ArticleNature communications2022
Splicing is an alternate oncogenic pathway activation mechanism in glioma.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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.
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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
35 citing papers in PubMed, 57 citations in OpenAlex.
- ARGLU1 in Glioma: A Novel Potential Regulator of Splicing, DNA Repair, and Therapeutic Resistance.Cells · 2026Review
- Review
- DeepSAP: improved RNA-seq alignment by integrating transcriptome guidance with transformer-based splice junction scoring.Genome biology · 2026Article
- CELF family of RNA-binding proteins: roles in disease biology and potential for therapeutic intervention.Cell communication and signaling : CCS · 2026Review
- HNRNPH1 drives glioblastoma progression by regulating the splicing of cell cycle genes.Cell death & disease · 2026Article
- Long-Read Transcriptome Sequencing and Functional Validation Reveals Novel and Oncogenic Gene Fusions in Fusion Panel-Negative Gliomas.bioRxiv : the preprint server for biology · 2026Article
- The Natural Triterpenoid Alisol B Overcomes Temozolomide Resistance in Glioblastoma Through Multi-Target Mechanisms: Coordinated Epigenetic, Metabolic, and Cell-Cycle Reprogramming.International journal of molecular sciences · 2026Article
- Alternative splicing in pediatric central nervous system tumors highlights oncofetal candidateNeuro-oncology pediatrics · 2026Article
- Unraveling the FGFR-RNA splicing axis: Mechanisms, oncogenic crosstalks and innovations for therapeutic purpose.Acta pharmaceutica Sinica. B · 2026Review
- C/EBPβ-induced alternative splicing of RCAN1 generates a potent TCR-T target in mesenchymal glioblastoma.Cellular & molecular immunology · 2026Article
- Adaptive immunotherapeutic paradigms in diffuse midline glioma: integrating epigenetic reprogramming, neuron-glioma interactions, and tumor microenvironment modulation.Journal of neuro-oncology · 2025Review
- A single-cell atlas of RNA alternative splicing in the glioma-immune ecosystem.Genome biology · 2025Article
- Clinical utility of targeted RNA sequencing in cancer molecular diagnostics.Nature medicine · 2025Article
- The proteomic landscape of diffuse midline glioma highlights the therapeutic potential of non-histone protein methyltransferases.Neuro-oncology · 2025Article
- Characterization of aberrant splicing in pediatric central nervous system tumors revealsbioRxiv : the preprint server for biology · 2025Article
- Establishment of an alternative splicing prognostic risk model and identification of FN1 as a potential biomarker in glioblastoma multiforme.Scientific reports · 2025Article
- Article
- Molecular Characterization and Inhibition of a Novel Stress-Induced Mitochondrial Protecting Role for Misfolded TrkAIII in Human SH-SY5Y Neuroblastoma Cells.International journal of molecular sciences · 2024Article
- MAPP unravels frequent co-regulation of splicing and polyadenylation by RNA-binding proteins and their dysregulation in cancer.Nature communications · 2024Article
- Development of a rapid and comprehensive genomic profiling test supporting diagnosis and research for gliomas.Brain tumor pathology · 2024Article
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 4 countries.
Funding
Abstract
High-grade diffuse glioma (HGG) is the leading cause of brain tumour death. While the genetic drivers of HGG have been well described, targeting these has thus far had little impact on survival suggesting other mechanisms are at play. Here we interrogate the alternative splicing landscape of pediatric and adult HGG through multi-omic analyses, uncovering an increased splicing burden compared with normal brain. The rate of recurrent alternative splicing in cancer drivers exceeds their mutation rate, a pattern that is recapitulated in pan-cancer analyses, and is associated with worse prognosis in HGG. We investigate potential oncogenicity by interrogating cancer pathways affected by alternative splicing in HGG; spliced cancer drivers include members of the RAS/MAPK pathway. RAS suppressor neurofibromin 1 is differentially spliced to a less active isoform in >80% of HGG downstream from REST upregulation, activating the RAS/MAPK pathway and reducing glioblastoma patient survival. Overall, our results identify non-mutagenic mechanisms by which cancers activate oncogenic pathways which need to accounted for in personalized medicine approaches.
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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.