ESR1 and breast carcinoma: Thus, to test this hypothesis and to identify determinants of differential splicing between ER+ and TN breast cancer subtypes, we selected several RNA processing factors that were differentially expressed between breast cancer subtypes (S7 Fig, S6 Table), were induced by estrogen in an estrogen time course in MCF7 cells[31], and/or have previously been identified as potential direct targets of ER based on the presence of ER binding sites in genome-wide chromatin immunoprecipitation experiments[31].