Prostate cancer is the second most common cancer among American men with about 1 in 6 men being diagnosed with prostate cancer during his lifetime. This cancer is slow growing with a survival rate of 93% fifteen years post treatment. However, the disease can be cured upon early diagnosis. Androgen Receptor (AR), controlled by androgen growth factor, plays a key role in the development of the prostate gland, maintenance of the male reproductive function and the progression to prostrate malignancy. Although advanced prostate cancer can be treated by androgen ablation, the recurrence is often associated with a more aggressive, androgen-independent phenotype. Understanding the mechanism underlying this aggressive, androgen-independent prostate cancer phenotype is imperative to identifying potential therapeutic targets and managing prostate cancer
Unique role for ERG in androgen-independent prostate cancer progression
Recent work performed by a group of researchers at the Cancer Center, University of Michigan led to the identification of an androgen regulated fusion gene, TMPRSSS2-ERG, that was specific to prostate cancer. Further investigation of this fusion gene revealed multiple levels of molecular cross-talk between AR and ERG, where the androgen-regulated ERG gene fusion product was found to regulate AR expression through a negative feedback loop. The key finding by the researchers that ERG regulates AR target genes and can emulate the effect of androgen in regulating prostate cancer oncogenesis in an androgen-independent manner has major implications for prostate cancer management.
- Clinical target for advanced prostate cancer
- Diagnostic marker for advanced prostate cancer
- Improved management and treatment of prostate cancer