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Institute of Pharmacology and Toxicology, University of Zürich-Vetsuisse, Winterthurerstrasse 260, CH-8057 Zürich, Switzerland¹ Laboratoire d'Etude des Résidus et Contaminants dans les Aliments (LABERCA), USC INRA 2013, Ecole Nationale Vétérinaire de Nantes, BP 50707, 44307 Nantes Cedex 3, France² Genedata AG, Maulbeerstrasse 46, CH-4016 Basel, Switzerland

(Correspondence should be addressed to H Naegeli; Email: naegelih{at}vetpharm.uzh.ch)

The nutritional intake of phytoestrogens seems to reduce the risk of breast cancer or other neoplastic diseases. However, these epidemiological findings remain controversial because low doses of phytoestrogens, achievable through soy-rich diets, stimulate the proliferation of estrogen-sensitive tumor cells. The question of whether such phytochemicals prevent cancer or rather pose additional health hazards prompted us to examine global gene expression programs induced by a typical soy product. After extraction from soymilk, phytoestrogens were deconjugated and processed through reverse- and normal-phase cartridges. The resulting mixture was used to treat human target cells that represent a common model system for mammary tumorigenesis. Analysis of mRNA on high-density microarrays revealed that soy phytoestrogens induce a genomic fingerprint that is indistinguishable from the transcriptional effects of the endogenous hormone 17β-estradiol. Highly congruent responses were also observed by comparing the physiologic estradiol with daidzein, coumestrol, enterolactone, or resveratrol, each representing distinct phytoestrogen structures. More diverging transcriptional profiles were generated when an inducible promoter was used to reconstitute the expression of estrogen receptor β (ERβ). Therefore, phytoestrogens appear to mitigate estrogenic signaling in the presence of both ER subtypes but, in late-stage cancer cells lacking ERβ, these phytochemicals contribute to a tumor-promoting transcriptional signature.