ReviewCell death discovery2025
The emerging roles of aberrant alternative splicing in glioma.
Review in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed.
- ARGLU1 in Glioma: A Novel Potential Regulator of Splicing, DNA Repair, and Therapeutic Resistance.Cells · 2026Review
- Article
- Long-read transcriptomic profiling of a glioma cell line following m6A regulator perturbations.Biochemistry and biophysics reports · 2026Article
- Tumor cell intrinsic mechanisms of immune escape.Cell communication and signaling : CCS · 2026Review
- Mapping glioblastoma's isoform diversity using long-read single-cell analysis.Nature communications · 2026Article
- Ataxin-2 as a candidate blood biomarker for estimating disease status in cases of suspected glioblastoma recurrence.Brain tumor pathology · 2026Article
- HNRNPH1 drives glioblastoma progression by regulating the splicing of cell cycle genes.Cell death & disease · 2026Article
- OY-TES-1 Splice Variant V5a in Glioma: A Driver of Malignancy and Potential Therapeutic Target.Current medical science · 2026Article
- Nano-Enabled Fluorescence Switching: A Novel Strategy for PDGFRβ Detection and TKI Therapy Monitoring.Research (Washington, D.C.) · 2026Article
- Review
- Revealing erythropoietin variant EV-3 as novel driving force and immunotherapeutic target in human glioblastoma.Journal of experimental & clinical cancer research : CR · 2025Article
- Spatial transcriptomics of glioblastoma defines biologically and clinically significant reprogramming patterns across unique spatial microenvironments.bioRxiv : the preprint server for biology · 2025Article
- Application of the Mass Spectrometry-High-Throughput Technique Over the Immunohistochemical Analysis for Human Brain Tumor Diagnosis and Prognosis: Insights Into Biomarkers' Identification for the Case Study of Grade IV Astrocytomas and Meningiomas.Biomedical chromatography : BMC · 2025Article
- Deregulating m6A regulators leads to altered RNA biology in glioma cell lines.bioRxiv : the preprint server for biology · 2025Article
- Integrative bioinformatic and experimental analysis reveals prognostic and immunological roles of MEX3 family genes in glioma.Frontiers in immunology · 2025Article
- Modeling craniofacial spliceosomopathies: a pathway toward deciphering disease mechanisms.Frontiers in cell and developmental biology · 2025Review
- Competitive Sequestration of miR-1183 by lncRNA DDX11-AS1 Drives Gliomagenesis through E2F7 Activation.Oncology research · 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gliomas represent a heterogeneous group of uniformly fatal brain tumors. Low and high-grade gliomas have diverse molecular signatures. Despite successful advances in understanding glioma, several genetic, epigenetic, and post-transcriptional alterations leave various targeted therapies ineffective, leading to a poor prognosis for high-grade glioma. Recent advances have revealed the implication of dysregulated alternative splicing (AS) events in glioma development. AS is a process that produces, from a single genomic sequence, several mature messenger RNAs. Splicing of pre-messenger RNAs concerns at least 95% of transcripts and constitutes an important mechanism in gene expression regulation. Dysregulation of this process, through variations in spliceosome components, aberrant splicing factors and RNA-binding protein activity, disproportionate regulation of non-coding RNAs, and abnormal mRNA methylation, can contribute to the disruption of AS. Such disruptions are usually associated with the development of several cancers, including glioma. Consequently, AS constitutes a key regulatory mechanism that could serve as a target for future therapies. In this review, we explore how AS events, spliceosome components, and their regulatory mechanisms play a critical role in glioma development, highlighting their potential as targets for innovative therapeutic strategies against this challenging cancer.
Identifiers
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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.