Radioligand-Labeled Binding Assay and Immunochemical Assay for Estrogen Receptor in 115 Human Breast Cancers

1988 ◽  
Vol 74 (2) ◽  
pp. 167-170 ◽  
Author(s):  
Angela Riccobon ◽  
Wainer Zoli ◽  
Antonella Capucci ◽  
Annalisa Volpi ◽  
Mara Vasini ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Breast Tumor ◽  
Binding Assay ◽  
Menopausal Status ◽  
Correlation Coefficients ◽  
Breast Cancers ◽  
Human Breast ◽  
Steroid Binding

The aim of this study was to evaluate the results obtained from a new enzyme immunoassay (Abbott-ER-EIA) for the determination of estrogen receptor levels in tumor cytosols in comparison with the currently used DCC method. One hundred and fifteen consecutive primary breast cancer specimens were examined; 66 of the women were postmenopausal and 49 were premenopausal. A good correlation (r = 0.88, p < 0.001 and a slope of 1.3) was found between ER-EIA and the steroid binding assay (DCC). When these data were analyzed according to menopausal status, no differences were observed for the slopes and correlation coefficients in pre’ and postmenopausal groups. The ER-EIA appears to produce results comparable to those obtained with the conventional DCC method for the determination of ER in breast tumor cytosols.

Breast cancers negative for estrogen receptor but positive for progesterone receptor, a true entity?

1987 ◽  
Vol 5 (4) ◽  
pp. 662-666 ◽  
Author(s):  
D T Kiang ◽  
R Kollander
Keyword(s):  
Estrogen Receptor ◽  
Progesterone Receptor ◽  
Staining Method ◽  
Binding Assay ◽  
Assay Method ◽  
Breast Cancers ◽  
Antibody Method ◽  
Steroid Binding ◽  
Rare Group ◽  
Er Status

By the conventional steroid-binding assay method for receptor, 3% of 1,095 primary breast cancers (or 10.6% of 263 premenopausal tumors) were classified as negative for estrogen receptor (ER), but positive for progesterone receptor (PR). The true ER status in this rare group of tumors was further investigated by the enzyme-immunoassay (EIA) or immunocytochemical (ICA) staining method using monoclonal antibodies H222 and D547. Immunoreactive ER was present in nine ER-/PR+ tumors studied, whereas it was not detectable in nine age-matched ER-/PR- tumors. Immunoreactive ER was also present in 24 ER+ breast cancers studied, and was particularly higher in tumors that were PR+. Measurement of immunoreactive ER by monoclonal antibody method provides certain advantages over the conventional dextran-coated charcoal (DCC) method, especially in ER-/PR+ tumors.

Determination of Estrogen Receptors in Human Breast Cancer: Comparison between Enzyme Immunoassay and Dextran-Coated Charcoal Method

1986 ◽  
Vol 72 (5) ◽  
pp. 511-514 ◽  
Author(s):  
Cecilia Bozzetti ◽  
Nadia Naldi ◽  
Annamaria Guazzi ◽  
Rita Nizzoli ◽  
Magda Benecchi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Estrogen Receptors ◽  
Enzyme Immunoassay ◽  
Strong Correlation ◽  
Human Breast Cancer ◽  
Human Breast ◽  
Dextran Coated Charcoal ◽  
The Mean

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 < 0.001). The mean ER-EIA value was significantly higher than the mean ER-DCC value in premenopausal (P < 0.001) as well in postmenopausal (P < 0.001) patients.

