Profiling of estrogen up- and down-regulated gene expression in human breast cancer cells: insights into gene networks and pathways underlying estrogenic control of proliferation and cell phenotype.

By J. Frasor, Jeanne M. Danes, B. Komm, Ken C. N. Chang, C. Lyttle, B. Katzenellenbogen. Endocrinology, 2003

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Mechanisms of tamoxifen resistance. (2004, background): “There is conﬂicting data concerning the relative co-expressions of ER a and ER b and their associations with established prognostic variables, endocrine responsiveness and survival (Dotzlaw et al. 1999, Jarvinen et al. 2000, Mann et al. 2001, Omoto et al. 2001, Iwase et al. 2003, Fuqua et al. 2003).”
Genome-wide analysis of estrogen receptor binding sites (2006, background): “Estrogen-mediated gene repression Most work investigating estrogen-regulated transcription focuses on upregulated genes, although downregulated genes constitute a significant fraction of all estrogen-dependent expression changes in cell line”
TOXICITY TESTING IN THE 21ST CENTURY: A VISION AND A STRATEGY (2010, background): “A familiar cellular-response network is signaling by estrogens in which initial exposure results in enhanced cell proliferation and growth of specific tissues or in proliferation of estrogen-sensitive cells in culture (Frasor et al., 2003).”
Estrogen signaling through the transmembrane G protein-coupled receptor GPR30. (2008, background): “Interestingly, recent gene expression profiling studies in breast cancer cells indicate that more genes are repressed than activated by estrogen stimulation (39).”