Abstract. Prostate cancer (PCa) is one of the most widespread malignancies in the world. The role of the human epidermal growth factor receptor 2 (HER2) in the pathogenesis and progression of human PCa remains poorly understood. In contradiction with breast cancer, studies on HER2 overexpression and gene amplification in PCa have produced varying results, although the HER2 oncogene has been implicated in the biology of numerous tumor types, and serves as a prognostic marker and therapeutic target in breast cancer. Technical challenges are considered the main reasons for data discrepancies. Amplification of the HER2 gene has previously been reported in PCa, in which it was associated with tumor progression. The present study aimed to evaluate the prevalence and clinical significance of HER2 amplification in PCa. A total of 32 biopsy samples obtained from human prostate adenocarcinomas were evaluated by chromogenic in situ hybridization (CISH) to determine the frequency of patients with HER2 gene amplifications. High copy numbers of HER2 were detected in 19 of the prostate tumors analyzed. The results of the present study suggested that, in patients without amplification of HER2, high levels of prostate-specific antigen or a high Gleason score were not significantly correlated with a high pathologic stage. Furthermore, amplification levels of the HER2 gene were directly associated with pathologic stage in patients with PCa. Therefore, the potential use of HER2 as a prognostic factor or therapeutic target for PCa warrants further study.
IntroductionProstate cancer (PCa), a common non-skin, sex-limited cancer, is the second cause of cancer-associated mortality (after lung cancer) in the USA (1,2) and the second most prevalent cancer among Iranian men (3). Worldwide, PCa is the second most commonly diagnosed cancer and, according to the International Agency for Research on Cancer's GLOBOCAN 2012 (4) database, it is the fifth leading cause of cancer-associated mortality in men. The incidence of PCa is increasing worldwide, although there is a marked variation in its incidence among different regions (5). The clinical configuration of PCa has noticeably altered over the past few years. As a localized disease, it is easily treated by radical radiation therapy or a prostatectomy; however, if the tumor becomes malignant, it transforms into a life-threatening disease (6).The progression and application of novel high-resolution technologies has enhanced the detection of genomic alterations, enabling elucidation of the complex nature and heterogeneity of PCa (7). The differentiation of PCa tumors is typically based on the serum expression levels of prostate-specific antigen (PSA), although, in certain cases, PSA levels do not accurately reflect tumor burden (8). Previous studies have identified a number of genetic, epigenetic and environmental risk factors for PCa (9-11). Among them, genetic aberrations and chromosomal changes have been suggested to serve a significant role in the development and progression of PCa (12)
