Despite nearly a century of awareness of the efficacy of various kinds of endocrine therapies in the management of patients with metastatic breast cancer, many facets of the mechanisms whereby hormones influence the growth of neoplastic tissue remain incompletely understood. Since the initial discovery in 1971 by Jensen et al1 that some breast cancers contain estrogen receptors, substantial progress has been made in understanding the critical role of these hormone binding sites in metabolism and neoplastic growth and in characterizing how these receptors are capable of interacting with nuclear material and activating transcription of specific genes.2,3 Many studies have shown that there is an excellent correlation between the presence of estrogen receptor activity and hormone triggered growth responses in breast tumors.4 Anti-estrogen or high dose estrogen mediated cytotoxicity of breast cancer also requires the presence of an estrogen receptor. Specifically, if the tumor lacks estrogen receptor the chance of seeing an objective response to endocrine therapy is only 5 percent or less. On the other hand, if the tumor contains receptor then the likelihood of a response to endocrine therapy is approximately 50 to 60 percent. Thus, there is a subset of patients who, despite the presence of estrogen binding activity, fail to show a response to endocrine therapy. The present article summarizes current information on cell culture models for this disease entity.KeywordsBreast CancerEstrogen ReceptorProgesterone ReceptorHuman Breast Cancer CellHuman Breast Cancer Cell LineThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.