Interferon-gamma and its functional receptors overexpression in benign prostatic hyperplasia and prostatic carcinoma: parallelism with c-myc and p53 expression

The therapeutic potential of IFN-gamma in prostatic cancer has been documen ted in several reports, although no immunohistochemical studies of this fac tor and its receptors in the prostate have been reported. The aim of the pr esent study was to investigate the expression of IFN-gamma and its receptor components (IFN-gamma-R alpha and IFN-gamma-R beta) in normal prostate, be nign prostatic hyperplasia (BPH) and prostatic cancer (PC), as well as the possible relationship between this factor and the products of the p53 gene (the wild and mutant forms) and the oncogene c-myc, by means of immunochemi cal techniques (Western blot, ELISA, and quantification of immunostaining i n histological sections). In normal prostate, IFN-gamma and its two recepto rs were expressed in the basal cells of the epithelium and some stromal cel ls. In BPH specimens, immunostaining of basal epithelial cells was signific antly increased for IFN-gamma and its alpha receptor, whereas stromal cell immunostaining was significantly increased for IFN-gamma and its beta recep tor. In addition, columnar epithelia; cells immunostained for IFN beta-R be ta. PC specimens differed from BPH specimens in the significantly increased immunostaining of epithelial cells for IFN-gamma, and its two receptors, a nd the immunostaining of columnar epithelial cells for IFN-gamma-R alpha, I mmunodetection of wild-p53 was weak and limited to some stromal cells in th e three types of specimens. Immunostainings for both mutant-p53 and c-myc w ere negative in normal prostate, and positive in the epithelium and stromal cells of both BPH and PC specimens. Immunostaining intensity in PC was sig nificantly higher than in BPH. These observations suggest that the expressi on of both mutant-p53 and c-myc, together with other factors, might be invo lved in the development of prostatic hyperplasia and neoplasia, while the i ncreased expression of IFN-gamma and its receptors could be regarded as an attempt, although insufficient, to inhibit the uncontrolled cell proliferat ion.