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- W94511596 endingPage "382" @default.
- W94511596 startingPage "351" @default.
- W94511596 abstract "The androgen receptor (AR) is fundamental for the growth and survival of normal and malignant prostate cells. Therefore, androgen deprivation therapy remains the first-line treatment for disseminated disease; however, relapse and progression to a castration-resistant phenotype for which no durable treatment currently exists, is inevitable. Restored AR activity is fundamental in the progression to castration-resistant prostate cancer. Multiple mechanisms by which AR is reactivated under androgen-depleted conditions may be involved in the development of this lethal phenotype. Recent studies have identified alternatively spliced transcripts encoding truncated AR isoforms that lack the ligand-binding domain, which is the therapeutic target of androgen deprivation therapy. Many of these truncated AR variants function as constitutively active, ligand-independent transcription factors that can support androgen-independent expression of AR target genes, as well as ligand-independent growth of prostate cancer cells. In this chapter, we will summarize the recent developments in the identification and characterization of AR splice variants in prostate cancer." @default.
- W94511596 created "2016-06-24" @default.
- W94511596 creator A5004467543 @default.
- W94511596 creator A5014512900 @default.
- W94511596 date "2013-01-01" @default.
- W94511596 modified "2023-09-23" @default.
- W94511596 title "Truncated Androgen Receptor Splice Variants in Prostate Cancer" @default.
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