Evaluation of HER-2/neu expression in clinically localized prostate cancer

4768 Background: The overexpression of HER-2/neu oncoprotein is found in 20–30% of patients with breast carcinoma and is an adverse prognostic factor. HER-2/neu overexpression has been reported to occur in up to 60% of patients with prostate carcinoma and may serve a possible new target for anti-tumour therapy. However, no conclusive studies have related oncogene activation with the development of prostatic neoplasia. Reported rates of HER-2/neu overexpression in patients with prostate carcinoma vary greatly. Methods: In order to determine the immunohistochemical expression of HER-2/neu protein in clinically localized prostate cancers and to compare immunohistochemical results and clinical prognostic factors, we have studied archival formalin-fixed, paraffin-embedded radical prostatectomy specimens. The HercepTest (DakoCytomation) was used to assess HER-2/neu expression. The level of HER-2/neu expression was evaluated on a scale from 0 (no staining) to 3+ according to the published guidelines. Fluorescent in situ hybridization for gene amplification was performed on all specimens. Results: Out of 114 cases 77 specimens (67,5%) had no staining, 15 (13,2%) specimens had 1+ staining, 14 (12,3%) specimens had 2+ staining and 8 (7%) specimens has 3+ staining. There was an association between the level of HER-2/neu expression and tumor stage (P = 0.03) as well as Gleason grade (P = 0.02), but none of the specimens had HER-2/neu gene amplification. This study demonstrates that more than a third of all clinically localized prostate cancers express HER-2/neu oncoprotein via immunohistochemistry using HercepTest on archival material of clinically localized prostate cancer. Conclusions: Although HER-2/neu oncoprotein expression was detected, no positive case demonstrated gene amplification. HER-2/neu oncoprotein expression does not appear to be a prognostic marker for prostate cancer on archival specimens. No significant financial relationships to disclose.