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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 been found to be the most frequent gene rearrangement in prostate cancers, occurring in 45-65% of North American patients.
A mouse monoclonal anti-ERG antibody was developed with an unprecedented 99.9% specificity for detecting prostatic adenocarcinoma. The report shows strong 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, ERG expression 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. Given the ease of performing IHC vs. FISH, ERG protein expression in formalin-fixed paraffinembedded (FFPE) tissues may be an extremely useful tool for the routine identification of the ERG gene rearrangement and diagnosis of prostatic adenocarcinoma.
Further utility for the mouse monoclonal anti-ERG antibody has been demonstrated recently in detecting endothelial malignancies, such as Kaposi sarcoma. ERG (M), 2X may be combined with AMACR (RM), 2X to form a primary antibody combination (see technical notes).
Note: ERG [9FY] was developed by the Center for Prostate Disease Research in association with the Henry M. Jackson Foundation, Rockville, Maryland. Patent Pending.
ERG positive prostate cancer and/or PIN glands.
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