phytoestrogens (from soy and other origins) effects vary from inhibition to stimulatn

[Lani]

depending on what stage tumor is in when exposed, status of ERbeta (not the ER measured normally which is ERa)

: Endocr Relat Cancer. 2008 Mar;15(1):161-173.
Global gene expression profiles induced by phytoestrogens in human breast cancer cells.

Dip R, Lenz S, Antignac JP, Le Bizec B, Gmuender H, Naegeli H.
Institute of Pharmacology and Toxicology, University of Zürich-Vetsuisse, Winterthurerstrasse 260, CH-8057 Zürich, Switzerland 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, France Genedata AG, Maulbeerstrasse 46, CH-4016 Basel, Switzerland.
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 17beta-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 beta (ERbeta). Therefore, phytoestrogens appear to mitigate estrogenic signaling in the presence of both ER subtypes but, in late-stage cancer cells lacking ERbeta, these phytochemicals contribute to a tumor-promoting transcriptional signature.
PMID: 18310284 [PubMed - as supplied by publisher]