Molecular biology of prostate-cancer pathogenesis

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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.


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.

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