ArticleHeliyon2025
Discovery of mutated oncodriver genes associated with glioblastoma originated from stem cells of subventricular zone through whole exome sequence profile analysis, and drug repurposing.
Article in Heliyon, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Donor-specific assemblies enhance somatic structural variant detection in complex genomic regions.bioRxiv : the preprint server for biology · 2026Article
- Novel Four-gene Panel for Detecting Senescence-associated Cell States in Skeletal Muscle Tissue.Juntendo medical journal · 2026Article
- Molecular Biomarkers of Glioma.Biomedicines · 2025Review
- Common molecular links and therapeutic insights between type 2 diabetes and kidney cancer.PloS one · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is one of the most aggressive cancers due to its high mortality rate in spite of intensive treatment. It may be happened because of drug resistance against their typical receptors, since these receptor genes are often mutated by environmental stress. So identifying mutated oncodriver genes which could be used as potential drug target is essential in order to develop effective new therapeutic drugs as well as better prognosis for GBM patients. In this study, we analyzed whole exome sequencing (WES) profiles of NCBI database on GBM and matched-normal (control) samples originated from astrocyte like neural stem cells (NSC) of subventricular zone (SVZ) to explore GBM-causing mutated oncodriver genes, since SVZ is considered as the origin of GBM development. We detected 16 mutated oncodriver genes. Then, filtering by differential co-expression analysis based on independent RNA-Seq profiles of CGGA database revealed 10 genes as dysregulated oncodriver genes. Following that, 3 significantly overexpressed oncodriver genes (MTCH2, VWF, and WDR89) were identified as potential drug targets. Then molecular mechanisms of GBM development were investigated by these three overexpressed driver genes through gene ontology (GO), KEGG-pathways, Gene regulatory network (GRN) and mutation analysis. Finally, overexpressed oncodriver genes guided top-ranked six drug agents (Irinotecan, Imatinib, etoposide, pazopanib, trametinib and cabozanitinib) were recommended against GBM through molecular docking study. Most of our findings received support by the literature review also. Therefore, the findings of this study might carry potential values to the wet-lab researchers for further investigation in terms of diagnosis and therapies of GBM.
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.