ArticleFrontiers in oncology2026
Assessing the prognostic role of androgen receptor expression in non-metastatic triple-negative breast cancer.
Article in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Triple negative breast cancer (TNBC) represents 15-20% of all invasive breast cancer with poor breast cancer survival. Androgen receptor (AR) expression in TNBC shows significant variability in the literature, with rates ranging from 7% to 75%. The association between AR expression and prognosis in TNBC remains controversial. Methods: A comparative retrospective design was utilized including all TNBC cases between 2014-2020. AR receptor expression was evaluated by immunohistochemical staining using whole tissue sections from archived paraffin-embedded formalin fixed blocks. Correlation of AR expression with standard clinical pathological factors and clinical outcomes of interest were assessed; including disease free survival (DFS), breast cancer specific survival (BCSS), and overall survival (OS). Results: 149 patients with non-metastatic TNBC were included. 94 patients (63.3%) being AR negative and 55 patients (36.7%) were AR positive. No statistical difference in tumor characteristics between the two groups was found. The 5-year OS rates for AR negative and positive patients were 60% and 70% respectively (p= 0.021). However, this statistical significance was lost with longer follow-up (103 months, p=0.25). The 5-year DFS was similar for both groups (AR negative and AR positive, 64.3%, 62.9% respectively, p=0.39) in addition to the BCSS (73%, 78.8% respectively, p= 0.84). In univariable and multivariable analyses, AR expression did not significantly impact OS or DFS (HR: 0.71 and 1.07, p= 0.3, 0.8, respectively). Conclusion: In this study, AR status showed no association with DFS, BCSS, or OS; and was not a prognostic factor in TNBC. Further studies exploring the role of AR in TNBC are warranted as AR expression could be a potential target with antiandrogen therapy.
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