New monoclonal antibody can detect ERG oncoprotein in prostate cancer patients


A media release from the Uniformed Services University of the Health Sciences last week announced the development of a highly specific assay for the detection of ERG oncoprotein. The assay is based on the development of an anti-ERG monoclonal antibody that appears to be capable of detecting the presence of ERG oncoprotein with > 99 percent accuracy. The actual paper by Furusato et al. is available in full on line. This research was conducted by scientists working at the Center for Prostate Disease Research (CPDR), the Armed Forces Institute of Pathology (AFIP), and Walter Reed Army Medical Center.

Basically, what Furusato et al. have shown is that they are able to identify the presence of the ERG oncoprotein with close to 100 percent accuracy in the prostatic tissues of men who have prostate cancer. But why is this important?

The ERG oncoprotein is the most common of the transcription factors that is produced as a consequence of the many gene fusion events that affect the regulation of androgen-receptor, prostate-associated genes. The new ERG oncoprotein monoclonal antibody can detect the presence of ERG oncoprotein with a very high degree of specificity in about 65 percent of all patients with prostate cancer. In addition, there appears to be no sign of ERG oncoprotein in the (benign) epithelial cells of men who do not have prostate cancer. According to Furusato et al., nearly half (44.8 percent) of 261 individual tumors that they tested were ERG positive, whereas 70.6 percent of 51 specimens with a single tumor were ERG positive and 62 percent of 81 specimens with more than one tumor were ERG positive.

What is also clear at present, however, is that there is a lot  more work to be done before we will know whether the ability to identify expression of the ERG oncoprotein has significant prognostic impact.

We know that the ERG oncoprotein is commonly expressed in patients with prostate cancer. We now know how to test for that expression very early in the development of prostate cancer. The unanswered question is whether the expression of the ERG oncoprotein early in development of prostate cancer is a key factor in the development of clinically significant as opposed to indolent disease. Based on the current paper, all that Furusato and colleagues can tell us is that, “when all of the tumor foci in a given whole-mount section were taken into account, higher Gleason sum and less-differentiated tumors showed correlation with ERG immunostaining.” They haven’t (yet) been able to demonstrate a correlation between ERG expression and disease progression.

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