ArticleScientific reports2025
Transcriptomic analysis identifies a potential target for bevacizumab resistant glioblastoma.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Dissecting the aberrant vasculature of glioblastoma: mechanisms and therapeutic targets.Cancer metastasis reviews · 2026Review
- Sevoflurane is associated with reduced EGFR-VEGF-AKT signaling in glioma tissues relative to propofol: a bioinformatics and clinical pilot study.Frontiers in oncology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors.
Funding
Abstract
Glioblastoma, IDH wild-type (WHO grade 4) (GBM), is the most common primary brain tumor in adults with a 21-month median overall survival, despite surgical-resection and radio-chemotherapy. Bevacizumab, a monoclonal antibody towards vascular endothelial growth factor-A, is used to treat recurrent-GBM. To find predictors of poor-response, patient-derived xenograft (PDX)-tumors were treated with bevacizumab or vehicle and subsequently grouped based on survival-response; RNAseq expression was then compared by responder-status. Bioinformatic-analysis demonstrated differential gene expression in tumors from poor-responders (six-PDXs) as compared to tumors from good-responders (three-PDXs), along with upregulation of angiogenesis and collagen gene-sets in poor-responders. Within these gene-sets, multiple genes known to be regulated by the early growth response-1 (EGR1) transcription factor, which was also upregulated, were identified and CHRNA7 (α7-nicotinic-acetylcholine receptor, α7-nAChR) was selected for validation. In terms of protein/functional studies, in the bevacizumab-treated poor-responders, nuclear-EGR1 was elevated, Ki67-labeling was increased in EGR1
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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 Socratic graph.