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lüll Partners in crime: deregulation of AR activity and androgen synthesis in prostate cancer Knudsen KE; Penning TMTrends Endocrinol Metab 2010[May]; 21 (5): 315-24Prostate cancer remains a leading cause of cancer death, as there are no durable means to treat advanced disease. Treatment of non-organ-confined prostate cancer hinges on its androgen dependence. First-line therapeutic strategies suppress androgen receptor (AR) activity, via androgen ablation and direct AR antagonists, whereas initially effective, incurable, 'castration-resistant' tumors arise as a result of resurgent AR activity. Alterations of AR and/or associated regulatory networks are known to restore receptor activity and support resultant therapy-resistant tumor progression. However, recent evidence also reveals an unexpected contribution of the AR ligand, indicating that alterations in pathways controlling androgen synthesis support castration-resistant AR activity. In this report, the mechanisms underlying the lethal pairing of AR deregulation and aberrant androgen synthesis in prostate cancer progression will be discussed.|Androgen Antagonists/therapeutic use[MESH]|Androgens/*biosynthesis[MESH]|Castration[MESH]|Humans[MESH]|Male[MESH]|Prostate/*metabolism[MESH]|Prostatic Neoplasms/genetics/pathology/*physiopathology[MESH]|Receptors, Androgen/drug effects/*physiology[MESH] |