Ben Jemaa et al. Journal of Experimental & Clinical Cancer Research 2010, 29:171 http://www.jeccr.com/content/29/1/171 Page 5 of 9 Figure 2 Distribution of tissue PSMA (A), PSA (B) and CD34 (C) immunostaining intensity (measured as average optical density) according to normal prostate (NP), benign prostatic hyperplasia (BPH) and prostatic carcinoma (PC). Average optical densities were evaluated only in patients showing immunopositivity. (50% vs. 53% vs. 90%, respectively). Compared to BPH patients, the profile (PSA-, PSMA-) was absent in both NP and PC tissues. This profile was found in 30% of hyperplastic prostate tissues. Discussion A variety of pathological processes lead to the loss of the normal prostate glandular architecture including benign prostatic hyperplasia and prostate cancer and its associated metastases. Aberrant prostate epithelial cells growth may result in direct production of prostate-asso- ciated antigens such as the secreted protease prostate- specific antigen (PSA) and the highly specific membrane antigen present in their plasma membrane, prostate- specific membrane antigen (PSMA) [4]. PSMA is an integral cell surface membrane protein which is highly specific to prostate gland [14]. Adenocarcinoma of the prostate, like many epithelial malignancies, initiates in the terminally differentiated secretory epithelial cells [33]. In the present study we demonstrated expression of PSMA within the cells of the prostatic secretory epithelium in normal, hyperplastic and malignant pros- tate specimens. We observed an increase of PSMA expression in prostate cancer. It’ is seems to indicate a more extensive role of PSMA in prostate cancer. Low expression in normal tissue would suggest a limited role of PSMA in normal human prostate and low expression in benign prostate hyperplasia tissue may suggest a lim- ited role of this protein in hyperplastic tissue [17,34]. Our finding is consistent with previous reports using immunohistochemistry and multiplex PCR reactions to demonstrate the association between PSMA and tumor progression [17,34,35]. A notable finding in our study revealed that in NP the expression of PSMA and PSA seems to be identical. However, PSMA expression in hyperplastic and neoplastic prostates tissues appears to be inversed to the PSA expression. Although PSMA is more expressed in malignant prostate than benign pro- static hyperplasia, PSA is highly expressed in hyperplas- tic tissues. This is in part, thought to be due to the differences observed in several biological features between peripheral and transition zone of the prostate gland [2]. Although, the majority of the glandular tissue in prostate is located in the peripheral zone, the PSA tissue is secreted at higher levels by benign prostate epithelium arising exclusively in the transition zone compared to prostate cancer developing mainly in per- ipheral zone [36,22]. The majority of our samples diag- nosed with prostate cancer have a Gleason grade ≥7. However, regarding to PSA expression we observed a bi-modal distribution of expression of this marker in