Molecular Localization of Epstein Barr Virus and Rb Tumor Suppressor Gene Expression in Tissues from Prostatic Adenocarcinoma and Benign Prostatic Hyperplasia
Abstract
Epstein- Barr virus (EBV) is a ubiquitous in that infecting more than 90% of adult population worldwide. Recently, EBV has been linked to the development of variety of human malignancies including prostate tissues that range from benign prostatic hyperplasia (BPH) to prostatic adenocarcinoma (PAC). Somatic point mutations in Rb gene have been detected in prostate cancer and are involved in progression steps of prostate carcinogenesis. To analyze the distribution and impact of concordant Rb expression and latent EBV infection on a group of prostate adenocarcinoma and benign prostatic hyperplasia. Seventy- two formalin-fixed, paraffin- embedded prostatic tissues were obtained in this study; 40 biopsies from prostatic carcinoma and 20 from benign prostate hyperplasia as well as 12 apparently normal prostatic autopsies control group. Detection of EBV-EBERs was done by ultra-sensitive version of in situ hybridization method where as immunohistochemistry detection system was used to demonstrate the expression of Rb gene. Detection of EBV-EBERs -ISH reactions in tissues with PAC was observed in 19 out of 40 (47.5%), while in the tissues from BPH was detected in 10% (2 out of 20). No EBV-EBERs positive – ISH reaction was detected in healthy prostate tissues in the control group. The differences between the percentages of EBERs detection in tissues PAC and each of BPH & control groups were statistically highly significant (p < 0.01). Positive Rb immune histo chemical (IHC) reactions were observed in 19 PAC cases (47.5%) and in 2 BPH cases (10%). Our results indicate that the EBV might contribute to the development of subset of prostate tumors. In addition, the significant percentage of expression of possible Rb gene as well as EBV in prostate adenocarcinoma could indicate for an important role of these molecular and viral factors in prostatic carcinogenesis.
