Truncated androgen receptor splice variants in prostate cancer

Peter E. Lonergan, Donald J. Tindall

Research output: Chapter in Book/Report/Conference proceedingChapter

1 Scopus citations

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 androgenindependent 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.

Original languageEnglish (US)
Title of host publicationProstate Cancer
Subtitle of host publicationBiochemistry, Molecular Biology and Genetics
PublisherSpringer New York
Pages351-382
Number of pages32
ISBN (Electronic)9781461468288
ISBN (Print)9781461468271
DOIs
StatePublished - Jan 1 2013

ASJC Scopus subject areas

  • Medicine(all)

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    Lonergan, P. E., & Tindall, D. J. (2013). Truncated androgen receptor splice variants in prostate cancer. In Prostate Cancer: Biochemistry, Molecular Biology and Genetics (pp. 351-382). Springer New York. https://doi.org/10.1007/978-1-4614-6828-8_13