作者: Abde M. Abukhdeir , Brian G. Blair , Keith Brenner , Bedri Karakas , Hiroyuki Konishi
DOI: 10.1007/S10549-006-9177-0
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摘要: Currently, a number of breast cancer cell lines exist that serve as models for both estrogen receptor alpha (ERα) positive and ERα negative disease. Models are also available pre-neoplastic epithelial cells do not express ERα; however, there no ideal systems studying positive. This has been largely due to the inability establish an growth stimulated, non-tumorigenic line, most human engineered overexpress have found be inhibited by estrogens. We developed independently derived clones from non-cancerous MCF-10A line stimulated 17-beta-estradiol (E2) in absence epidermal factor (EGF), cytokine normally required proliferation. effect is blocked selective modulator (SERM), Tamoxifen downregulator, ICI 182,780 (Faslodex, Fulvestrant). Exposure these EGF E2 results inhibitory phenotype similar previous reports. These data present reconciling explanation previously described paradoxical effects overexpression, provide model examining carcinogenic estrogens cells.