ArticleCell reports2018
A Distinct DNA Methylation Shift in a Subset of Glioma CpG Island Methylator Phenotypes during Tumor Recurrence.
Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers.
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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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Who cites it
121 citing papers in PubMed.
- Review
- DNA Methylation Profiling in IDH-Mutant Gliomas: Biological Evolution, Molecular Grading and Clinical Implementation.Neuropathology and applied neurobiology · 2026Review
- Chromosomal Instability Drives Glioblastoma Heterogeneity and Therapeutic Opportunities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Longitudinal changes in DNA methylation in IDH-mutant glioma fuel disease progression through altered cell state differentiation.Nature genetics · 2026Article
- Single-nucleus multiomics unveils malignant cellular states, regulatory architectures and microenvironmental reorganization across the G-CIMP epigenomic transition in IDH-mutant glioma.bioRxiv : the preprint server for biology · 2026Article
- KRAS and MYC synergistic inhibition: a powerful strategy targeting KRAS-mutant cancers.Molecular cancer · 2026Review
- TET CpG sequence-context-specific DNA demethylation shapes progression of IDH-mutant gliomas.Cell reports. Medicine · 2026Article
- Review
- Repeat resection for recurrent glioblastoma - does timing matter?Journal of neuro-oncology · 2026Article
- TUBB2A and TM4SF1 Methylation Define Prognostic Subgroups in Adult-Type Diffuse Glioma.Cancers · 2026Article
- Epigenomic and Metabolic Interplay in the Development of Metastatic Brain Tumors.Oncology research · 2026Review
- Glioportal: a comprehensive transcriptomic resource unveiling ligand-mediated mesenchymal transition in glioblastoma.Neuro-oncology · 2025Article
- DNA methylation analysis reveals an epigenetic signature distinctive of high-grade oligodendroglioma.Acta neuropathologica · 2025Article
- Multi-Layered Analysis of TGF-β Signaling and Regulation via DNA Methylation and microRNAs in Astrocytic Tumors.International journal of molecular sciences · 2025Article
- DNA methylation remodeling in temozolomide resistant recurrent glioblastoma: comparing epigenetic dynamics in vitro and in vivo.Journal of translational medicine · 2025Article
- The role of vorasidenib in the treatment of isocitrate dehydrogenase-mutant glioma.Neuro-oncology · 2025Review
- Review
- NDRG1/2 as a prognostic predictive biomarker of cervical cancer and its correlation with immune infiltration.Biomarkers in medicine · 2025Article
- Simulation-guided pan-cancer analysis identifies a novel regulator of CpG island hypermethylation heterogeneity.Briefings in bioinformatics · 2025Article
- The molecular history of IDH-mutant astrocytomas without adjuvant treatment.Brain pathology (Zurich, Switzerland) · 2025Article
61 more citing papers are in PubMed but not listed here.
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Authors and funding
23 authors.
Funding
Abstract
Glioma diagnosis is based on histomorphology and grading; however, such classification does not have predictive clinical outcome after glioblastomas have developed. To date, no bona fide biomarkers that significantly translate into a survival benefit to glioblastoma patients have been identified. We previously reported that the IDH mutant G-CIMP-high subtype would be a predecessor to the G-CIMP-low subtype. Here, we performed a comprehensive DNA methylation longitudinal analysis of diffuse gliomas from 77 patients (200 tumors) to enlighten the epigenome-based malignant transformation of initially lower-grade gliomas. Intra-subtype heterogeneity among G-CIMP-high primary tumors allowed us to identify predictive biomarkers for assessing the risk of malignant recurrence at early stages of disease. G-CIMP-low recurrence appeared in 9.5% of all gliomas, and these resembled IDH-wild-type primary glioblastoma. G-CIMP-low recurrence can be characterized by distinct epigenetic changes at candidate functional tissue enhancers with AP-1/SOX binding elements, mesenchymal stem cell-like epigenomic phenotype, and genomic instability. Molecular abnormalities of longitudinal G-CIMP offer possibilities to defy glioblastoma progression.
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