ReviewFuture oncology (London, England)2009
Therapeutic potential of manipulating VEGF splice isoforms in oncology.
Review in Future oncology (London, England), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed.
- A Splice Form of VEGF, a Potential Anti-Angiogenetic Form of Head and Neck Squamous Cell Cancer Inhibition.International journal of molecular sciences · 2024Review
- How VEGF-A and its splice variants affect breast cancer development - clinical implications.Cellular oncology (Dordrecht, Netherlands) · 2022Review
- Review
- Targeting VEGF pathway to normalize the vasculature: an emerging insight in cancer therapy.OncoTargets and therapy · 2018Review
- Dynamics and implications of circulating anti-angiogenic VEGF-AScientific reports · 2017Article
- RNA-Sequencing data supports the existence of novel VEGFA splicing events but not of VEGFAScientific reports · 2017Article
- Novel mechanisms of resistance to vemurafenib in melanoma - V600E B-Raf reversion and switching VEGF-A splice isoform expression.American journal of cancer research · 2015Article
- Antiangiogenic actions of vascular endothelial growth factor-A165b, an inhibitory isoform of vascular endothelial growth factor-A, in human obesity.Circulation · 2014Article
- Effect of tumor microenvironment on tumor VEGF during anti-VEGF treatment: systems biology predictions.Journal of the National Cancer Institute · 2013Article
- Compartment model predicts VEGF secretion and investigates the effects of VEGF trap in tumor-bearing mice.Frontiers in oncology · 2013Article
- Predicting the effects of anti-angiogenic agents targeting specific VEGF isoforms.The AAPS journal · 2012Article
- VEGF gene alternative splicing: pro- and anti-angiogenic isoforms in cancer.Journal of cancer research and clinical oncology · 2012Review
- Article
- Refining orthologue groups at the transcript level.BMC genomics · 2010Article
- Pazopanib for the treatment of patients with advanced renal cell carcinoma.Clinical Medicine Insights. Oncology · 2010Article
- The mouse retina as an angiogenesis model.Investigative ophthalmology & visual science · 2010Review
- Alternative RNA splicing and cancer.Wiley interdisciplinary reviews. RNAReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Anti-angiogenic therapies currently revolve around targeting vascular endothelial growth factor-A (VEGF-A) or its receptors. These therapies are effective to some degree, but have low response rates and poor side-effect profiles. Part of these problems is likely to be due to their lack of specificity between pro- and anti-angiogenic isoforms, and their nonspecific effects on proactive, pleiotropic survival and maintenance roles of VEGF-A in endothelial and other cell types. An alternative approach, and one which has recently been shown to be effective in animal models of neovascularization in the eye, is to target the mechanisms by which the cell generates pro-angiogenic splice forms of VEGF-A, its receptors and, co-incidentally, by targeting the upstream processes, other oncogenes that have antagonistic splice isoforms. The concept here is to target the splicing mechanisms that control splice site choice in the VEGF-A mRNA. Recent evidence on the pharmacological possibilities of such splice factors is described.
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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.