Growth Factor Stimulation Induces a Distinct ERalpha Cistrome Underlying Breast Cancer Endocrine Resistance

INSTRUCTIONS: Please enter one of the following Topic Classifications in the section below: Bioinformatics & Computational Biology Genes & Environment Genetic & Molecular Epidemiology Medical Genomics Molecular Genetics Proteomics Statistical Genetics, Genomics, and Omics Estrogen receptor a (ERa) expression in breast cancer is predictive of response to endocrine therapy; however,resistance is common in ERa-positive tumors that overexpress the growth factor receptor ERBB2.

Even in the absence of estrogen, ERa can be activated by growth factors, including the epidermal growth factor (EGF). EGF induces a transcriptional program distinct from estrogen; however, the mechanism of the stimulus-specific response is unknown. Here we show that the EGF-induced ERa genomic targets, its cistromes, are distinct from those induced by estrogen in a process dependent on the transcription factor AP-1.