In human prostate cancer, the ERG oncogene is frequently overexpressed due to chromosomal translocations involving ERG and regulatory sequences of the TMPRSS2 or other androgen responsive genes. In particular, the TMPRSS2:ERG fusion gene has recently been found to be the most frequent gene rearrangement in prostate cancers, occurring in 45- 65% of North American patients. The mouse monoclonal anti-ERG antibody, clone 9FY, shows an unprecedented 99.9% specificity for detecting prostatic adenocarcinoma. Independent reports demonstrate 97-100% correlation between the expression of the ERG protein and the presence of TMPRSS2:ERG rearrangement and a remarkable concordance (96.5%) of ERG positive prostatic intraepithelial neoplasia (PIN) and ERG positive carcinoma in prostatectomy specimens.
Therefore, as a hallmark of the TMPRSS2:ERG chromosomal translocation, detection of ERG expression by 9FY offers a rare, but definitive marker of adenocarcinoma of prostatic origin, and unique opportunities to indicate oncogenic activations in PIN, to stratify prostate cancer patients for ERG oncogene status and to monitor treatment efficacy. Towards the stratification of patients, comparative evaluations of ERG protein expression status with 9FY and TMPRSS2-ERG gene fusions in hormone-naïve and castration resistant prostate cancers have shown promise for defining a subgroup of cases with dispensed androgen signaling pathway. Given the ease of performing IHC vs. FISH, ERG protein expression in formalin-fixed paraffin-embedded (FFPE) tissues may be an extremely useful tool for the routine identification of the ERG gene rearrangement and
diagnosis of prostatic adenocarcinoma.
Further utility of the mouse monoclonal anti-ERG antibody, 9FY, has been shown in detecting endothelial malignancies, including Kaposi sarcoma. Reports have also demonstrated the superior performance of 9FY in chromatin immunoprecipitation (ChIP), immunofluorescence (IF) and immunoblot assays.
Note: Clone 9FY [U.S. Patent 8,765,916 and patents pending] was developed by the Center for Prostate Disease Research with the Henry M. Jackson Foundation for the Advancement of Military Medicine, Rockville, Maryland, USA.