Estradiol mouse breast cancer

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Mycoestrogens are naturally occurring endocrine disruptors found primarily in grains. Certain mycoestrogens, including especially zearalenone, may advance the growth of breast cancer cells. An important metabolite breakdown product of zearalenone is zeranol, a compound that is also produced as a synthetic compound brand name Ralgro and is largely used in the U.

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In addition to their well-known role in growth and differentiation of the breast, ovary and uterus in females, and testes and prostate in males, estrogen is also required for proper functioning of the cardiovascular, immune, gastrointestinal, musculoskeletal, and nervous systems as well as skin. Two metabolites of E 2estrone E 1 and estriol E 3circulate at high levels at certain phases in the menstrual cycle and during pregnancy Gruber et al. E 1 and E 3 have been thought to be the inactive metabolites of E 2but E 3 has significant effects on the immune system Zang et al.

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A role for estrogens in breast cancer is widely accepted, however, recent evidence highlights that timing and exposure levels are important in determining whether they elicit harmful versus beneficial effects. The rat chemical carcinogen model has been widely used to study the effects of estrogens but conclusions on the levels that lead to tumor development and an absolute requirement for progesterone P4 are lacking. A newer method of hormone administration mixes hormones with nut butter for peroral consumption allowing for a less stressful method of long-term administration with lower spikes in serum estradiol E2 levels.

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Estrogen promotes breast cancer development and progression mainly through estrogen receptor ER. However, blockage of estrogen production or action prevents development of and suppresses progression of ER-negative breast cancers. How estrogen promotes ER-negative breast cancer development and progression is poorly understood.

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Breast Cancer Research and Treatment. Estrogen is important for breast carcinogenesis and the majority of breast cancers maintain hormone dependency. Estrogen has the ability to stimulate both breast epithelial cell growth and angiogenesis, and a well-characterized in vivo cancer model where these functional interactions can be studied is lacking.

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Background: Long-term tamoxifen treatment of breast cancer can result in tamoxifen-stimulated breast cancer, in which estrogen inhibits tumor growth after tamoxifen withdrawal. We investigated the molecular mechanism s of estradiol-induced tumor regression by using an in vivo model of tamoxifen-stimulated human breast cancer. Methods: Growth of parental estradiol-stimulated MCF-7E 2 and long-term tamoxifen-stimulated MCF-7TAMLT xenografts in athymic mice was measured during treatment with vehicle, estradiol, estradiol plus tamoxifen, tamoxifen alone, estradiol plus fulvestrant, or fulvestrant alone.

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Endocrine therapy with estrogen deprivation or with antiestrogens results in tumor regression in a subset of patients with advanced breast cancer. To better understand the mechanisms by which estrogens and antiestrogens modulate breast cancer growth in vivo, we have studied the effects of endocrine manipulation on the development and growth of tumors derived from cultured human breast cancer cells in the athymic nude mouse. Tumor growth did not occur in ovariectomized mice. Cells remained viable, however, since estrogen supplementation more than 30 days later resulted in tumor formation.

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