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Estrogen in breast cancer

Aromatase inhibitors serve to eliminate ex-traovarian synthesis of estrogens in breast cancer patients. This can be achieved effectively only in postmenopause because, as an FSH-dependent enzyme, ovarian aromatase is subject to feedback regulation of female Luellmann, Color Atlas of Pharmacology 2005 Thieme All rights reserved. Usage subject to terms and conditions of license. [Pg.256]

Anastrazole is a nonsteroidal, type H, aromatase inhibitor that is 200 times more potent than aminoglutethimide. It is eliminated primarily via hqDatic metabolism, has a terminal half life of 50 h with steady state concentrations achieved approximately 10 days with once daily dosing regimens. It is administered orally at a dose of 1 mg/day that achieves near maximal aromatase inhibition and hence estrogen suppression in breast cancer patients. No effect on adrenal steroidogenesis has been observed at up to ten times the daily recommended dose. When used in the metastatic setting, anastrozole has been shown... [Pg.220]

TWADDLE G M, TURBOV J, LIU N, MURTHY s (1999) Tyrosine kinase inhibitors as antiprohferative agents against estrogen-dependent breast cancer cell line in vitro. JSurg Oncol. 70 ... [Pg.86]

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. [Pg.86]

Anastrozole is a selective nonsteroidal aromatase inhibitor that lowers estrogen levels. The pharmacokinetics of anastrozole demonstrate good absorption, with hepatic metabolism the primary route of elimination and only 10% excreted unchanged by the kidney. The elimination half-life is approximately 50 hours. Anastrozole is used for the adjuvant treatment of postmenopausal women with hormone-positive breast cancer and in breast cancer patients who have had disease progression following tamoxifen. Side effects include hot flashes, arthralgias, osteoporosis/bone fractures, and thrombophlebitis. [Pg.1296]

Riera J, Simpson JF, Tamayo R, et al. Use of cultured cells as a control for quantitative immunocytochemical analysis of estrogen receptor in breast cancer. The Quicgel method. Am. J. Clin. Pathol. 1999 111 329-335. [Pg.85]

Chung GG, Zerkowski MP, Ghosh S, et al. Quantitative analysis of estrogen receptor heterogeneity in breast cancer. Lab. Invest. 2007 87 662-669. [Pg.85]

Yaziji H, Taylor CR, Goldstein NS, et al. Consensus recommendations on estrogen receptor testing in breast cancer by immu nohistochemistry. A/ / /. Immunohistochem. Mol. Morphol. 2008 16 513-520. [Pg.185]

The oral estrogen-alone arm was stopped early after a mean of 7 years of follow-up. Estrogen-only therapy had no effect on coronary heart disease risk and caused no increase in breast cancer risk. [Pg.355]

Fuqua SA (2001) The role of estrogen receptors in breast cancer metastasis. J Mammary Gland Biol Neoplasia 6 407... [Pg.57]

Lee AV, Cui X, Oesterreich S (2002) Cross-talk among estrogen receptor, epidermal growth factor, and insulin-like growth factor signaling in breast cancer. Clin Cancer Res 7(12 Suppl) 4429s... [Pg.58]

Palmieri C, Cheng GJ, Saji S, Zelada-Hedman M, Warri A, Weihua Z, Van Noorden S, Wahlstrom T, Coombes RC, Warner M, Gustafsson JA (2002) Estrogen receptor beta in breast cancer. Endocr Relat Cancer 9 1... [Pg.60]

Howell SJ, Johnston SRD, Howell A (2004b) The use of selective estrogen receptor modulators and selective estrogen receptor down-regulators in breast cancer. Best Pract Res Clin Endocrinol Metab 18 47-66... [Pg.166]

Osipo C, Liu H, Meeke K, Jordan VC (2004) The consequences of exhaustive antiestrogen therapy in breast cancer estrogen-induced tumor cell death. Exp Biol Med 229 ... [Pg.167]

Pink JJ, Jordan VC (1996) Models of estrogen receptor regulation by estrogens and antiestrogens in breast cancer cell fines. Cancer Res 56 2321-2330... [Pg.167]

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