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.
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.
High AR-V9 mRNA expression in CRPC metastases was predictive of primary resistance to abiraterone acetate (HR = 4.0; 95% confidence interval, 1.31-12.2; <i>P</i> = 0.02).<b>Conclusions:</b> AR-V9 may be an important component of therapeutic resistance in CRPC.<i></i>.
Metastases with AR amplification showed high AR and AR-V7 mRNA levels, increased nuclear AR immunostaining, and co-amplification of genes such as YIPF6 in the AR proximity at Xq12.
Moreover, brain dissemination is probably the result of progressive dedifferentiation of primary tumor, shown by reduction of ER and AR expression in metastases.
The concordance of <sup>18</sup>F-FDHT and <sup>18</sup>F-FES uptake on PET with immunohistochemical expression of AR and ER in biopsies of corresponding metastases was analyzed.
Patients and Methods Fifty-six patients with metastatic castration-resistant prostate cancer (mCRPC) with osseous metastases had NaF PET/CT scans performed at baseline and after three cycles of chemotherapy (n = 16) or androgen receptor pathway inhibitors (n = 40).
Accordingly, infiltration of CD3<sup>+</sup> and CD68<sup>+</sup> cells was lower in AR-driven than in non-AR-driven metastases, and tumor cell HLA class I ABC immunoreactivity was inversely correlated with nuclear AR immunoreactivity.
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.
Lesions affecting tumour suppressor genes usually occur as single events, whereas mutations in genes involved in androgen receptor signalling commonly involve multiple, convergent events in different metastases.
We showed androgen induced epithelial-mesenchymal transition (EMT) in AR-positive bladder cancer cells and promoted tumor metastasis in xenograft models.