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Author Spotlight: Computing the Effects of a Local Radiofrequency Hyperthermia Intervention on Tumor Biomechanics
Published on: December 1, 2023
Experimental and computational analyses reveal dynamics of tumor vessel cooption and optimal treatment strategies
Chrysovalantis Voutouri1, Nathaniel D Kirkpatrick2, Euiheon Chung2
1Cancer Biophysics Laboratory, Department of Mechanical and Manufacturing Engineering, University of Cyprus, 1678 Nicosia, Cyprus.
Abstract:
Cooption of the host vasculature is a strategy that some cancers use to sustain tumor progression without-or before-angiogenesis or in response to antiangiogenic therapy. Facilitated by certain growth factors, cooption can mediate tumor infiltration and confer resistance to antiangiogenic drugs. Unfortunately, this mode of tumor progression is difficult to target because the underlying mechanisms are not fully understood. Here, we analyzed the dynamics of vessel cooption during tumor progression and in response to antiangiogenic treatment in gliomas and brain metastases. We followed tumor evolution during escape from antiangiogenic treatment as cancer cells coopted, and apparently mechanically compressed, host vessels. To gain deeper understanding, we developed a mathematical model, which incorporated compression of coopted vessels, resulting in hypoxia and formation of new vessels by angiogenesis. Even if antiangiogenic therapy can block such secondary angiogenesis, the tumor can sustain itself by coopting existing vessels. Hence, tumor progression can only be stopped by combination therapies that judiciously block both angiogenesis and cooption. Furthermore, the model suggests that sequential blockade is likely to be more beneficial than simultaneous blockade.
Insights
Cancer cells can hijack host blood vessels (cooption) to grow, even during antiangiogenic therapy. Blocking both cooption and angiogenesis, potentially sequentially, is crucial for halting tumor progression.
Area of Science:
- Oncology
- Cancer Biology
- Mathematical Modeling
Background:
- Some cancers utilize host vasculature (vessel cooption) for growth, independent of or resistant to antiangiogenic therapies.
- Vessel cooption facilitates tumor infiltration and drug resistance, but underlying mechanisms remain poorly understood.
- Understanding cooption dynamics is critical for developing effective cancer treatments.
Purpose of the Study:
- To analyze vessel cooption dynamics during tumor progression and antiangiogenic treatment escape in gliomas and brain metastases.
- To investigate the mechanical compression of host vessels by coopted cancer cells.
- To develop a mathematical model to understand the interplay between cooption, angiogenesis, and hypoxia.
Main Methods:
- Observational analysis of tumor evolution during antiangiogenic treatment escape.
- Development of a mathematical model incorporating vessel cooption, mechanical compression, hypoxia, and angiogenesis.
- Simulation of tumor progression under different therapeutic blockade strategies.
Main Results:
- Cancer cells coopt host vessels, leading to mechanical compression and hypoxia.
- Coopted vessels enable tumor survival even when secondary angiogenesis is blocked by therapy.
- Mathematical model confirms that cooption can sustain tumors independently of angiogenesis.
- Sequential blockade of angiogenesis and cooption is predicted to be more effective than simultaneous blockade.
Conclusions:
- Vessel cooption is a critical mechanism for tumor progression and therapeutic resistance.
- Combination therapies targeting both angiogenesis and cooption are necessary to halt tumor growth.
- Sequential therapeutic blockade strategies may offer superior outcomes compared to simultaneous approaches.
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