Background: The progression of normal prostatic epithelium to androgen-dependent cancer and, eventually, hormone-refractory prostate cancer is a complex process involving many different growth regulatory signals. Activation of epidermal growth factor receptor (EGFR) has been implicated in prostate cancer cell growth.
Methods: This study was undertaken to investigate both amplification of EGFR gene by fluorescence in situ hybridization (FISH) and over-expression of EGFR by immunohistochemical staining in prostate tissue from 71 patients treated by hormonal therapy.
Results: EGFR gene amplification was present in 1 of 71 tumors, and polysomy of chromosome 7 was present in 24 of 71 tumors. Immunohistochemically, EGFR expression was demonstrable in 57 of 71 tumors. Membranous immunostaining for EGFR was observed in >75% of tumor cells in 11% of cases, in 51-75% of tumor cells in 20% of cases, in 26-50% of tumor cells in 21% of cases, in 11-25% of tumor cells in 21% of cases, and in 1-10% of tumor cells in 7% of cases. No immunostaining for EGFR was seen in 20% of cases. There was no correlation between EGFR protein expression and gene amplification. There was also no correlation between EGFR expression and clinicopathological characteristics or clinical outcome.
Conclusions: We found that EGFR gene expression was detectable in 35% of this large series of hormone-treated prostate cancer, and that EGFR protein is frequently expressed in tissue from these patients. EGFR over-expression may serve as a reasonable target for therapeutic intervention in this otherwise difficult to treat subset of prostate cancer.