Abstract
Castration-resistant prostate cancer (CRPC) is now the second most common cause of male cancer-related mortality. Recent evidence confirms that androgen receptor signalling continues to drive a significant proportion of progressing prostate cancers despite castrate serum levels of testosterone and multiple hormonal interventions. An increased understanding of the molecular biology underlying CRPC is informing on therapeutic targets for this disease, and we hypothesise that this will lead to the development of more efficacious drugs.
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