ERα, PR and AR receptor status converted from positive in the primary tumor to negative in the effusion metastases or <i>vice versa</i> in 25-30%, 30-35% and 46-51% of cases for the 1% and 10% thresholds for positivity, respectively.
Androgen receptor (AR) is a validated drug target for prostate cancer based on its role in proliferation, survival, and metastases of prostate cancer cells.
Recent genome-wide analysis of prostate cancer metastases illustrate the importance of the Wnt/β-catenin pathway in prostate cancer and compel us to reexamine the interaction of the AR and Wnt/β-catenin signaling pathways.
We sought to identify the plausible stemness factor that determines the "molecular signature" of prostate cancer (PCa) cells derived from different metastases (PC3, PCa2b, LNCaP, and DU145) and whether androgen receptor (AR) influences the maintenance of stemness features.
We did not find any GATA3 or AR expression in the metastases from endometrial or salivary gland carcinomas, while GATA3 expression was seen in the majority of metastases from urothelial or breast carcinomas.
Body mass index (P = .023) and DACH1 (P = .034) were correlated with MBC prognosis, whereas the expression of AR (P = .049), SIX1 (P = .048), surgery (P < .001), and chemotherapy (P = .001) were important for FBC in addition to already known factors: tumor size and location, TNM stage (lymph nodes and organ metastasis), radiotherapy, and ER and human epidermalgrowth factor receptor-2 (HER2) expression.
Although most metastases (21/22, 95%) had concordant AR expression with the primary tumors, one treatment-naïve tumor (5%) had complete loss of AR immunoexpression in the metastasis without detectable molecular alterations in AR or AR co-regulators.
Coexpression analyses showed an increase of the double-positive (AR<sup>+</sup> /ARv7<sup>+</sup> ) population in metastases compared to benign, and an increase of the double-negative population in PRCA samples compared to benign.