A novel therapeutic strategy for ER-negative human breast cancers, targeting AP-1 activity

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 14129-14129
Author(s):  
K. Sakaguchi ◽  
H. Nakajima ◽  
I. Fujiwara ◽  
N. Mizuta ◽  
J. Magae
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Human Breast Cancer ◽  
Human Breast Cancer Cell ◽  
Breast Cancers ◽  
Human Breast ◽  
Er Positive

14129 Background: While agents targeting estrogen receptors are the most effective in adjuvant therapy for human breast cancers expressing estrogen receptor(ER), breast cancers lacking ER are clinically serious, because they are highly malignant and exhibit resistance to the usual anti-cancer drugs, including estrogen receptor-antagonists and DNA breaking agents. Although a transcription factor, AP-1, is known to be related to tumor malignancy including metastasis, invasion and drug-resistance, it remains to be elucidated how AP-1 plays in development and expression of malignant characters of human breast cancers. Methods and Results: Here, we used MX-1, a human breast cancer cell line lacking ER and several ER positive cell lines, to clarify the roles of AP-1 and the therapeutic efficacy of ascochlorin, a newly developed prenylphenol antibiotic on ER-negative breast cancer. We found that MX-1 exhibited higher AP-1 activity and expressed higher levels of c-Jun, c-Fos and Fra-1 when compared with conventional ER-positive human breast cancer cell lines. Consistent with this study in vitro, histological study on human breast cancer tissues suggests that ER-negative cancers express high Fra-1 protein, and that paclitaxel- sensitive cancers express low Fra-1 protein. The ascochlorin, which inhibits AP-1 through the Erk signaling pathway, suppressed the AP-1 activity of MX-1 cells, and selectively killed MX-1 cells, partly due to induction of apoptosis. Moreover, administration of ascochlorin elongated life span of mice intraperitoneally implanted with murine mammary carcinoma cells. Conclusions: Our results suggest that AP-1 is an effective clinical target molecule for the treatment of ER-negative human breast cancer, and that ascochlorin is promising therapeutic agent for these refractory breast cancers. No significant financial relationships to disclose.

Determination of turnover of androstenedione to estrone via aromatase in estrogen receptor positive and negative human breast cancer cell lines [Poster 48]

Steroids ◽  
1987 ◽  
Vol 50 (4-6) ◽  
pp. 651-652
Author(s):  
Kurt W. Possinger ◽  
Annette Staebler ◽  
Sophia Sgouropoulou ◽  
Peter J. Langecker ◽  
Till C. Lorenz ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Cell Lines ◽  
Breast Cancer Cell ◽  
Human Breast Cancer ◽  
Human Breast Cancer Cell ◽  
Breast Cancer Cell Lines ◽  
Human Breast ◽  
Estrogen Receptor Positive

How to target estrogen receptor-negative breast cancer?

2003 ◽  
pp. 261-266 ◽  
Author(s):  
H Rochefort ◽  
M Glondu ◽  
M E Sahla ◽  
N Platet ◽  
M Garcia
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Targeted Therapies ◽  
Cathepsin D ◽  
Human Breast Cancer ◽  
Breast Cancers ◽  
Human Breast

Estrogen receptor (ER)-positive breast cancers generally have a better prognosis and are often responsive to anti-estrogen therapy, which is the first example of a successful therapy targeted on a specific protein, the ER. Unfortunately ER-negative breast cancers are more aggressive and unresponsive to anti-estrogens. Other targeted therapies are thus urgently needed, based on breast cancer oncogene inhibition or suppressor gene activation as far as molecular studies have demonstrated the alteration of expression, or structure of these genes in human breast cancer. Using the MDA-MB.231 human breast cancer cell line as a model of ER-negative breast cancers, we are investigating two of these approaches in our laboratory. Our first approach was to transfect the ER or various ER-deleted variants into an ER-negative cell line in an attempt to recover anti-estrogen responsiveness. The unliganded receptor, and surprisingly estradiol, were both found to inhibit tumor growth and invasiveness in vitro and in vivo. The mechanisms of these inhibitions in ER-negative cancer cells are being studied, in an attempt to target the ER sequence responsible for such inhibition in these cancer cells. Another strategy is trying to inhibit the activity or expression of an oncogene specifically overexpressed in most breast cancers. This approach was recently shown by others to be efficient in breast cancer therapy with HER2-Neu oncogene amplification using Herceptin. Without excluding other molecular putative targets, we have focused our research on cathepsin D as a potential target, since it is often overexpressed in aggressive human breast cancers, including ER-negative tumors, and rarely associated with HER2-Neu amplification. Our first results obtained in vitro on cell lines and in vivo in tumor xenografts in nude mice, illustrate that the mode of action of cathepsin D in breast cancer is useful to guide the development of these therapies. In the past 20 years we have learned that the action of cathepsin D is complex and involves both intracellular and extracellular activities due to its proteolytic activity and to interactions with membrane components without catalytic activity. Each of these mechanisms could be potentially inhibited in an attempt to prevent tumor growth. Breast cancer is a very heterogeneous and multigenic disease and different targeted therapies adapted to each category of breast cancer are therefore required. Validated assays in the primary tumor of molecular markers such as ER, HER2-Neu and cathepsin D should help to predict which targeted therapy should be applied to cure breast cancer patients.

