Anti-AMACR polyclonal antibody

Nephrogenic adenoma (NA) is a rare benign lesion of the urinary tract. Although its histogenesis is still debated, several reports suggest that the lesion has a renal tubular cell origin or differentiation. As NA can be difficult to distinguish from malignant conditions such as prostate cancer, there is a need for reliable markers. Unfortunately, it has been reported that NA cells also stained positive for the prostate cancer marker alpha-methylacyl-coenzyme A racemase (AMACR). Because all the previous studies have used an avidin-biotin (AB) detection procedure, and because cells with tubular renal differentiation are likely to contain a high level of endogenous biotin, we investigated in NA the expression of several markers including AMACR, using both AB and biotin-free detection systems. We assessed the expression of p63, cytokeratins 7 and 20, CD10 (proximal tubule marker), MUC1 (distal tubule marker), PAX2, and AMACR on 14 NAs (from 6 patients) grouped on a tissue microarray. The tissue microarray also included renal, urothelial, and prostate tissues. Staining was detected using both AB and biotin-free Envision systems. Detection with the AB procedure leads to nonspecific staining in kidney samples and NA. More specific expression was obtained by using the Envision kit, and only CK7, PAX2, and MUC1 remained positive in NA, without any AMACR staining. These findings provide supporting evidence that NA has the differentiation of distal renal tubules, and strongly suggest that AMACR, when detected with a biotin-free procedure, can be used as a reliable marker for distinguishing NA from prostate cancer.

Background: Because of the numerous limitations of prostate-specific antigen (PSA), alpha-methylacyl-CoA racemase (AMACR) and hepsin have recently been suggested as potential biomarkers in prostate cancer (PC). This report presents a comparison study of the presence of AMACR and hepsin in urine collected before and after digital rectal examination (DRE) as a previously suggested diagnostic marker for PC. Methods: Seventy-six urine samples (38 before and 38 after prostate massage) from patients with benign prostate hyperplasia (BPH) and 66 urine samples (33 before and 33 after prostate massage) from patients with PC were analyzed. PC was confirmed by prostate biopsy. Urinary levels of AMACR and hepsin were determined by ELISA and related to the tumor stage, Gleason score and PSA level. Results: AMACR and hepsin levels in urine collected after prostate massage were higher only in the PC group. There were no correlations between AMACR levels, hepsin levels, tumor stage and Gleason score. AMACR and hepsin did not differentiate between BPH and PC with better true positive and false negative rates than serum PSA. Conclusions: AMACR and hepsin were unable to diagnose PC with better true positive and false negative rates than PSA. An additional procedure combined with other markers should be applied for the reliable diagnosis of PC.