Targeted disruption of the p160 coactivator interface of androgen receptor (AR) selectively inhibits AR activity in both androgen-dependent and castration-resistant AR-expressing prostate cancer cells

The evidence that androgen blockade-resistant prostate cancer, termed castration resistant, remains androgen receptor (AR) dependent is compelling. AR is re-activated through multiple mechanisms including expression of constitutively active splice variants that lack hormone binding domains (HBD). Th...

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Main Authors: Nakka, Manjula, Agoulnik, Irina U., Weigel, Nancy L.
Formato: Artigo
Idioma:Inglês
Publicado: 2012
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Article
Acceso en liña:https://ncbi.nlm.nih.gov/pmc/articles/PMC3593820/
https://ncbi.nlm.nih.gov/pubmed/23270728
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1016/j.biocel.2012.12.012
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