Lookup NU author(s): Dr Judith Bulmer
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
Background: Endometrial cancer (EC) is a hormone-driven disease, and androgen receptor (AR) expression in high-grade EC (HGEC) and metastatic EC has not yet been described.Methods: The expression pattern and prognostic value of AR in relation to oestrogen (ER alpha and ER beta) and progesterone (PR) receptors, and the proliferation marker Ki67 in all EC subtypes (n = 85) were compared with that of healthy and hyperplastic endometrium, using immunohistochemisty and qPCR.Results: Compared with proliferative endometrium, postmenopausal endometrtial epithelium showed significantly higher expression of AR (P<0.001) and ERa (P = 0.035), which persisted in hyperplastic epithelium and in low-grade EC (LGEC). High-grade EC showed a significant loss of AR (P<0.0001), PR (P<0.0001) and ERb (P<0.035) compared with LGEC, whilst maintaining weak to moderate ER alpha. Unlike PR, AR expression in metastatic lesions was significantly (P = 0.039) higher than that in primary tumours. Androgen receptor expression correlated with favourable clinicopathological features and a lower proliferation index. Loss of AR, with/without the loss of PR was associated with a significantly lower disease-free survival (P<0.0001, P<0.0001, respectively).Conclusions: Postmenopausal endometrial epithelium acquires AR whilst preserving other steroid hormone receptors. Loss of AR, PR with retention of ER alpha and ER beta may promote the unrestrained growth of HGEC. Androgen receptor may therefore be a clinically relevant prognostic indicator and a potential therapeutic target in EC.
Author(s): Kamal AM, Bulmer JN, DeCruze SB, Stringfellow HF, Martin-Hirsch P, Hapangama DK
Publication type: Article
Publication status: Published
Journal: British Journal of Cancer
Print publication date: 15/03/2016
Online publication date: 01/03/2016
Acceptance date: 22/12/2015
ISSN (print): 0007-0920
ISSN (electronic): 1532-1827
Publisher: Nature Publishing Group
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