Partners in crime: deregulation of AR activity and androgen synthesis in prostate cancer
Prostate 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 d...
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| Veröffentlicht in: | Trends in endocrinology and metabolism 2010-05, Vol.21 (5), p.315-324 |
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| container_title | Trends in endocrinology and metabolism |
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| creator | Knudsen, Karen E Penning, Trevor M |
| description | Prostate 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. |
| doi_str_mv | 10.1016/j.tem.2010.01.002 |
| format | Article |
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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. 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Urinary tract diseases ; Prostate - metabolism ; Prostatic Neoplasms - genetics ; Prostatic Neoplasms - pathology ; Prostatic Neoplasms - physiopathology ; Receptors, Androgen - drug effects ; Receptors, Androgen - physiology ; Tumors ; Tumors of the urinary system ; Urinary tract. Prostate gland ; Vertebrates: endocrinology</subject><ispartof>Trends in endocrinology and metabolism, 2010-05, Vol.21 (5), p.315-324</ispartof><rights>Elsevier Ltd</rights><rights>2010 Elsevier Ltd</rights><rights>2015 INIST-CNRS</rights><rights>2010 Elsevier Ltd. All rights reserved.</rights><rights>2010 Elsevier Ltd. 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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.</description><subject>Androgen Antagonists - therapeutic use</subject><subject>Androgens - biosynthesis</subject><subject>Biological and medical sciences</subject><subject>Castration</subject><subject>Endocrinology & Metabolism</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Male</subject><subject>Male genital diseases</subject><subject>Medical sciences</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Prostate - metabolism</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Prostatic Neoplasms - physiopathology</subject><subject>Receptors, Androgen - drug effects</subject><subject>Receptors, Androgen - physiology</subject><subject>Tumors</subject><subject>Tumors of the urinary system</subject><subject>Urinary tract. 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Psychology</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Male</topic><topic>Male genital diseases</topic><topic>Medical sciences</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Prostate - metabolism</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Prostatic Neoplasms - pathology</topic><topic>Prostatic Neoplasms - physiopathology</topic><topic>Receptors, Androgen - drug effects</topic><topic>Receptors, Androgen - physiology</topic><topic>Tumors</topic><topic>Tumors of the urinary system</topic><topic>Urinary tract. 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| ispartof | Trends in endocrinology and metabolism, 2010-05, Vol.21 (5), p.315-324 |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Androgen Antagonists - therapeutic use Androgens - biosynthesis Biological and medical sciences Castration Endocrinology & Metabolism Fundamental and applied biological sciences. Psychology Gynecology. Andrology. Obstetrics Humans Male Male genital diseases Medical sciences Nephrology. Urinary tract diseases Prostate - metabolism Prostatic Neoplasms - genetics Prostatic Neoplasms - pathology Prostatic Neoplasms - physiopathology Receptors, Androgen - drug effects Receptors, Androgen - physiology Tumors Tumors of the urinary system Urinary tract. Prostate gland Vertebrates: endocrinology |
| title | Partners in crime: deregulation of AR activity and androgen synthesis in prostate cancer |
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