EPCA-2: A Highly Specific Serum Marker for Prostate Cancer
Received 9 January 2007; accepted 27 January 2007.
Objectives
To describe the initial assessment of early prostate cancer antigen (EPCA)-2 as a serum marker for the detection of prostate cancer and to examine its sensitivity and specificity.
Methods
Serum samples were obtained from 385 men: those with prostate-specific antigen (PSA) levels less than 2.5 ng/mL, PSA levels of 2.5 ng/mL or greater with negative biopsy findings, benign prostatic hyperplasia, organ-confined prostate cancer, non-organ-confined disease, and prostate cancer with PSA levels less than 2.5 ng/mL. In addition, a diverse group of controls was assessed with an enzyme-linked immunosorbent assay to detect an epitope of the EPCA-2 protein, EPCA-2.22.
Results
Using a cutoff of 30 ng/mL, the EPCA-2.22 assay had a 92% specificity (95% confidence interval 85% to 96%) for healthy men and men with benign prostatic hyperplasia and 94% sensitivity (95% confidence interval [CI] 93% to 99%) for overall prostate cancer. The specificity for PSA in these selected groups of patients was 65% (95% CI 55% to 75%). Additionally, EPCA-2.22 was highly accurate in differentiating between localized and extracapsular disease (area under the curve 0.89, 95% CI 0.82 to 0.97, P <0.0001) in contrast to PSA (area under the curve 0.62, 95% CI 0.50 to 0.75, P = 0.05).
Conclusions
The results of our study have shown that EPCA-2 is a novel biomarker associated with prostate cancer that has high sensitivity and specificity and accurately differentiates between men with organ-confined and non-organ-confined disease.
aBrady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland
bDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland
Reprint requests: Robert H. Getzenberg, Ph.D., Brady Urological Institute, Johns Hopkins Hospital, Marburg 121, 600 North Wolfe Street, Baltimore, MD 21287.
None of the other authors declare a conflict of interest.
This study was supported by a grant from the National Institutes of Health, National Cancer Institute (CA65463) and a research grant from Onconome Incorporated.
1 R. Getzenberg holds a patent for the technology described in this study. This patent is owned by the University of Pittsburgh and Johns Hopkins University and has been licensed to Onconome Inc. He has also received a research grant from Onconome Inc. and is a consultant to the company. The terms of this arrangement are managed by the Johns Hopkins University in accordance with its conflict of interest policies.
ABSTRACT