Oncogenic activation of ERG: A predominant mechanism in prostate cancer

Taduru Sreenath*, Albert Dobi, Gyorgy Petrovics, Shiv Srivastava

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

48 Scopus citations


Prevalent gene fusions involving regulatory sequences of the androgen receptor (AR) regulated genes (primarily TMPRSS2) and protein coding sequences of nuclear transcription factors of the ETS gene family (predominantly ERG) result in unscheduled androgen dependent ERG expression in prostate cancer (CaP).Cumulative data from a large number of studies in the past six years accentuate ERG alterations in more than half of all CaP patients in Western countries. Studies underscore that ERG functions are involved in the biology of CaP. ERG expression in normal context is selective to endothelial cells, specific hematopoetic cells and pre-cartilage cells. Normal functions of ERG are highlighted in hematopoetic stem cells. Emerging data continues to unravel molecular and cellular mechanisms by which ERG may contribute to CaP. Herein, we focus on biological and clinical aspects of ERG oncogenic alterations, potential of ERG-based stratification of CaP and the possibilities of targeting the ERG network in developing new therapeutic strategies for the disease.

Original languageEnglish
Article number37
Pages (from-to)10-21
Number of pages12
JournalJournal of Carcinogenesis
StatePublished - 2011
Externally publishedYes


  • ERG
  • androgen receptor
  • oncoprotein
  • patient stratification
  • prostate cancer


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