Androgen receptor expression in glioblastoma: molecular profiling and association with tumor burden.

BACKGROUND: Glioblastoma (GBM) is the most aggressive primary brain tumor in adults, characterized by higher incidence and poorer outcomes in males. Increasing evidence suggests that androgen receptor (AR) expression may influence GBM progression, yet its clinical significance remains uncertain. This study aimed to evaluate AR expression at both mRNA and protein levels in GBM tissue and to explore its potential association with magnetic resonance imaging (MRI)-defined tumor volume. METHODS AND RESULTS: Tumor samples from 34 patients with primary GBM were analyzed. AR mRNA expression was quantified by real-time PCR in 30 cases, while immunohistochemistry was performed in 24 cases to assess AR protein expression. Tumor volumes were determined from T1-contrast-enhancing and FLAIR-hyperintense MRI regions. Statistical analyses included unpaired t-tests with Welch’s corrections and Spearman’s rank correlations with additional multivariable linear regression analyses (pre-steroid imaging status was not included). Mean AR mRNA and protein expression levels were higher in males than females, though not statistically significant. AR mRNA expression showed a strong trend toward positive correlation with Ki67 proliferation index (r = 0.44, p = 0.07) and tumor volume (r = 0.36, p = 0.06 for T1-enhancing regions; r = 0.40, p = 0.03 for non-enhancing FLAIR-hyperintense regions). Exploratory multivariable model adjusted for age, sex, and MGMT status revealed that higher AR mRNA expression was independently associated with FLAIR-hyperintense tumor volume (β = 0.50, p = 0.037), while AR protein expression and all other covariates showed no significant associations. CONCLUSION: AR expression is consistently detectable in GBM tissue and shows a trend toward association at the transcriptional level with non-contrast-enhancing tumor volume, suggesting a potential role in GBM biology and warranting further investigation in larger studies.