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. 2014 Feb 4;18(5):863–874. doi: 10.1111/jcmm.12232

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© 2014 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.

This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Fig. 1 — Expression of Olfactomedin 4 (OLFM4), estrogen receptor-α (ERα) and progesterone receptor (PR) in normal endometrium, endometrial hyperplasia and endometrioid adenocarcinoma detected by immunohistochemistry. Haematoxylin-eosin, Morphology of normal endometrium (A), simple hyperplasia without atypia (E), complex atypical hyperplasia (I), and well-(M), moderately-(Q) and poorly-differentiated endometrioid adenocarcinomas (U) stained by haematoxylin-eosin. OLFM4, OLFM4 staining was undetectable in normal endometrium (B). Immunoreactivity of OLFM4 gradually increased from endometrial hyperplasia (F), atypical endometrial hyperplasia (J) to well-differentiated endometrioid adenocarcinoma (N), and gradually decreased with lower degrees of differentiation in endometrioid adenocarcinomas (N, R, V). ER, Immunoreactivity of ER gradually decreased from normal endometrium (C), endometrial hyperplasia (G), atypical endometrial hyperplasia (K) to well-differentiated endometrioid adenocarcinoma (O). ER staining was hardly detectable in moderately-(S) and poorly-(W) differentiated endometrioid adenocarcinomas. PR, Immunoreactivity of PR gradually decreased from normal endometrium (D), endometrial hyperplasia (H), atypical endometrial hyperplasia (L), well- (P), moderately-(T) to poorly-(X) differentiated endometrioid adenocarcinomas. NE: normal endometrium; EH: endometrial hyperplasia; AEH: atypical endometrial hyperplasia; WD-EAC: well-differentiated endometrioid adenocarcinoma; MD-EAC: moderately-differentiated endometrioid adenocarcinoma; PD-EAC: poorly-differentiated endometrioid adenocarcinomas.