scholarly journals Inhibition of estrogen receptor signaling

2005 ◽  
Vol 8 (3) ◽  
Author(s):  
E. M. Rosen ◽  
S. Fan
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Estrogen Receptor Alpha ◽  
Dietary Factors ◽  
Type I ◽  
Breast Cancers ◽  
Human Breast ◽  
Estrogen Receptor Signaling ◽  
Reduce Breast Cancer Risk ◽  
Pharmacologic Agents

The estrogen receptor-alpha (ER-α) is a Type I nuclear receptor that is over-expressed in the majority of human breast cancers and plays a significant role in the development and progression of these cancers. As estrogen plays important roles in the etiology of breast cancer and the growth of established ER-α expressing cancers, intense interest has been generated in understanding the mechanisms by which ER-α signaling is regulated physiologically and using this knowledge to develop interventions to inhibit ER-α signaling. These efforts have met with some success in the development of pharmacologic agents that can reduce breast cancer risk, prevent recurrence of established cancers, and treat advanced cancers with considerably less side effects than cytotoxic chemotherapy. Here, we will review some of the mechanisms that operate to inhibit ER-α signaling and describe how pharmacologic agents and dietary factors interact with ER-α to block its activity. In the process of reviewing these mechanisms, we will highlight their clinical implications.

scholarly journals Interactions between estrogen and insulin-like growth factor signaling pathways in human breast tumor cells.

2003 ◽  
pp. 331-345 ◽  
Author(s):  
I H L Hamelers ◽  
P H Steenbergh
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Signaling Pathways ◽  
Breast Tumor ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Synergistic Effects ◽  
Human Breast ◽  
Breast Tumor Cells ◽  
Igf I

Estrogens and insulin-like growth factors (IGFs) act as mitogens promoting cell proliferation in normal breast tissue as well as in breast carcinomas. Both hormones have been shown to play a role in the development of breast cancer and were found to activate multiple signaling pathways leading to proliferation of human breast cancer cell lines in vitro. Originally, it was considered that these agents manifest their mitogenic actions through separate pathways, but a growing body of evidence suggests that the IGF- and estrogen-mediated signaling pathways are intertwined. 17beta-Estradiol (E2) has been shown to enhance IGF signaling at multiple levels. E2 treatment of breast cancer cells alters expression of nearly all of the IGF family members including IGF-I, IGF-II, IGF-binding proteins, IGF type I receptor (IGF-RI), and insulin receptor substrate 1. The ligand-bound estrogen receptor has been reported to bind to and to activate the IGF-RI directly. Vice versa, IGF signaling has been reported to enhance estrogen receptor activation in human breast cancer cells by inducing phosphorylation of the estrogen receptor. Finally, several groups have described synergistic effects of the combination of E2 and IGF-I on S phase entry in breast tumor cell lines. Here, we review recent, often contradictory, reports describing the effects of E2 and IGFs on the proliferation of breast tumor cells, with special emphasis on the synergistic effects of the two hormones.

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