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- W2114883280 abstract "Manipulation of patients’ androgen status pervades so much of the management of prostate cancer (PCa). It commences with neoadjuvant androgen deprivation therapy (ADT) in combination with radiation therapy for intermediate-risk and high-risk organ-confined disease and extends to various modulations of ADT in patients with nonlocalised and metastatic disease. Permutations include continuous and intermittent monotherapy as well as combined androgen blockade for hormone-responsive cancer, with both the addition and subtraction of single therapeutic agents for short-term responses in castrateresistant PCa (CRPC). Although initial response toADT is excellent (>90%), these therapies inevitably fail with the emergence of CRPC. Extensive preclinical and clinical data indicate that the androgen receptor (AR) signalling pathway is not only present but continues to mediate androgen signalling after failure of androgen agonist therapy, despite castrate levels of circulating androgens [1]. AR overexpression, amplification, mutation, and altered coregulator interactionsmay sensitise the AR to lower levels of ligand, thereby contributing to failure of hormonal therapies. It has been documented recently that intratumoural androgen levels in CRPC are sufficient to stimulate tumour growth [2], indicating that local synthesis of androgens is another mechanism for maintaining AR signalling in the castrate environment. The clinical importance of these findings is highlighted by the recent reports of clinical efficacy of abiraterone acetate, an irreversible inhibitor of 17a-hydroxylase/C17,20 lyase that" @default.
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- W2114883280 date "2009-08-01" @default.
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- W2114883280 title "Testosterone Therapy in Castrate-Resistant Prostate Cancer: A Possible New Approach" @default.
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- W2114883280 doi "https://doi.org/10.1016/j.eururo.2009.04.030" @default.
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