AR variant ARv567es induces carcinogenesis in a novel transgenic mouse model of prostate cancer.

ABSTRACT: Androgen deprivation therapy remains the primary treatment modality for patients with metastatic prostate cancer but is uniformly marked by progression to castration-resistant prostate cancer (CRPC) after a period of regression. Continued activation of androgen receptor (AR) signaling is attributed as one of the most important mechanisms underlying failure of therapy. Recently, the discovery of constitutively active AR splice variants (AR-Vs) adds more credence to this idea. Expression of AR-Vs in metastases portends a rapid progression of the tumor. However, the precise role of the AR-Vs in CRPC still remains unknown. ARv567es is one of the two AR variants frequently found in human CRPC xenografts and metastases. Herein, we developed a probasin (Pb) promoter-driven ARv567es transgenic mou

ORGANISM(S): Mus musculus

SUBMITTER: Ilsa Coleman 

PROVIDER: E-GEOD-61303 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress