Abstract
Background: The androgen receptor (AR) pathway has emerged as a potential therapeutic target in breast cancer with increased attention to provide biological insight into triple negative breast cancer (TNBC). The present study assessed the role of AR within the tumour microenvironment in patients with invasive ductal breast cancer. Methods: Immunohistochemical analysis of AR was performed on a breast cancer tissue microarray of 850 patients. These results were correlated with clinicopathological data and cancer specific survival (CSS). Results: Positive AR expression was seen in 75% of luminal A, 70% of B, 47% of Her2 like and 31% of TNBC. AR was associated with invasive grade (p<0.001), estrogen receptor /progesterone receptor (p<0.001), molecular subtypes (p<0.001), necrosis (p<0.001), reduced inflammation (p<0.001), and increased tumour budding (p=0.001). AR was consistently associated with tumour budding in molecular subtypes; luminal A (p=0.022), Her2 like (p=0.035) and TNBC (p=0.034). In TNBC, AR was associated with poor CSS (P=0.013). Conclusion: AR may be an important regulator of tumour budding in breast cancer. AR is a potential prognostic marker and therapeutic target for patients with TNBC.
Highlights
The androgen receptor (AR) pathway has emerged as a potential therapeutic target in breast cancer with increased attention to provide biological insight into triple negative breast cancer (TNBC)
The majority of breast cancers are slow growing and convey good clinical outcome [2], a subset acquires an aggressive phenotype in terms of molecular, genotypic, and phenotypic features resulting in multiple subtypes and classifications of breast cancer [3,4]
Breast cancer has been classified as ER positive or negative based on expression or lack of expression of ER or progesterone receptor (PR)
Summary
The androgen receptor (AR) pathway has emerged as a potential therapeutic target in breast cancer with increased attention to provide biological insight into triple negative breast cancer (TNBC). The majority of breast cancers are slow growing and convey good clinical outcome [2], a subset acquires an aggressive phenotype in terms of molecular, genotypic, and phenotypic features resulting in multiple subtypes and classifications of breast cancer [3,4]. Based on cell-type and molecular signature, molecular subtypes have emerged as into luminal A, luminal B, Her (human epidermal growth factor receptor 2) like and basal-like or triple negative breast cancer (TNBC) [3]. The luminal subtypes have good prognosis and usually treated with ER targeted therapy. With the exception of EGFR targeted therapy [6], to date there is no targeted treatment for this group
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