Nuclear β‐catenin is a molecular feature of type I endometrial carcinoma

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Abstract
Two types of endometrial carcinoma can be distinguished: type I tumours, which are oestrogen‐related and are typically low‐grade endometrioid carcinomas; and type II tumours, which are unrelated to oestrogen stimulation and are often non‐endometrioid carcinomas. The molecular abnormalities involved in carcinogenesis appear to be different for these tumour types. The aim of this study was to test the hypothesis that an abnormality in the Wnt/β‐catenin signalling pathway is a molecular feature of type I endometrial carcinoma. This study investigated nuclear β‐catenin by immunohistochemistry in 233 endometrial carcinomas and analysed its correlation with several immunohistochemical, histological, and clinical parameters, such as proliferation rate (Ki‐67), expression of oestrogen and progesterone receptors, and survival. Nuclear β‐catenin expression was observed in 39 cases (16%). All tumours expressing nuclear β‐catenin were endometrioid adenocarcinomas, were significantly better differentiated, and were more often hormone receptor‐positive than tumours without nuclear β‐catenin. No correlation with proliferation rate was found. It was found that several features of type I endometrial carcinoma occur significantly more often in tumours expressing nuclear β‐catenin, suggesting that an abnormality in the Wnt/β‐catenin signalling pathway, resulting in nuclear β‐catenin immunopositivity, is a molecular feature of a subset of type I endometrial carcinomas. Copyright © 2003 John Wiley & Sons, Ltd.