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Estrogen Status Affects Breast Cancer Resistance Mechanisms

Last Updated: April 30, 2009.

Breast cancer cells develop different mechanisms of resistance to compounds such as tamoxifen depending on whether the cells are grown under premenopausal or postmenopausal conditions, researchers report in the May issue of Endocrinology.

THURSDAY, April 30 (HealthDay News) -- Breast cancer cells develop different mechanisms of resistance to compounds such as tamoxifen depending on whether the cells are grown under premenopausal or postmenopausal conditions, researchers report in the May issue of Endocrinology.

Ping Fan, and colleagues from the University of Virginia Health Sciences System in Charlottesville, Va., grew breast cancer cells resistant to antiestrogens (tamoxifen, 4-hydroxytamoxifen, fulvestrant) under conditions of high estrogen, mimicking the premenopausal state, and under conditions of low estrogen, mimicking the postmenopausal state.

The researchers found that estradiol stimulated growth and blocked apoptosis in resistant cells grown under premenopausal conditions but had the opposite effect on cells grown under postmenopausal conditions. Tamoxifen-resistant cells grown under premenopausal conditions showed a marked movement of the estrogen receptor from the nucleus to the cytoplasm but less markedly under postmenopausal conditions. Epidermal growth factor receptor was upregulated under postmenopausal but not premenopausal conditions, according to the study.

"Together, these data demonstrate that culture of breast cancer cells under premenopausal and postmenopausal conditions and structurally diverse antiestrogens results in adaptive responses with differing biological signatures," Fan and colleagues conclude.

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