction with sites distinct from ER. Antiestrogen binding sites and calmodulin have been suggested to mediate antiproliferative effects of drugs. Interaction of ligands with the former sites has been proposed to antagonize the growth promoting effect of histamine. Although 2 and 3 had high affinities for these sites, their inhibitory effects on MCF 7 cell growth were largely unaffected by the presence of histidine, the source of intracellular histamine. Thus, the relationship between antiestrogen binding site affinity and antiproliferative effects of 2 and 3 was not clarified. In contrast, MCF 7 cell growth suppression potencies paralleled calmodulin antagonist potencies of 1 and 2 suggesting that interaction of 1 and 2 with calmodulin may contribute to their anticancer effects.
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PMID:Characterization of MCF 7 breast cancer cell growth inhibition by the antiestrogen nitromifene (CI 628) and selected metabolites. 255 Jul 4

Estrogen receptor (ER) content is a well-known predictor of clinical outcome in human breast cancer. The recent cloning of a human ER complementary DNA has made possible the characterization of the ER gene on a molecular level. We have examined in human breast cancers a single, two-allele restriction fragment length polymorphism using the restriction enzyme PvuII. Initial studies in human breast cancer cell lines suggested a possible association between the absence of one allele and the absence of ER expression; subsequent analysis of allele distribution and frequency in 188 primary human breast tumor biopsies did indeed show a significant but not complete correlation between the absence of one allele and the failure to express ER. Preliminary data suggest that this restriction fragment length polymorphism is located within gene sequences coding for the putative DNA or hormone-binding domains of the ER.
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PMID:Estrogen receptor expression in human breast cancer associated with an estrogen receptor gene restriction fragment length polymorphism. 256 95

Estrogen receptor (ER) and progestin receptor (PR) concentrations in tumor biopsies are important predictive indicators of a clinical response to endocrine therapy of breast cancer. To assess interference of O.C.T. (optimum cutting temperature) embedding compound in assays of ER and PR by radioligand binding, we determined specific binding capacities and affinities of ER and PR in cytosols by a multipoint titration method, using split samples of 14 breast-tumor biopsies, one portion serving as untreated control, the other treated with O.C.T. There was no statistically significant difference between these two groups. We then compared these data with those of historical controls analyzed both in the presence and absence of sodium molybdate (10 mmol/L). Eighty breast-tumor specimens (mean +/- SD patients' ages, 59 +/- 14 y) embedded in O.C.T. compound and analyzed without molybdate gave ER and PR values that differed insignificantly from those for 306 samples (patients' ages, 61 +/- 14 y) untreated with O.C.T. Thirty-nine specimens (patients' ages, 58 +/- 15 y) embedded in O.C.T. compound were analyzed in the presence of molybdate and compared with the results for 288 specimens (patients' ages, 61 +/- 14 y) untreated with O.C.T. Again, there was an insignificant difference in the concentrations and affinities of receptors in the two groups. Evidently O.C.T. compound does not alter the receptor status of tumor biopsies.
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PMID:Influence of O.C.T. embedding compound on determinations of estrogen and progestin receptors in breast cancer. 259 Oct 50

Athymic (nu/nu) mice are T cell deficient and can accept xenografts of human tumor material. Hormone-dependent tumor growth can be demonstrated in ovariectomized athymic mice by estrogen administration. Estrogen receptor (ER) positive MCF-7 breast cancer cells implanted into the axillary mammary fat do not grow into palpable tumors unless sustained release preparations of estrogen are administered. The non-steroidal antiestrogen tamoxifen, though it exhibits estrogenic properties in the mouse, does not facilitate MCF-7 tumor growth (during short term, i.e. 8 weeks of therapy) and can prevent estradiol-stimulated growth. In contrast, ER negative MDA-MB-231 cells grow with or without estrogen administration and tamoxifen does not control tumor growth. These statements reflect current dogma concerning the value of athymic mice to confirm the hormone dependent growth of cancer cells in vivo. Our aim has been to define the limits of this dogma and to investigate the growth relationship of hormone-dependent and independent cells with their host environment. The potential endocrine or paracine effect of ER negative tumors on the growth of ER positive tumors was evaluated by transplantation on opposite sides of athymic mice or by the inoculation of different ratios of ER positive/negative cells (MCF-7:MDA-MB-231 9:1, 99:1, 999:1). MCF-7 cells could not be encouraged to grow by a rapidly growing MDA-MB-231 tumor on the opposite side of the animal. Similarly ER negative tumors grew out of the mixed tumor inoculates suggesting that ER positive tumors could not be encouraged to grow preferentially by the paracrine influences of ER negative cells. However, estrogen facilitates the growth of an ER positive tumor following inoculation of mixed cell populations. Antiestrogen treatment can blunt estrogen-stimulated growth but cannot control the growth of ER positive/negative containing tumors. ER positive endometrial tumors grow in response to estrogen treatment and some (EnCa101) have been shown to grow in response to tamoxifen or a combination of tamoxifen and estrogen. More unusual though is our recent observation that an ER negative primary endometrial tumor (BR) and its metastasis (BR-MET) grow more rapidly in estrogen-treated athymic mice. This finding seems to have far-ranging consequences for our view of hormone-dependent growth. Either our view of estrogen-stimulated growth needs to be modified or the host is specifically altered during estrogen treatment. We have taken the position that since natural killer cells (present in athymic mice) can be lowered by estrogen this may result in an increased tumor cell survival in the heterotransplant model.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Immune-deficient animals to study "hormone-dependent" breast and endometrial cancer. 262 14

Biochemical quantitation of estrogen receptors has been used to predict prognosis in breast cancer. Immunocytochemical analysis of estrogen receptors correlates with biochemical analysis but has very few follow-up studies in the literature to validate it as a prognostic indicator. 257 patients were followed for up to 10 years (median, 6.2 years) after primary surgical treatment. Estrogen receptor analysis using both biochemical and immunocytochemical techniques was performed on their tumor specimens. Patients with positive estrogen receptor values had longer survival than patients with negative values. This was demonstrated by both methods in the first 5 years of follow-up but only by immunochemistry after 5 years. The relationship between estrogen receptor status and disease-free interval was less strong than with survival. This study demonstrates that immunocytochemical estrogen receptor analysis was of prognostic significance.
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PMID:Immunocytochemical analysis of estrogen receptors as a predictor of prognosis in breast cancer patients: comparison with quantitative biochemical methods. 264 60

Recurrences of breast cancer are more responsive to hormone therapy if the tumors are positive for estrogen receptors or progesterone receptors. To assess the relationship between hormone receptor content, mammographic tumor morphology, and breast parenchymal patterns, we reviewed charts and mammograms of 210 patients with primary unilateral breast cancer. Mammograms of tumors in 97 patients were divided morphologically into five groups: (1) spiculated mass, (2) architectural distortion, (3) calcifications only, (4) circumscribed mass, and (5) tumor not visible. Estrogen receptor positivity was 81% (39/48) in group 1, 37% (7/19) in group 2, 17% (2/12) in group 3, 31% (4/13) in group 4, and 60% (3/5) in group 5 (P less than .001). Mean estrogen receptor content was also significantly different among groups (P less than .001). There was no statistically significant association between tumor morphology and progesterone receptors, or between calcifications and receptor status. In all 210 patients, hormone-receptor-positive tumors showed no association with mammographic parenchymal pattern. When direct assay of estrogen receptors is unavailable, mammographic appearance of the tumor may suggest the estrogen receptor status.
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PMID:Relationship between mammographic features and hormone receptor content in patients with breast cancer. 268 29


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