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Epithelial\u2013mesenchymal transition (EMT) endows cells with migratory and invasive properties and can be induced by oestrogen. We hypothesized that oestrogen\u2010induced EMT is critical in the pathogenesis of adenomyosis. We first investigated whether EMT occurred in adenomyotic lesions and whether it correlated with serum 17\u03b2\u2010oestradiol (E2) levels. Immunohistochemistry was performed on adenomyotic lesions and corresponding eutopic endometrium samples from women with adenomyosis. Endometria from women without endometrial disorders were used as a control. In the epithelial component of adenomyotic lesions, vimentin expression was up\u2010regulated and E\u2010cadherin expression was down\u2010regulated compared to the eutopic endometrium, suggesting that EMT occurs in adenomyosis. In adenomyosis, the serum E2 level was negatively correlated with E\u2010cadherin expression in the epithelial components of the eutopic endometrium and adenomyotic lesions, suggesting the involvement of oestrogen\u2010induced EMT in endometrial cells. In oestrogen receptor\u2010positive Ishikawa endometrial epithelial cells, oestrogen induced a morphological change to a fibroblast\u2010like phenotype, a shift from epithelial marker expression to mesenchymal marker expression, increased migration and invasion, and up\u2010regulation of the EMT regulator Slug. Raloxifene, a selective oestrogen receptor modulator, abrogated these effects. To determine the role of oestrogen\u2010induced EMT in the implantation of ectopic endometrium, we xenotransplanted eutopic endometrium or adenomyotic lesions from adenomyosis patients into ovariectomized SCID mice. The implantation of endometrium was oestrogen\u2010dependent and was suppressed by raloxifene. Collectively, these data highlight the crucial role of oestrogen\u2010induced EMT in the development of adenomyosis and suggest that raloxifene may be a potential therapeutic agent for adenomyosis patients. Copyright \u00a9 2010 Pathological Society of Great Britain and Ireland. 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