Fibroblast growth factor signaling as a bypass mechanism of the androgen receptor pathway: new perspectives for castrationresistant prostate cancer

Till now, prostate cancer (PC) appears among the most critical public health concerns in men in developed as well as developing countries. Androgens operating through androgen receptor (AR) nourish the development and function of normal prostate and may pathologically contribute to PC in case of any deformation or deregulation (1). Based on this, inhibiting the production of androgens by castration or their effects by using anti-AR agents is employed as a treatment of advanced PC disease. However, in most instances, upon therapy, cancer will develop in a form called castrate-resistant prostate cancer (CRPC). Reactivation of AR expression and activity is often noticed in this disease stage (2,3). Treatment with more potent anti-AR agents can be useful in this setting but their efficacy can be limited in time, while high therapeutic pressure will select for aggressive and highly adaptable cancer variants leading to therapeutic impasse