BackgroundThe present study was undertaken to relate the co-expression of prostate-associated antigens, PSMA and PSA, with the degree of vascularization in normal and pathologic (hyperplasia and cancer) prostate tissues to elucidate their possible role in tumor progression.MethodsThe study was carried out in 6 normal, 44 benign prostatic hyperplastic and 39 cancerous human prostates. Immunohistochemical analysis were performed using the monoclonal antibody CD34 to determine the angiogenic activity, and the monoclonal antibodies 3E6 and ER-PR8 to assess PSMA and PSA expression, respectively.ResultsIn our study we found that in normal prostate tissue, PSMA and PSA were equally expressed (3.7 ± 0.18 and 3.07 ± 0.11). A significant difference in their expression was see in hyperplastic and neoplastic prostates tissues (16.14 ± 0.17 and 30.72 ± 0.85, respectively) for PSMA and (34.39 ± 0.53 and 17.85 ± 1.21, respectively) for PSA. Study of prostate tumor profiles showed that the profile (PSA+, PSMA-) expression levels decreased between normal prostate, benign prostatic tissue and primary prostate cancer. In the other hand, the profile (PSA-, PSMA+) expression levels increased from normal to prostate tumor tissues. PSMA overexpression was associated with high intratumoral angiogenesis activity. By contrast, high PSA expression was associated with low angiogenesis activity.ConclusionThese data suggest that these markers are regulated differentially and the difference in their expression showed a correlation with malignant transformation. With regard to the duality PSMA-PSA, this implies the significance of their investigation together in normal and pathologic prostate tissues.

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The aim of this study was determined the expression of pro inflammatory cytokines in prostate epithelial cells. Furthermore, we analysed the relation between these cytokines and sera PSA levels according the three groups: 0-4, 4-20 and >20 ng/mL. The study was carried out in five normal prostate (NP), 27 benign prostate hyperplastic (BPH) and 18 prostate cancer (PC). Immunohistochemical and Western blot analysis was performed. Serum levels of PSA were assayed by Immulite autoanalyser. The western Blotting analysis revealed an immunoexpression of IL-1alpha, IL-6 and TNFalpha in BPH and PC. IL-1alpha, was absent in NP. Immunohistochemical analysis showed significant high optical density to IL-1alpha and IL-6 in cancer epithelial cells (19.45 +/- 3.25 and 26.2 +/- 3.19) compared to normal cells (1.73 +/- 1.51 and 4.83 +/- 2.65). While, TNFalpha optical densities were not significant in NP (12.03 +/- 2.9), BPH (9.87 +/- 3.85) and PC (13.34 +/- 2.34). The different profiles of cytokines according sera PSA levels showed a high immunoexpression of the profile (IL-6+, IL-1alpha+) in BPH patients with PSA between 0-4 and 4-20 ng/mL. However, PC patients with sera PSA between 4 and 20 ng/mL, showed a significant high immunoexpression of the profile (IL-6+, IL-1alpha-). This data demonstrate a locally production of pro-inflammatory cytokines by prostate epithelial cells and a cross talk between PSA and these cytokines in prostate pathologies.

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The estrogen receptors (ERs) ERα and ERβ are important factors in breast cancer progression. Nevertheless, the molecular interplay between ERα and ERβ and its clinical significance in breast cancer is controversial. The establishment of a clear association is required; therefore, the current study analyzed the expression patterns of ERα and ERβ in 32 breast tumor tissues using reverse transcription-quantitative polymerase chain reaction. Furthermore, human epidermal growth factor receptor 2 (HER2) and the Ki-67 status were detected by immunohistochemistry. The results revealed that the ERα and ERβ expression rates recorded were 68 and 65%, respectively. The ERα:ERβ ratio exhibited a decline along with disease progression. ERα and ERβ were found to be negatively correlated with HER2 status but positively correlated with Ki-67. Co-expression of ERα and ERβ was associated with breast cancer aggressiveness, including higher histological grade and positive nodal status, which commonly occur following the menopause. In addition, in cases where ERβ was coexpressed with ERα, HER2 expression was frequently found to be negative, whereas the Ki-67 index was upregulated. These data suggest that ERα and ERβ co-expression may be an indicator of tumor aggressiveness and the sensitivity of hormonal therapy via the downregulation of HER2.