Prostate cancer is a leading cause of male cancer mortality. The androgen receptor (AR) is important for normal development and maintenance of the prostate and is also critical for the survival and progression of prostate cancer. Current treatment of advanced or metastatic prostate cancer relies on androgen deprivation by inhibiting androgen synthesis or anti-androgens that bind to the AR ligand binding domain. The initial response to androgen deprivation therapy is favorable, however, most patients inevitably relapse to a more aggressive, castration-resistant prostate cancer (CRPC), caused by continued transactivation of AR. CWR-R1ca was derived from the castration-resistant or recurrent CWR-R1 human prostate cancer cell line . The original parental CWR-R1 is a human prostate carcinoma epithelial cell line derived from the recurrent CWR22 human xenograft tumors that were harvested from nude mice 140-160 days after castration and express AR full length (AR-FL), AR-V7 and PSA mRNA and protein .
Synonyms: Fibroblast-Free CWR-R1 cell line
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