Molecular biology of prostate-cancer pathogenesis

Randi L. Shand, Edward P. Gelmann

Research output: Contribution to journalReview articlepeer-review

64 Scopus citations


Purpose of review: The genetic and molecular basis of prostate-cancer pathogenesis is reviewed. Recent findings: Several genetic loci have been found that are associated with hereditary predisposition to prostate cancer, but they account for a small fraction of all cases. A number of suppressor genes have been identified that are activated by either complete or partial genetic loss in sporadic prostate cancer. Chromosomal translocation results in transcriptional activation of truncated ETS transcription factors ERG and ETV1, the first candidates for dominant oncogenes for prostate cancer. Lastly, the androgen receptor is active throughout the course of prostate cancer and, in androgen-independent prostate cancer, takes on the role of a dominant oncogene as the target of gene amplification, overexpression, and the activation of mutations. Summary: Genetic lesions responsible for familial and sporadic prostate cancer are being revealed and they suggest that prostate cancer often initiates owing to an increased susceptibility to oxidative damage; it then progresses by affecting transcription factors, the PI3 kinase pathway, and other growth stimulatory pathways. The final common pathway after androgen ablation appears to be activation of androgen receptor.

Original languageEnglish (US)
Pages (from-to)123-131
Number of pages9
JournalCurrent Opinion in Urology
Issue number3
StatePublished - May 2006
Externally publishedYes


  • Hereditary cancer
  • Oncogene
  • Prostate cancer
  • Suppressor gene

ASJC Scopus subject areas

  • Urology


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