Most advanced prostate tumors are dependent upon hormonal regulation of the transcriptional activity of the
androgen receptor (AR). Current ASCO recommendations for initial treatment of advanced disease target the hormonal
mediated regulation of AR activation through androgen deprivation therapy. Despite early treatment efficacy, most
prostate tumors progress and re-activate AR transcriptional regulation through alternative biological mechanisms that
allow them to circumvent the requirement for androgen. It is the temporal and spatial recruitment of specific AR
transcriptional complexes to the promoters of cancer associated target genes that promotes the tumorigenic phenotype in
prostate cancer. Increasing published data associates the E Twenty Six (ETS) family of transcription factors with prostate
cancer progression and with the transcriptional activity of the AR. Evidence suggests that ETS factors act in concert to
both positively and negatively regulate the pathways that control progression to metastatic cancer in prostate tissues.
Given the critical roles both ETS factors and the AR play in the development of prostate cancer, mechanistic insight into
their transcriptional co-regulation during the hormone sensitive and hormone refractory phases of progression will be
provided by determining the contribution of ETS, AR and ETS-AR mediated regulatory control. This review examines the
current depth of understanding of the role of the ETS family of transcription factors as transcriptional elements that confer
the carcinogenic response to aberrant hormonal activity during prostate cancer progression.