ArticleJournal of neuro-oncology2011
Bevacizumab can induce reactivity to VEGF-C and -D in human brain and tumour derived endothelial cells.
Article in Journal of neuro-oncology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- Article
- Advancing Systemic Treatment beyond First Line for Advanced Hepatocellular Carcinoma.Current oncology reports · 2026Review
- Bispecific receptor decoy proteins block ocular neovascularization via simultaneous blockade of vascular endothelial growth factor A and C.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- The Landscape of Vascular Endothelial Growth Factor Inhibition in Retinal Diseases.Investigative ophthalmology & visual science · 2025Review
- Phase 1b Dose Escalation Study of Sozinibercept Inhibition of Vascular Endothelial Growth Factors C and D With Aflibercept for Diabetic Macular Edema.Translational vision science & technology · 2024Article
- Vascular Endothelial Growth Factor C and D Signaling Pathways as Potential Targets for the Treatment of Neovascular Age-Related Macular Degeneration: A Narrative Review.Ophthalmology and therapy · 2024Review
- Emerging therapeutic strategies for unmet need in neovascular age-related macular degeneration.Journal of translational medicine · 2023Review
- New and Innovative Treatments for Neovascular Age-Related Macular Degeneration (nAMD).Journal of clinical medicine · 2021Review
- Targeting the Tumor Microenvironment in Renal Cell Cancer Biology and Therapy.Frontiers in oncology · 2019Review
- VEGF-C sustains VEGFR2 activation under bevacizumab therapy and promotes glioblastoma maintenance.Neuro-oncology · 2018Article
- Subserous invasion of VEGF-C-producing cancer cells is a possible risk factor for ileal ulceration in the non-metastatic mucosal layer during bevacizumab-combined chemotherapy for recurrent ovarian cancer: A case report.Molecular and clinical oncology · 2017Article
- Vascular endothelial growth factor-D modulates oxidant-antioxidant balance of human vascular endothelial cells.Journal of cellular and molecular medicine · 2017Article
- Current status and future directions of anti-angiogenic therapy for gliomas.Neuro-oncology · 2016Review
- Senescence from glioma stem cell differentiation promotes tumor growth.Biochemical and biophysical research communications · 2016Article
- The relevance of cell type- and tumor zone-specific VEGFR-2 activation in locally advanced colon cancer.Journal of experimental & clinical cancer research : CR · 2015Article
- Resistance to sunitinib in renal clear cell carcinoma results from sequestration in lysosomes and inhibition of the autophagic flux.Autophagy · 2015Article
- Direct effect of bevacizumab on glioblastoma cell lines in vitro.Neuromolecular medicine · 2014Article
- Article
- The propeptides of VEGF-D determine heparin binding, receptor heterodimerization, and effects on tumor biology.The Journal of biological chemistry · 2013Article
- Sozinibercept (Anti-VEGF-C/-D) Combined with Ranibizumab for Polypoidal Choroidal Vasculopathy: Phase IIb Predefined Subgroup Analysis.Ophthalmology scienceArticle
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Though clinical trials demonstrated effectiveness of the anti-VEGF antibody bevacizumab (Avastin) in adjuvant therapies for some solid tumours, there are rather few experimental data about cellular effects of bevacizumab on tumour cells and tumour associated endothelial cells. Recent reports demonstrate resistance mechanisms and secondary re-angiogenesis after a transient normalization of tumour vessels. Therefore we investigated the influence of bevacizumab on human glioma cells and human brain derived as well as tumour derived endothelial cells focussing on the role of VEGF-C and -D as potential alternative pro-angiogenic factors. Bevacizumab treatment showed no influence on proliferation after short term exposure (1-5 days) but slowed down endothelial cell proliferation by 25-30% after 14 days treatment. There was no significant induction of apoptosis after short or long term exposure. Tube formation capabilities were significantly impaired by bevacizumab with a continuing effect after 14 days of treatment even after omitting the antibody. VEGF-C and -D had no effect on endothelial cells in untreated or short term treatment groups. However, cells developed responsiveness to these factors in terms of increased proliferation and tube formation after 14 days bevacizumab treatment. Furthermore, bevacizumab induced expression of VEGF-C and -D in glioma cells. Treatment with bevacizumab may induce alterations in human brain and tumour endothelial cells leading to escape mechanisms from anti-VEGF therapy. VEGF-C and -D thus might act as alternative pro-angiogenic factors during anti-VEGF therapy.
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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.