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On the other hand, tamoxifen therapy constitutes a major risk factor for endometrial carcinoma development. Amplification of the <jats:italic>ESR1<\/jats:italic> gene encoding ER was recently shown to constitute a mechanism for ER over\u2010expression in breast carcinoma. This study was designed to determine the potential role of <jats:italic>ESR1<\/jats:italic> amplifications in endometrial carcinoma. Tissue microarrays of 368 endometrial carcinomas and large sections of 43 cases of endometrial hyperplasia were analysed for <jats:italic>ESR1<\/jats:italic> gene amplification and ER protein expression by means of fluorescence <jats:italic>in situ<\/jats:italic> hybridization (FISH) and immunohistochemistry. FISH revealed <jats:italic>ESR1<\/jats:italic> amplification in 40\/176 (23%) cancers, 6\/19 (32%) atypical complex hyperplasias, 3\/10 (30%) complex hyperplasias without atypia and 2\/14 (14%) simple hyperplasias without atypia. Strong ER protein expression was significantly linked to <jats:italic>ESR1<\/jats:italic> amplification in endometrial carcinoma (<jats:italic>p<\/jats:italic> = 0.0036). These data indicate that <jats:italic>ESR1<\/jats:italic> amplification might be one mechanism for ER over\u2010expression in endometrial carcinoma, and suggest an early role for <jats:italic>ESR1<\/jats:italic> amplification in the development of a significant fraction of endometrial carcinoma. Given the predictive role of <jats:italic>ESR1<\/jats:italic> amplification for tamoxifen response in breast carcinoma, it will be interesting to investigate the response of <jats:italic>ESR1<\/jats:italic>\u2010amplified endometrial cancers to anti\u2010oestrogenic drugs. Copyright \u00a9 2008 Pathological Society of Great Britain and Ireland. 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