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Updated: May 24, 2026

A Mouse Model to Investigate the Role of Cancer-Associated Fibroblasts in Tumor Growth
Published on: December 22, 2020
Importance of fibroblast growth factor receptor in neovascularization and tumor escape from antiangiogenic therapy
Philip J Saylor1, Bernard Escudier, M Dror Michaelson
1Division of Hematology-Oncology, Massachusetts General Hospital, Boston, MA 02114, USA.
Abstract:
Therapeutic inhibition of pathways involved in angiogenesis has become the standard of care in renal cell carcinoma (RCC). Most currently available antiangiogenic agents inhibit the vascular endothelial growth factor (VEGF) pathway. Although these drugs have produced exciting benefits, some tumors do not respond to these agents. In addition most if not all tumors that initially respond will eventually develop resistance. Tumor escape from antiangiogenic therapy may include various signaling pathways that are involved in angiogenesis, including the fibroblast growth factor (FGF) signaling pathway. Emerging preclinical data suggest that FGF and VEGF act distinctly and synergistically to promote tumor vascularization. The current review discusses the role of FGF signaling in resistance to anti-VEGF therapies and outlines potential therapeutic implications.
Insights
Fibroblast growth factor (FGF) signaling may drive resistance to anti-vascular endothelial growth factor (VEGF) therapies in renal cell carcinoma. Targeting FGF pathways could overcome treatment resistance and improve outcomes.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Antiangiogenic therapies targeting the vascular endothelial growth factor (VEGF) pathway are standard treatments for renal cell carcinoma (RCC).
- Tumor resistance to VEGF inhibitors is a significant clinical challenge, limiting long-term efficacy.
- Alternative signaling pathways, such as fibroblast growth factor (FGF), may contribute to tumor angiogenesis and treatment escape.
Purpose of the Study:
- To review the role of FGF signaling in the development of resistance to anti-VEGF therapies in RCC.
- To explore the distinct and synergistic interactions between FGF and VEGF signaling in promoting tumor vascularization.
- To discuss potential therapeutic strategies targeting the FGF pathway to overcome anti-VEGF resistance.
Main Methods:
- Literature review of preclinical studies and clinical data.
- Analysis of signaling pathways involved in angiogenesis and RCC.
- Synthesis of information on FGF and VEGF interactions in tumor vascularization.
Main Results:
- FGF signaling pathways play a critical role in tumor angiogenesis.
- FGF and VEGF signaling pathways can act distinctly and synergistically to promote tumor vascularization.
- Emerging evidence suggests FGF signaling contributes to resistance against anti-VEGF therapies in RCC.
Conclusions:
- FGF signaling is implicated in resistance to anti-VEGF therapy in renal cell carcinoma.
- Targeting FGF pathways represents a promising therapeutic strategy to overcome resistance.
- Further investigation into combined FGF and VEGF inhibition may enhance RCC treatment outcomes.
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