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The great escape; the hallmarks of resistance to antiangiogenic therapy
Judy R van Beijnum1, Patrycja Nowak-Sliwinska1, Elisabeth J M Huijbers1
1Angiogenesis Laboratory, Department of Medical Oncology, VU University Medical Center, Amsterdam, The Netherlands (J.R.v.B., E.J.M.H., V.L.T., A.W.G.); and Institute of Chemical Sciences and Engineering, Swiss Federal Institute of Technology, Lausanne, Switzerland (P.N.-S.).
Abstract:
The concept of antiangiogenic therapy in cancer treatment has led to the approval of different agents, most of them targeting the well known vascular endothelial growth factor pathway. Despite promising results in preclinical studies, the efficacy of antiangiogenic therapy in the clinical setting remains limited. Recently, awareness has emerged on resistance to antiangiogenic therapies. It has become apparent that the intricate complex interplay between tumors and stromal cells, including endothelial cells and associated mural cells, allows for escape mechanisms to arise that counteract the effects of these targeted therapeutics. Here, we review and discuss known and novel mechanisms that contribute to resistance against antiangiogenic therapy and provide an outlook to possible improvements in therapeutic approaches.
Insights
Antiangiogenic therapy shows limited clinical efficacy due to tumor resistance. Understanding complex tumor-stromal interactions is key to overcoming these escape mechanisms and improving cancer treatment outcomes.
Area of Science:
- Oncology
- Cancer Biology
- Pharmacology
Background:
- Antiangiogenic therapy targets tumor vascularization, primarily via the vascular endothelial growth factor (VEGF) pathway.
- While effective in preclinical models, clinical efficacy of antiangiogenic agents is often limited.
- Emerging evidence highlights resistance mechanisms as a major challenge in antiangiogenic therapy.
Purpose of the Study:
- To review and discuss known and novel mechanisms of resistance to antiangiogenic therapy.
- To provide an outlook on potential therapeutic strategies to overcome resistance.
Main Methods:
- Literature review of preclinical and clinical studies on antiangiogenic therapy resistance.
- Analysis of tumor-stromal cell interactions contributing to resistance.
- Discussion of emerging therapeutic approaches.
Main Results:
- Tumor resistance to antiangiogenic therapy arises from complex interactions between tumor cells, endothelial cells, and mural cells.
- These interactions facilitate escape mechanisms that counteract therapeutic effects.
- Various novel resistance pathways have been identified.
Conclusions:
- Resistance significantly limits the clinical success of antiangiogenic therapies.
- Targeting tumor-stromal interplay is crucial for developing more effective antiangiogenic strategies.
- Future therapeutic approaches should aim to overcome identified resistance mechanisms.
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