The variability in the biological behaviour of prostate cancer and the inadequacy of markers used for assessing prognosis cause difficulties in the management of patients. We conducted a study of 74 prostate carcinomas to identify the significance of Her-2/neu oncogene in the initiation and progression of prostate carcinoma. Tissue array blocks were constructed and overexpression of Her-2/neu protein was assessed in areas of carcinoma, low and high grade intraepithelial neoplasia and benign prostate hyperplasia by immunohistochemistry. Flourescence in-situ hybridization (FISH) method was used to investigate Her-2/neu gene amplification in areas of carcinoma of 56 cases. Her-2/neu protein was expressed in a cytoplasmic/membranous manner. The expression rate significantly increased from areas of benign prostate hyperplasia to prostatic intraepithelial neoplasia and reached the highest degree in areas of carcinoma. Her-2/neu overexpression was observed in 72.97% of prostate carcinomas while gene amplification was present in 4.05% of the cases. Polisomy or any other anomaly involving chromosome 17 was not detected. There was no relationship between the ratio of Her-2/neu protein expression or gene amplification and known prognostic parameters as Gleason grade, and stage of the tumor. The discordance between the expression and amplification rates suggested that expression may be the cause of some other factors rather than true gene amplification. According to the results of the present study involving mostly the clinically localized prostate carcinomas, it can be suggested that Her-2/neu oncogene does not seem to have any role in clinically localized prostate carcinoma, but no assessment could be made for advanced stage carcinomas and the progression to androgen independent disease.