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A Combined 3D Tissue Engineered In Vitro/In Silico Lung Tumor Model for Predicting Drug Effectiveness in Specific Mutational Backgrounds
Published on: April 6, 2016
Multiscale modeling of tumor response to vascular endothelial growth factor (VEGF) inhibitor
Melisa Hendrata1, Janti Sudiono2
1Department of Mathematics, California State University, Los Angeles, CA, USA.
Abstract:
Vascular endothelial growth factor (VEGF) has been known as a key mediator of angiogenesis in cancer. Bevacizumab is anti-VEGF monoclonal antibody that has been approved by the FDA as a first-line treatment in many types of cancer. In this paper, we extend a previously validated multiscale tumor model to comprehensively include the multiple roles of VEGF during the course of angiogenesis and its binding mechanism with bevacizumab. We use the model to simulate tumor system response under various bevacizumab concentrations, both in stand-alone treatment and in combination with chemotherapy. Our simulation indicates that periodic administration of bevacizumab with lower concentration can achieve greater efficacy than a single treatment with higher concentration. The simulation of the combined therapy also shows that the continuous administration of bevacizumab during the maintenance phase can lead to antitumor activity which further suppresses its growth. Agreement with experimental results indicates the potential of the model in predicting the efficacy of anti-VEGF therapies and could therefore contribute to developing prospective clinical trials.
Insights
Periodic, lower-dose bevacizumab (anti-VEGF antibody) shows greater efficacy than high-dose single treatments. This anti-VEGF therapy model aids in predicting treatment outcomes for cancer clinical trials.
Area of Science:
- Oncology
- Biomedical Engineering
- Pharmacology
Background:
- Vascular endothelial growth factor (VEGF) is crucial for tumor angiogenesis.
- Bevacizumab, an anti-VEGF monoclonal antibody, is an FDA-approved cancer therapeutic.
- Existing tumor models require enhancement to fully capture VEGF's roles and bevacizumab interactions.
Purpose of the Study:
- To extend a multiscale tumor model to incorporate VEGF's multifaceted roles in angiogenesis.
- To simulate the binding mechanism of bevacizumab with VEGF.
- To predict tumor response to bevacizumab, alone and with chemotherapy.
Main Methods:
- Utilized a previously validated multiscale tumor model.
- Integrated comprehensive VEGF functions and bevacizumab binding kinetics.
- Performed simulations of tumor system response under varying bevacizumab concentrations and treatment schedules.
Main Results:
- Simulations suggest periodic, lower-concentration bevacizumab administration is more effective than single high-dose treatments.
- Combined therapy simulations indicate continuous bevacizumab during maintenance phases enhances antitumor activity.
- Model predictions align with experimental data, validating its predictive capabilities.
Conclusions:
- The enhanced multiscale model accurately predicts the efficacy of anti-VEGF therapies like bevacizumab.
- Optimized bevacizumab dosing strategies, including periodic and continuous administration, can improve treatment outcomes.
- The model serves as a valuable tool for designing future clinical trials for anti-VEGF cancer therapies.
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