ArticleTranslational oncology2014
Integrin inhibitor suppresses bevacizumab-induced glioma invasion.
Article in Translational oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed.
- Tinostamustine (EDO-S101) and Its Combination with Celecoxib or Temozolomide as a Therapeutic Option for Adult-Type Diffuse Gliomas.International journal of molecular sciences · 2025Article
- Diamond Nanoparticles Suppress Migration of T98G Glioblastoma Cells by Targeting ECM-Integrin Interactions and Intracellular Signaling, Leading to Extensive Proteome Alterations.Nanotechnology, science and applications · 2025Article
- Advances in antitumour therapy with oncolytic herpes simplex virus combinations.Discover oncology · 2024Review
- Inference of glioblastoma migration and proliferation rates using single time-point images.Communications biology · 2023Article
- The complex relationship between integrins and oncolytic herpes Simplex Virus 1 in high-grade glioma therapeutics.Molecular therapy oncolytics · 2022Review
- Molecular Mechanisms and Clinical Challenges of Glioma Invasion.Brain sciences · 2022Review
- Combination of Ad-SGE-REIC and bevacizumab modulates glioma progression by suppressing tumor invasion and angiogenesis.PloS one · 2022Article
- Anoikis resistance in diffuse glioma: The potential therapeutic targets in the future.Frontiers in oncology · 2022Review
- Differentiated glioblastoma cells accelerate tumor progression by shaping the tumor microenvironment via CCN1-mediated macrophage infiltration.Acta neuropathologica communications · 2021Article
- Mechanisms of Invasion in Glioblastoma: Extracellular Matrix, CaFrontiers in cellular neuroscience · 2021Review
- The Current State of Oncolytic Herpes Simplex Virus for Glioblastoma Treatment.Oncolytic virotherapy · 2021Review
- Article
- Visualization of Diagnostic and Therapeutic Targets in Glioma With Molecular Imaging.Frontiers in immunology · 2020Review
- Antitumor activity of integrin αTranslational cancer research · 2019Article
- Adaptive adhesion systems mediate glioma cell invasion in complex environments.Journal of cell science · 2018Article
- Fibroblast growth factor 13 regulates glioma cell invasion and is important for bevacizumab-induced glioma invasion.Oncogene · 2018Article
- Anti-high mobility group box-1 (HMGB1) antibody attenuates delayed cerebral vasospasm and brain injury after subarachnoid hemorrhage in rats.Scientific reports · 2016Article
- A super gene expression system enhances the anti-glioma effects of adenovirus-mediated REIC/Dkk-3 gene therapy.Scientific reports · 2016Article
- Periostin (POSTN) Regulates Tumor Resistance to Antiangiogenic Therapy in Glioma Models.Molecular cancer therapeutics · 2016Article
- Induction of WNT11 by hypoxia and hypoxia-inducible factor-1α regulates cell proliferation, migration and invasion.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma is known to secrete high levels of vascular endothelial growth factor (VEGF), and clinical studies with bevacizumab, a monoclonal antibody to VEGF, have demonstrated convincing therapeutic benefits in glioblastoma patients. However, its induction of invasive proliferation has also been reported. We examined the effects of treatment with cilengitide, an integrin inhibitor, on bevacizumab-induced invasive changes in glioma. U87ΔEGFR cells were stereotactically injected into the brain of nude mice or rats. Five days after tumor implantation, cilengitide and bevacizumab were administered intraperitoneally three times a week. At 18 days after tumor implantation, the brains were removed and observed histopathologically. Next, the bevacizumab and cilengitide combination group was compared to the bevacizumab monotherapy group using microarray analysis. Bevacizumab treatment led to increased cell invasion in spite of decreased angiogenesis. When the rats were treated with a combination of bevacizumab and cilengitide, the depth of tumor invasion was significantly less than with only bevacizumab. Pathway analysis demonstrated the inhibition of invasion-associated genes such as the integrin-mediated cell adhesion pathway in the combination group. This study showed that the combination of bevacizumab with cilengitide exerted its anti-invasive effect. The elucidation of this mechanism might contribute to the treatment of bevacizumab-refractory glioma.
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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.