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Updated: May 20, 2025

Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model
Published on: March 20, 2020
Therapies targeting triple-negative breast cancer: a perspective on anti-FGFR
Jinhao Chen1,2,3, Qianru Wang1,3, Hongyan Wu1,3
1Hubei Key Laboratory of Tumor Microenvironment and Immunotherapy, China Three Gorges University, Yichang, Hubei, China.
Abstract:
Triple-negative breast cancer (TNBC) is one of the subtypes with the worst prognosis due to tumour heterogeneity and lack of appropriate treatment. This condition is a consequence of the distinctive tumour microenvironment (TME). The TME is associated with factors such as the promotion of proliferation, angiogenesis, inhibition of apoptosis, suppression of the immune system and drug resistance. Therefore, remodelling the TME is critical for the treatment of TNBC. A key role in the formation of the TME is played by the fibroblast growth factor/fibroblast growth factor receptor(FGF/FGFR) signalling pathway. Thus, the FGFRs may be a potential target for treating TNBC. Over-activated FGFRs promote growth, migration and drug resistance in TNBC by influencing the onset of TME events, tumour angiogenesis and immune rejection. A thorough comprehension of the FGF/FGFR signalling pathway's mechanism of action in the development of TNBC could offer valuable insights for discovering new therapeutic strategies and drug targets. Inhibiting the FGF/FGFR axis could potentially hinder the growth of TNBC and its drug resistance by disrupting crucial biological processes in the TME, such as angiogenesis and immune evasion. This review evaluates the potential of inhibiting the FGF/FGFR axis as a strategy for treating TNBC. It explores the prospects for developing related therapeutic approaches. This study explores the research and application prospects of the FGF/FGFR axis in TNBC. The aim is to provide guidance for further therapeutic research and facilitate the development of innovative approaches targeting TNBC.
Insights
Targeting the fibroblast growth factor/fibroblast growth factor receptor (FGF/FGFR) pathway offers a promising strategy to combat triple-negative breast cancer (TNBC). Inhibiting this axis disrupts the tumor microenvironment, potentially overcoming treatment resistance.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Triple-negative breast cancer (TNBC) presents a poor prognosis due to tumor heterogeneity and limited treatment options.
- The tumor microenvironment (TME) significantly influences TNBC progression, promoting proliferation, angiogenesis, immune suppression, and drug resistance.
- The fibroblast growth factor/fibroblast growth factor receptor (FGF/FGFR) signaling pathway plays a crucial role in TME formation and TNBC development.
Purpose of the Study:
- To evaluate the potential of inhibiting the FGF/FGFR axis as a therapeutic strategy for TNBC.
- To explore the role of FGF/FGFR signaling in TNBC progression, including TME modulation, angiogenesis, and immune evasion.
- To identify new therapeutic targets and strategies for TNBC treatment by understanding the FGF/FGFR pathway's mechanisms.
Main Methods:
- This review synthesizes current research on the FGF/FGFR signaling pathway in TNBC.
- Analysis of the impact of FGF/FGFR overactivation on TME components and TNBC characteristics.
- Evaluation of preclinical and clinical data regarding FGF/FGFR inhibitors in TNBC models.
Main Results:
- Overactivated FGFRs contribute to TNBC growth, migration, and drug resistance by influencing TME events.
- Inhibition of the FGF/FGFR axis demonstrates potential in disrupting tumor angiogenesis and overcoming immune evasion.
- Targeting FGF/FGFR signaling may hinder TNBC proliferation and enhance sensitivity to existing therapies.
Conclusions:
- Inhibiting the FGF/FGFR axis is a viable therapeutic strategy for TNBC, addressing critical aspects of the TME.
- Further research into FGF/FGFR pathway inhibitors could lead to innovative treatments for TNBC.
- Understanding the FGF/FGFR mechanism provides a foundation for developing novel drugs and therapeutic approaches for TNBC.
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