Abstract
Although androgen-deprivation therapy is the standard therapy for advanced and metastatic prostate cancer, this treatment is only palliative. Prostate cancer recurs then grows despite low circulating testicular androgens, using several mechanisms that remain dependent on androgen-receptor signaling in most cases. This article reviews the diversity of mechanisms used for growth by castration-recurrent prostate cancer.
Copyright © 2012 Elsevier Inc. All rights reserved.
MeSH terms
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Androgen Antagonists / therapeutic use
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Antineoplastic Agents / pharmacology
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Gene Amplification
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Gene Expression Regulation, Neoplastic / physiology
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Humans
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Male
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Neoplasm Recurrence, Local / pathology
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Neoplasm Recurrence, Local / physiopathology*
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Neoplasms, Hormone-Dependent / physiopathology*
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Prostate / chemistry
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Prostatic Neoplasms / drug therapy
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Prostatic Neoplasms / genetics
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Prostatic Neoplasms / metabolism
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Prostatic Neoplasms / pathology
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Prostatic Neoplasms / physiopathology*
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Protein Isoforms / physiology
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Receptors, Androgen / biosynthesis
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Receptors, Androgen / drug effects
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Receptors, Androgen / physiology*
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Testosterone / biosynthesis
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Transcriptional Activation / physiology
Substances
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Androgen Antagonists
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Antineoplastic Agents
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Protein Isoforms
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Receptors, Androgen
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Testosterone