ArticleJournal of hematology & oncology2013
Development and characterization of a high-throughput in vitro cord formation model insensitive to VEGF inhibition.
Article in Journal of hematology & oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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
13 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Efficacy and safety evaluations of anlotinib in patients with advanced non-small cell lung cancer treated with bevacizumab.Frontiers in pharmacology · 2022Pooled it
- Vascularized in vitro bone model as 3D quadruple culture with primary human osteoblasts, osteocytes, osteoclasts and endothelial cells.Materials today. Bio · 2025Article
- PD-1 and PD-L1 inhibitors in cold colorectal cancer: challenges and strategies.Cancer immunology, immunotherapy : CII · 2023Review
- Gold nanoparticles enhance antibody effect through direct cancer cell cytotoxicity by differential regulation of phagocytosis.Nature communications · 2021Article
- Article
- Understanding the Role of Innate Immune Cells and Identifying Genes in Breast Cancer Microenvironment.Cancers · 2020Review
- Anti-VEGFR2 therapy delays growth of preclinical pediatric tumor models and enhances anti-tumor activity of chemotherapy.Oncotarget · 2019Article
- Synergistic effect of immune checkpoint blockade and anti-angiogenesis in cancer treatment.Molecular cancer · 2019Review
- Human iPSC-derived endothelial cell sprouting assay in synthetic hydrogel arrays.Acta biomaterialia · 2016Article
- Article
- A method to assess target gene involvement in angiogenesis in vitro and in vivo using lentiviral vectors expressing shRNA.PloS one · 2014Article
- An in vitro cord formation assay identifies unique vascular phenotypes associated with angiogenic growth factors.PloS one · 2014Article
- Adverse reactions of immune checkpoint inhibitors combined with angiogenesis inhibitors: A pharmacovigilance analysis of drug-drug interactions.International journal of immunopathology and pharmacologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAnti-VEGF therapy reduces tumor blood vessels, however, some vessels always remain. These VEGF insensitive vessels may help support continued tumor growth and metastases. Many in vitro assays examining multiple steps of the angiogenic process have been described, but the majority of these assays are sensitive to VEGF inhibition. There has been little focus on the development of high-throughput, in vitro assays to model the vessels that are insensitive to VEGF inhibition.
methodsHere, we describe a fixed end-point and kinetic, high-throughput stem cell co-culture model of cord formation.
resultsIn this system, cords develop within 24 hours, at which point they begin to lose sensitivity to VEGF inhibitors, bevacizumab, and ramucirumab. Consistent with the hypothesis that other angiogenic factors maintain VEGF-independent vessels, pharmacologic intervention with a broad spectrum anti-angiogenic antagonist (suramin), a vascular disrupting agent (combretastatin), or a combination of VEGF and Notch pathway inhibitors reduced the established networks. In addition, we used our in vitro approach to develop an in vivo co-implant vasculogenesis model that connects with the endogenous vasculature to form functional blood vessels. Similar to the in vitro system, over time these vessels become insensitive to VEGF inhibition.
conclusionTogether, these models may be used to identify novel drugs targeting tumor vessels that are not sensitive to VEGF inhibition.
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.