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Updated: May 19, 2026
An Orthotopic Bladder Cancer Model for Gene Delivery Studies
Published on: December 1, 2013
A Decade of FGF Receptor Research in Bladder Cancer: Past, Present, and Future Challenges
Erica di Martino1, Darren C Tomlinson, Margaret A Knowles
1Section of Experimental Oncology, Leeds Institute of Molecular Medicine, St James's University Hospital, Leeds LS9 7TF, UK.
Abstract:
Fibroblast growth factors (FGFs) orchestrate a variety of cellular functions by binding to their transmembrane tyrosine-kinase receptors (FGFRs) and activating downstream signalling pathways, including RAS/MAPK, PLCγ1, PI3K, and STATs. In the last ten years, it has become clear that FGF signalling is altered in a high proportion of bladder tumours. Activating mutations and/or overexpression of FGFR3 are common in urothelial tumours with low malignant potential and low-stage and -grade urothelial carcinomas (UCs) and are associated with a lower risk of progression and better survival in some subgroups. FGFR1 is not mutated in UC, but overexpression is frequent in all grades and stages and recent data indicate a role in urothelial epithelial-mesenchymal transition. In vitro and in vivo studies have shown that FGFR inhibition has cytotoxic and/or cytostatic effects in FGFR-dependent bladder cancer cells and FGFR-targeted agents are currently being investigated in clinical studies for the treatment of UC. Urine-based tests detecting common FGFR3 mutations are also under development for surveillance of low-grade and -stage tumours and for general population screening. Overall, FGFRs hold promise as therapeutic targets, diagnostic and prognostic markers, and screening tools for early detection and clinical management of UC.
Insights
Fibroblast growth factor receptors (FGFRs) are frequently altered in bladder cancer. Targeting FGFRs shows promise for new treatments and early detection of urothelial carcinoma.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Fibroblast growth factors (FGFs) signal through tyrosine-kinase receptors (FGFRs), influencing cellular functions.
- Altered FGF signalling is prevalent in bladder tumours, particularly involving FGFR3 mutations or overexpression.
- FGFR1 overexpression is common in urothelial carcinoma (UC) and linked to epithelial-mesenchymal transition.
Purpose of the Study:
- To review the role of FGFRs in urothelial carcinoma.
- To explore FGFRs as therapeutic targets and diagnostic/prognostic markers for UC.
- To assess the potential of FGFR-targeted agents and urine-based FGFR3 mutation tests.
Main Methods:
- Literature review of studies on FGF signalling in bladder cancer.
- Analysis of data on FGFR mutations and overexpression in urothelial tumours.
- Evaluation of in vitro and in vivo evidence for FGFR inhibition efficacy.
Main Results:
- Activating FGFR3 alterations are common in low-grade/stage UCs, correlating with better outcomes in some subgroups.
- FGFR1 overexpression occurs across all UC grades/stages and may drive epithelial-mesenchymal transition.
- FGFR inhibition demonstrates cytotoxic/cytostatic effects in FGFR-dependent bladder cancer cells.
Conclusions:
- FGFRs are promising therapeutic targets for urothelial carcinoma treatment.
- FGFRs can serve as diagnostic and prognostic markers for UC.
- Urine-based FGFR tests offer potential for early detection and surveillance of UC.
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