ArticleBMC systems biology2011
Pharmacokinetics and pharmacodynamics of VEGF-neutralizing antibodies.
Article in BMC systems biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
38 citing papers in PubMed, 66 citations in OpenAlex.
- Modeling VEGF and GLUT1 Expression as Coadapted Foraging Strategies in Cancer.bioRxiv : the preprint server for biology · 2026Article
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- Modeling treatment of diabetic wounds with oxygen therapy and senolytic drug.Scientific reports · 2025Article
- Predicting oxytocin binding dynamics in receptor genetic variants through computational modeling.npj women's health · 2025Article
- Plasma and serum concentrations of VEGF-A121, but not of VEGF-A165, increase post-bevacizumab administration.PloS one · 2024Article
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- VEGF-A splice variants bind VEGFRs with differential affinities.Scientific reports · 2020Article
- The Convergence of Cell-Based Surface Plasmon Resonance and Biomaterials: The Future of Quantifying Bio-molecular Interactions-A Review.Annals of biomedical engineering · 2020Review
- Sex differences in cancer mechanisms.Biology of sex differences · 2020Review
- Systems Biology Will Direct Vascular-Targeted Therapy for Obesity.Frontiers in physiology · 2020Article
- A QSP Model for Predicting Clinical Responses to Monotherapy, Combination and Sequential Therapy Following CTLA-4, PD-1, and PD-L1 Checkpoint Blockade.Scientific reports · 2019Article
- In Vitro Characterization of Hypoxia Preconditioned Serum (HPS)-Fibrin Hydrogels: Basis for an Injectable Biomimetic Tissue Regeneration Therapy.Journal of functional biomaterials · 2019Article
- Challenges in Translating from Bench to Bed-Side: Pro-Angiogenic Peptides for Ischemia Treatment.Molecules (Basel, Switzerland) · 2019Review
- Predictive Approach Identifies Molecular Targets and Interventions to Restore Angiogenesis in Wounds With Delayed Healing.Frontiers in physiology · 2019Article
- VEGF-121 plasma level as biomarker for response to anti-angiogenetic therapy in recurrent glioblastoma.BMC cancer · 2018Article
- VEGFR1 promotes cell migration and proliferation through PLCγ and PI3K pathways.NPJ systems biology and applications · 2018Article
- Mechanistic modeling quantifies the influence of tumor growth kinetics on the response to anti-angiogenic treatment.PLoS computational biology · 2017Article
- Monitoring Severity of Multiple Organ Dysfunction Syndrome: New Technologies.Pediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies · 2017Review
- A multiscale computational model predicts distribution of anti-angiogenic isoform VEGFScientific reports · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundVascular endothelial growth factor (VEGF) is a potent regulator of angiogenesis, and its role in cancer biology has been widely studied. Many cancer therapies target angiogenesis, with a focus being on VEGF-mediated signaling such as antibodies to VEGF. However, it is difficult to predict the effects of VEGF-neutralizing agents. We have developed a whole-body model of VEGF kinetics and transport under pathological conditions (in the presence of breast tumor). The model includes two major VEGF isoforms VEGF121 and VEGF165, receptors VEGFR1, VEGFR2 and co-receptors Neuropilin-1 and Neuropilin-2. We have added receptors on parenchymal cells (muscle fibers and tumor cells), and incorporated experimental data for the cell surface density of receptors on the endothelial cells, myocytes, and tumor cells. The model is applied to investigate the action of VEGF-neutralizing agents (called "anti-VEGF") in the treatment of cancer.
resultsThrough a sensitivity study, we examine how model parameters influence the level of free VEGF in the tumor, a measure of the response to VEGF-neutralizing drugs. We investigate the effects of systemic properties such as microvascular permeability and lymphatic flow, and of drug characteristics such as the clearance rate and binding affinity. We predict that increasing microvascular permeability in the tumor above 10-5 cm/s elicits the undesired effect of increasing tumor interstitial VEGF concentration beyond even the baseline level. We also examine the impact of the tumor microenvironment, including receptor expression and internalization, as well as VEGF secretion. We find that following anti-VEGF treatment, the concentration of free VEGF in the tumor can vary between 7 and 233 pM, with a dependence on both the density of VEGF receptors and co-receptors and the rate of neuropilin internalization on tumor cells. Finally, we predict that free VEGF in the tumor is reduced following anti-VEGF treatment when VEGF121 comprises at least 25% of the VEGF secreted by tumor cells.
conclusionsThis study explores the optimal drug characteristics required for an anti-VEGF agent to have a therapeutic effect and the tumor-specific properties that influence the response to therapy. Our model provides a framework for investigating the use of VEGF-neutralizing drugs for personalized medicine treatment strategies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.