HER-2/neu receptor in prostate cancer development and progression to androgen independence

• Published in: Tumori 2004-03, Vol.90 (2), p.163-170
• Main Authors: Di Lorenzo, Giuseppe, Autorino, Riccardo, De Laurentiis, Michele, Cindolo, Luca, D'Armiento, Massimo, Bianco, Angelo Raffaele, De Placido, Sabino
• Format: Article
• Language: English
• Subjects: Androgens - metabolism; Antineoplastic Agents - pharmacology; Biomarkers, Tumor - metabolism; Disease Progression; Gene Expression Regulation, Neoplastic - drug effects; Humans; Immunohistochemistry; Male; Neoplasms, Hormone-Dependent - metabolism; Prostate - metabolism; Prostatic Neoplasms - drug therapy; Prostatic Neoplasms - metabolism; Receptor Cross-Talk - drug effects; Receptor, Epidermal Growth Factor - drug effects; Receptor, Epidermal Growth Factor - metabolism; Receptor, ErbB-2 - drug effects; Receptor, ErbB-2 - metabolism; Signal Transduction
• ISSN: 0300-8916; 2038-2529
• DOI: 10.1177/030089160409000201

Development of prostate cancer and progression to androgen-independent disease is correlated with increased expression of growth factors and receptors capable of establishing autocrine and/or paracrine growth-stimulatory loops. A thorough review was made of the current literature and recent abstract presentations at scientific meetings focusing on the role of the HER-2/neu (c-erbB2) receptor in prostate cancer and the potential clinical usefulness of its specific inhibitors. In the past 10 years, conflicting results on HER-2/neu expression in prostate cancer have been reported. More recently, four studies have shown experimental evidence of HER-2/neu in the development of prostate cancer and, more specifically, in the progression to a hormone-refractory clinical behavior. Furthermore, it has been proposed that HER-2 family and androgen receptors function synergistically in the absence of androgen, which suggests a cross-talk between the HER-2/neu and androgen receptor pathways. Finally, clinical trials are in progress in prostate cancer patients to test novel agents that selectively interfere with HER-2/neu activity.