ArticleJournal of cancer science & therapy2016
Anti-VEGFR2 driven nuclear translocation of VEGFR2 and acquired malignant hallmarks are mutation dependent in glioblastoma.
Article in Journal of cancer science & therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 7 citations in OpenAlex.
- Nrf2 and PGC-1α signaling in temozolomide resistance in glioblastoma under hypoxia.Biomedical reports · 2026Article
- The IL13α 2R paves the way for anti-glioma nanotherapy.Genes & diseases · 2023Review
- Spatial and temporal VEGF receptor intracellular trafficking in microvascular and macrovascular endothelial cells.Scientific reports · 2021Article
- Modulating microenvironments for treating glioblastoma.Current tissue microenvironment reports · 2020Article
- Identification of signature genes associated with therapeutic resistance to anti-VEGF therapy.Oncotarget · 2020Article
- Apatinib suppresses cell growth and metastasis and promotes antitumor activity of temozolomide in glioma.Oncology letters · 2018Article
- Targeted Theranostic Nanoparticles for Brain Tumor Treatment.Pharmaceutics · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
objectiveAnti-angiogenic therapies (AATs), targeting VEGF-VEGFR pathways, are being used as an adjuvant to normalize glioblastoma (GBM) vasculature. Unexpectedly, clinical trials have witnessed transient therapeutic effect followed by aggressive tumor recurrence. In pre-clinical studies, targeting VEGFR2 with vatalanib, increased GBM growth under hypoxic microenvironment. There is limited understanding of these unanticipated results. Here, we investigated tumor cell associated phenotypes in response to VEGFR2 blockade.
methodsHuman U251 cells were orthotopically implanted in mice (day 0) and were treated with vehicle or vatalanib on day 8. Tumor specimens were collected for immunohistochemistry and protein array. Nuclear translocation of VEGFR2 was analyzed through IHC and western blot.
resultsVatalanib treated animals displayed distinct patterns of VEGFR2 translocation into nuclear compartment of U251 tumor cells.
conclusionsStudy suggests that AAT- induced molecular and phenotypic alterations in tumor cells are associated with mutation status and are responsible for aggressive tumor growth. Therefore, mutation status of the tumor in GBM patients should be taken in to consideration before applying targeted therapy to overcome unwanted effects.
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.