For all histological specimens, the profile (PSA+, PSMA+) was the most expressed in 66% of NP, 70% of patients with BPH and 71% of PC patients. However, no significance was observed between the different groups of prostatic specimens according to the percentage of immunoexpression of the profile (PSA+, PSMA+). To obtain insights into the relationship between PSA and

PSMA production in the subgroup (PSA+, PSMA+) along prostatic diseases, we analysed the intensities of immunoreactions to PSA and to PSMA in NP, BPH and PC patients for the above profile. As observed in Figure 5, optical density of PSA increases significantly from NP to BPH and declines in PC samples in the profile (PSA+, PSMA+) (p < 0.0001). However, the intensity of immunoreaction to PSMA increases significantly from NP to BPH and malignant prostate specimens (p < 0.0001) Eltanexor in the

same profile. Figure 4 Percentage of prostatic specimens with positive or negative immunoreactions to PSA and PSMA according to groups: normal prostate (NP), benign prostatic hyperplasia (BPH) and prostatic carcinoma (PC). Statistical analysis refers to each group separately at p≤0.05. Figure 5 Comparison of the intensity of immunoreactivity (measured as average optical density ± SEM) for PSA and PSMA according to groups: normal prostate (NP), benign prostatic hyperplasia (BPH) and prostatic carcinoma (PC) among (PSA+, PSMA+) profile. Values denoted by different superscripts are significantly different from each selleck chemical other. Those values sharing the same superscript are not statistically different from each other. Statistical analysis refers to each antibody separately. Significance was determined at p≤0. 05. The prostate tumour profile (PSA+, PSMA-) expression levels decreases from NP to benign prostatic tissue and primary prostate cancer (50% vs. 15% vs.

2%, respectively). Inversely, the profile (PSA-, PSMA+) expression increases from NP to BPH and PC patients (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. Baf-A1 in vitro Aberrant prostate epithelial cells growth may result in direct production of prostate-associated 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]. buy AZD1152 Adenocarcinoma of the prostate, like many epithelial malignancies, initiates in the terminally differentiated secretory epithelial cells [33].