Estrogen receptors cancer

Schafer JI, Liu H, Tonetti DA, Jordan VC (1999) The interaction of raloxifene and the active metabolite of the antiestrogen EM-800 (SC 5705) with the human estrogen receptor. Cancer Res 59 4308-4313... 

Levenson AS, Jordan YC. The key to the antiestrogenic mechanism of raloxifene is amino acid 351 (Aspartate) in the estrogen receptor. Cancer Res 1998 58(9) 1872-1875. 

Dewhirst, M.W. and McDonnell, D.P. (2001) Circumventing tamoxifen resistance in breast cancers using antiestrogens that induce unique conformational changes in the estrogen receptor. Cancer Research, 61,... 

B4. Bocchinfuso, W. P., Hively, W. P., Couse, J. F., Varmus, H. E., and Korach, E. S., A mouse mammary tumor virus- Wnt-1 transgene induces mammary gland hyperplasia and tumorigenesis in mice lacking estrogen receptor. Cancer Res. 59, 1869-1876 (1999). 

B.D., Dyck, P.A., and Jordan, V.C., Gene expression profiles with activation of the estrogen receptor oc-selective estrogen receptor modulator complex in breast cancer cells expressing wild-type estrogen receptor. Cancer Res., 62,4419,2002. 

EM-800 is a pure estrogen receptor antagonist that has recently been used clinically for breast cancer patients who have failed tamoxifen therapy. 

The test system was considerably less sensitive to endosulfan when mouse ER, rather than human ER, was used to mediate (3-gal activity (Ramamoorthy et al. 1997). In similar assays, endosulfan at 10 jM had no effect on (3-gal activity in yeast Saccharomyces) transfected with either the human or rainbow trout ER (Andersen et al. 1999). In addition, no effect was observed on transcriptional activation of HeLa cells transfected with plasmids containing an estrogen receptor as a responsive element (Shelby et al. 1996). Endosulfan also did not induce transient reporter gene expression in MCF-7 human breast cancer cells at an incubation concentration of 2.5 pM (Andersen et al. 1999). Maximum endosulfan-induced ER-mediated luciferase reporter gene expression occurred in vitro in a T47D human breast adenocarcinoma cell line at approximately 10 pM, while 50% expression of luciferase occurred at about 5.9 pM the maximum expression was approximately 59% of the effect from exposure to 0.03 nM estradiol (0.00003 pM) (Legler et al. 1999). Luciferase expression from combined treatment with endosulfan and dieldrin was additive over concentrations ranging from 3 to 8 pM. 

Legler J, van den Brink CE, Brouwer A, et al. 1999. Development of a stably transfected estrogen receptor-mediated luciferase reporter gene assay in the human T47D breast cancer cell line. Toxicol Sci 48 55-66. 

Ramamoorthy K, Wang F, Chen I-C, et al. 1997. Estrogenic activity of a dieldrin/toxaphene mixture in the mouse uterus, MCF-7 human breast cancer cells, and yeast-based estrogen receptor assays No apparent synergism. Endocrinology 138(4) 1520-1527. 

HSIEH c Y, SANTELL R c, HASLAM s z, HELFERICH w G (1998) Estrogenic effects of genistein on the growth of estrogen receptor-positive human breast cancer (MCF-7) cells in vitro and in vivo. Cancer Res. 58 3883-3838. 

VLADUSic E A, HORNBY A E, GUERRA-VLADUSic F K, Lupu R (1998) Expression of estrogen receptor beta messenger RNA variant in breast cancer. Cancer Res. 58 210-14. 

PETERSON G and BARNES s (1991) Genistein inhibition of the growth of hiunan hreast cancer cells independence from estrogen receptors and the multi-drug resistance gene. Biochem Biophys Res Commun. 179 (1) 661-7. 

Toremifene is an estrogen receptor antagonist. The pharmacokinetics of toremifene are best described by a two-compartment model, with an a half-life of 4 hours and an elimination half-life of 5 days. Peak plasma concentrations are achieved approximately 3 hours after an oral dose. Toremifene is metabolized extensively, with metabolites found primarily in the feces. Toremifene is used for the treatment of metastatic breast cancer in postmenopausal women with estrogen-receptor-positive or unknown tumors. Toremifene causes hot flashes, vaginal bleeding, thromboembolism, and visual acuity changes. 

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