ArticleThe AAPS journal2012
Predicting the effects of anti-angiogenic agents targeting specific VEGF isoforms.
Article in The AAPS journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
37 citing papers in PubMed, 57 citations in OpenAlex.
- Novel Role of Pin1-Cis P-Tau-ApoE Axis in the Pathogenesis of Preeclampsia and Its Connection with Dementia.Biomedicines · 2024Review
- Quantitative systems pharmacology modeling of macrophage-targeted therapy combined with PD-L1 inhibition in advanced NSCLC.Clinical and translational science · 2024Article
- Generating immunogenomic data-guided virtual patients using a QSP model to predict response of advanced NSCLC to PD-L1 inhibition.NPJ precision oncology · 2023Article
- Generating immunogenomic data-guided virtual patients using a QSP model to predict response of advanced NSCLC to PD-L1 inhibition.bioRxiv : the preprint server for biology · 2023Article
- Mechanistic insights into the development of severe fetal growth restriction.Clinical science (London, England : 1979) · 2023Review
- Nanocarriers for the Delivery of Neuroprotective Agents in the Treatment of Ocular Neurodegenerative Diseases.Pharmaceutics · 2023Review
- Article
- Cancer combination therapies by angiogenesis inhibitors; a comprehensive review.Cell communication and signaling : CCS · 2022Review
- Isoforms of soluble vascular endothelial growth factor in stress-related mental disorders: a cross-sectional study.Scientific reports · 2021Article
- Melatonin ameliorates microvessel abnormalities in the cerebral cortex and hippocampus in a rat model of Alzheimer's disease.Neural regeneration research · 2021Article
- 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
- Review
- Network-based method for drug target discovery at the isoform level.Scientific reports · 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
- Discovery of High-Affinity PDGF-VEGFR Interactions: Redefining RTK Dynamics.Scientific reports · 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
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Vascular endothelial growth factor (VEGF) is a key mediator of angiogenesis, whose effect on cancer growth and development is well characterized. Alternative splicing of VEGF leads to several different isoforms, which are differentially expressed in various tumor types and have distinct functions in tumor blood vessel formation. Many cancer therapies aim to inhibit angiogenesis by targeting VEGF and preventing intracellular signaling leading to tumor vascularization; however, the effects of targeting specific VEGF isoforms have received little attention in the clinical setting. In this work, we investigate the effects of selectively targeting a single VEGF isoform, as compared with inhibiting all isoforms. We utilize a molecular-detailed whole-body compartment model of VEGF transport and kinetics in the presence of breast tumor. The model includes two major VEGF isoforms, VEGF(121) and VEGF(165), receptors VEGFR1 and VEGFR2, and co-receptors Neuropilin-1 and Neuropilin-2. We utilize the model to predict the concentrations of free VEGF, the number of VEGF/VEGFR2 complexes (considered to be pro-angiogenic), and the receptor occupancy profiles following inhibition of VEGF using isoform-specific anti-VEGF agents. We predict that targeting VEGF(121) leads to a 54% and 84% reduction in free VEGF in tumors that secrete both VEGF isoforms or tumors that overexpress VEGF(121), respectively. Additionally, 21% of the VEGFR2 molecules in the blood are ligated following inhibition of VEGF(121), compared with 88% when both isoforms are targeted. Targeting VEGF(121) reduces tumor free VEGF and is an effective treatment strategy. Our results provide a basis for clinical investigation of isoform-specific anti-VEGF agents.
Indexed as
Identifiers
What OpenQuestion holds
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.