ArticlePloS one2010
r84, a novel therapeutic antibody against mouse and human VEGF with potent anti-tumor activity and limited toxicity induction.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 43 citations in OpenAlex.
- VEGF-A-mediated venous endothelial cell proliferation results in neoangiogenesis during neuroinflammation.Nature neuroscience · 2024Article
- Pancreatic Cancer-Secreted Proteins: Targeting Their Functions in Tumor Microenvironment.Cancers · 2023Review
- Direct and indirect regulation of the tumor immune microenvironment by VEGF.Journal of leukocyte biology · 2022Review
- VEGFR2 activity on myeloid cells mediates immune suppression in the tumor microenvironment.JCI insight · 2021Article
- Cyclooxygenase-2 Inhibition Potentiates the Efficacy of Vascular Endothelial Growth Factor Blockade and Promotes an Immune Stimulatory Microenvironment in Preclinical Models of Pancreatic Cancer.Molecular cancer research : MCR · 2019Article
- Skeletal Colonization by Breast Cancer Cells Is Stimulated by an Osteoblast and β2AR-Dependent Neo-Angiogenic Switch.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2017Article
- Hypoxia and Transforming Growth Factor β Cooperate to Induce Fibulin-5 Expression in Pancreatic Cancer.The Journal of biological chemistry · 2016Article
- Article
- Phosphatidylserine (PS) Is Exposed in Choroidal Neovascular Endothelium: PS-Targeting Antibodies Inhibit Choroidal Angiogenesis In Vivo and Ex Vivo.Investigative ophthalmology & visual science · 2015Article
- Inhibition of pathological brain angiogenesis through systemic delivery of AAV vector expressing soluble FLT1.Gene therapy · 2015Article
- Adipose VEGF Links the White-to-Brown Fat Switch With Environmental, Genetic, and Pharmacological Stimuli in Male Mice.Endocrinology · 2015Article
- Article
- Vascular channels formed by subpopulations of PECAM1+ melanoma cells.Nature communications · 2014Article
- Vascular endothelial growth factor promotes fibrosis resolution and repair in mice.Gastroenterology · 2014Article
- Collagen signaling enhances tumor progression after anti-VEGF therapy in a murine model of pancreatic ductal adenocarcinoma.Cancer research · 2014Article
- Tie1 deletion inhibits tumor growth and improves angiopoietin antagonist therapy.The Journal of clinical investigation · 2014Article
- Inhibition of VEGFR-2 reverses type 1 diabetes in NOD mice by abrogating insulitis and restoring islet function.Diabetes · 2013Article
- BIBF 1120 (nintedanib), a triple angiokinase inhibitor, induces hypoxia but not EMT and blocks progression of preclinical models of lung and pancreatic cancer.Molecular cancer therapeutics · 2013Article
- VEGF blockade enables oncolytic cancer virotherapy in part by modulating intratumoral myeloid cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2013Article
- Enhanced heme function and mitochondrial respiration promote the progression of lung cancer cells.PloS one · 2013Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Vascular endothelial growth factor (VEGF) is critical for physiological and pathological angiogenesis. Within the tumor microenvironment, VEGF functions as an endothelial cell survival factor, permeability factor, mitogen, and chemotactic agent. The majority of these functions are mediated by VEGF-induced activation of VEGF receptor 2 (VEGFR2), a high affinity receptor tyrosine kinase expressed by endothelial cells and other cell types in the tumor microenvironment. VEGF can also ligate other cell surface receptors including VEGFR1 and neuropilin-1 and -2. However, the importance of VEGF-induced activation of these receptors in tumorigenesis is still unclear. We report the development and characterization of r84, a fully human monoclonal antibody that binds human and mouse VEGF and selectively blocks VEGF from interacting with VEGFR2 but does not interfere with VEGF:VEGFR1 interaction. Selective blockade of VEGF binding to VEGFR2 by r84 is shown through ELISA, receptor binding assays, receptor activation assays, and cell-based functional assays. Furthermore, we show that r84 has potent anti-tumor activity and does not alter tissue histology or blood and urine chemistry after chronic high dose therapy in mice. In addition, chronic r84 therapy does not induce elevated blood pressure levels in some models. The ability of r84 to specifically block VEGF:VEGFR2 binding provides a valuable tool for the characterization of VEGF receptor pathway activation during tumor progression and highlights the utility and safety of selective blockade of VEGF-induced VEGFR2 signaling in tumors.
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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.