ReviewNature reviews. Cancer2008
VEGF-A splicing: the key to anti-angiogenic therapeutics?
Review in Nature reviews. Cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 276 papers, 2 of them syntheses 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
276 citing papers in PubMed, 2 syntheses or guidelines pooled it, 507 citations in OpenAlex.
- Alternative splicing and cancer: a systematic review.Signal transduction and targeted therapy · 2021Pooled it
- Association between VEGF-A and VEGFR-2 polymorphisms and response to treatment of neovascular AMD with anti-VEGF agents: a meta-analysis.The British journal of ophthalmology · 2017Pooled it
- VEGFA and VEGFR2 gene polymorphisms and response to anti-vascular endothelial growth factor therapy: comparison of age-related macular degeneration treatments trials (CATT).JAMA ophthalmology · 2014Trial
- RAISE quantifies RNA binding protein activity via transcriptomic profiling.Nature communications · 2026Article
- Review
- Review
- Alternative Splicing-Mediated Resistance to Antibody-Based Therapies: Mechanisms and Emerging Therapeutic Strategies.International journal of molecular sciences · 2025Review
- The Current Role of Antiangiogenics in Colorectal Cancer.International journal of molecular sciences · 2025Review
- Polymorphisms inBiomedicines · 2025Review
- Splicing factor kinase SRPK1 inhibition in monocyte: a novel therapeutic approach for peripheral arterial disease.American journal of physiology. Heart and circulatory physiology · 2025Article
- Disrupted Alternative Splicing of RAB11FIP3 Contributes to Diabetic Foot Ulcer Dysfunction.Journal of cellular and molecular medicine · 2025Article
- Contribution of tumor microenvironment (TME) to tumor apoptosis, angiogenesis, metastasis, and drug resistance.Medical oncology (Northwood, London, England) · 2025Review
- Global research landscape of antiangiogenic therapy for colorectal cancer: a bibliometric analysis of mechanistic insights and clinical advancements.Frontiers in oncology · 2025Review
- KDASDB: A comprehensive and user-friendly database of alternative splicing dedicated to kidney diseases.Computational and structural biotechnology journal · 2025Article
- The RNA revolution in medicine: from gene regulation to clinical therapeutics.Animal cells and systems · 2025Review
- Repurposing alternative splicing events as potential targets for the design of diagnostic and therapeutic tools in PCa.Frontiers in oncology · 2025Review
- Transcriptome-wide m6A landscape across diverse porcine tissues revealed by nanopore direct RNA sequencing.Frontiers in genetics · 2025Article
- Recent updates on potential of VEGFR-2 small-molecule inhibitors as anticancer agents.RSC advances · 2024Review
- Synthetic Antiangiogenic Vascular Endothelial Growth Factor-A Splice Variant Revascularizes Ischemic Muscle in Peripheral Artery Disease.Journal of the American Heart Association · 2024Article
- PAIP1 binds to pre-mRNA and regulates alternative splicing of cancer pathway genes including VEGFA.BMC genomics · 2024Article
216 more citing papers are in PubMed but not listed here.
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 2 countries.
Funding
Abstract
The physiology of microvessels limits the growth and development of tumours. Tumours gain nutrients and excrete waste through growth-associated microvessels. New anticancer therapies target this microvasculature by inhibiting vascular endothelial growth factor A (VEGF-A) splice isoforms that promote microvessel growth. However, certain VEGF-A splice isoforms in normal tissues inhibit growth of microvessels. Thus, it is the VEGF-A isoform balance, which is controlled by mRNA splicing, that orchestrates angiogenesis. Here, we highlight the functional differences between the pro-angiogenic and the anti-angiogenic VEGF-A isoform families and the potential to harness the synthetic capacity of cancer cells to produce factors that inhibit, rather than aid, cancer growth.
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.