Bladder cancer is the second most common genitourinary
tumor and constitutes a very heterogeneous disease. Molecular and pathologic studies suggest that low-grade noninvasive and high-grade invasive urothelial cell
carcinoma (UCC) arise via distinct pathways. Low-grade noninvasive UCC represent the majority of
tumors at presentation. A high proportion of patients with low-grade UCC develop recurrences but usually with no progression to invasive disease. At presentation, a majority of the
bladder tumors (70%-80%) are low-grade noninvasive (pTa). Several genetic changes may occur in
bladder cancer, but activating mutations in the
fibroblast growth factor receptor 3 (FGFR3) genes are the most common and most specific genetic abnormality in
bladder cancer. Interestingly, these mutations are associated with
bladder tumors of low stage and grade, which makes the FGFR3 mutation the first marker that can be used for diagnosis of noninvasive
bladder tumors. Since the first report of FGFR3 involvement in
bladder tumors, numerous studies have been conducted to understand its function and thereby confirm the oncogenic role of this receptor particularly in noninvasive groups. Efforts are on to exploit this receptor as a therapeutic target, which holds much promise in the treatment of
bladder cancer, particularly low-grade noninvasive
tumors. Further studies need to explore the potential use of FGFR3 mutations in
bladder cancer diagnosis, prognosis, and in surveillance of patients with
bladder cancer. This review focuses on the role of FGFR3 in
bladder tumors in the backdrop of various studies published.