Endocrine-disrupting chemicals (EDC) are abundant in our environment. A number of EDCs, including bisphenol A (BPA) can bind to the estrogen receptors, ERα and ERβ, and may contribute to estrogen-linked diseases such as breast cancer. Early-exposure is of particular concern; many EDCs cross the placenta and infants have measurable levels of e.g. BPA. In addition, infants are frequently fed soy-based formula that contains phytoestrogens. Effects of combined exposure to xeno- and phytoestrogens are poorly studied. Here, we extensively compared to what extent BPA, genistein and an extract of infant soy-based formula (SF) mimic estrogen-induced gene transcription and cell proliferation. We investigated ligand-specific effects on ER activation in HeLa-ERα and ERβ reporter cells; on proliferation, genome-wide gene regulation and non-ER mediated effects in MCF7 breast cancer cells; and how co-exposure influenced these effects. The biological relevance was explored using enrichment analyses of differentially regulated genes and clustering with clinical breast cancer profiles. We demonstrate that co-exposure to BPA and genistein, or SF, results in increased functional and transcriptional estrogenic effects. Using statistical modeling we determine that BPA and phytoestrogens act in an additive manner. The proliferative and transcriptional effects of the tested compounds mimic those of 17β-estradiol, and are abolished by co-treatment with an ER antagonist. Gene expression profiles induced by each compound clustered with poor-prognosis breast cancer, indicating that exposure may adversely affect breast cancer prognosis. This study accentuates that co-exposure to BPA and soy-based phytoestrogens results in additive estrogenic effects, and may contribute to estrogen-linked diseases, including breast cancer.