A mechanism for androgen receptor-mediated prostate cancer recurrence after androgen deprivation therapy

C. W. Gregory, B. He, R. T. Johnson, O. H. Ford, J. L. Mohler, F. S. French, E. M. Wilson

Research output: Contribution to journalArticle

509 Scopus citations

Abstract

The development and growth of prostate cancer depends on the androgen receptor and its high-affinity binding of dihydrotestosterone, which derives from testosterone. Most prostate tumors regress after therapy to prevent testosterone production by the testes, but the tumors eventually recur and cause death. A critical question is whether the androgen receptor mediates recurrent tumor growth after androgen deprivation therapy. Here we report that a majority of recurrent prostate cancers express high levels of the androgen receptor and two nuclear receptor coactivators, transcriptional intermediary factor 2 and steroid receptor coactivator 1. Overexpression of these coactivators increases androgen receptor transactivation at physiological concentrations of adrenal androgen. Furthermore, we provide a molecular basis for this activation and suggest a general mechanism for recurrent prostate cancer growth.

Original languageEnglish (US)
Pages (from-to)4315-4319
Number of pages5
JournalCancer research
Volume61
Issue number11
StatePublished - Jun 1 2001

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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