ArticleOncology letters2020
IDH1-R132H mutation radiosensitizes U87MG glioma cells via epigenetic downregulation of TIGAR.
Article in Oncology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 17 citations in OpenAlex.
- TIGAR Maintains Mitotic Spindle Organization and βII-Tubulin Stability in Glioma Stem Cells.CNS neuroscience & therapeutics · 2026Article
- Uncovering G Protein-Coupled Receptors: Novel Targets and Biomarkers for Predicting Glioma Prognosis.Annals of clinical and translational neurology · 2026Article
- Understanding the Radiobiology of Central Nervous System Diseases in the Golden Age of Radiosurgery-Does It Matter?Brain sciences · 2025Review
- Histogram analysis of diffusion weighted magnetic resonance imaging for predicting isocitrate dehydrogenase 1 mutation status in brain gliomas.Current journal of neurology · 2025Article
- Low expression of polo-like kinase 2 predicts high postoperative seizure recurrence in glioma-related epilepsy.American journal of translational research · 2025Article
- IDH1Scientific reports · 2023Article
- Article
- Radiosensitizing effect of dendrosomal nanoformulation of curcumin on cancer cells.Pharmacological reports : PR · 2022Article
- The implications of IDH mutations for cancer development and therapy.Nature reviews. Clinical oncology · 2021Review
- RUNX1 and REXO2 are associated with the heterogeneity and prognosis of IDH wild type lower grade glioma.Scientific reports · 2021Article
- Glioblastoma Primary Cells Retain the Most Copy Number Alterations That Predict Poor Survival in Glioma Patients.Frontiers in oncology · 2021Article
- Metabolic Rewiring in Radiation Oncology Toward Improving the Therapeutic Ratio.Frontiers in oncology · 2021Review
- Current biomarker-associated procedures of cancer modeling-a reference in the context of IDH1 mutant glioma.Cell death & disease · 2020Review
- Review
- Emerging Roles and Therapeutic Interventions of Aerobic Glycolysis in Glioma.OncoTargets and therapy · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Isocitrate dehydrogenase 1 (IDH1) is the most frequently mutated gene in World Health Organization grade II-III and secondary glioma. The majority of IDH1 mutation cases involve the substitution from arginine to histidine at codon 132 (IDH1-R132H). Although the oncogenic role of IDH1-R132H has been confirmed, patients with IDH1-R132H brain tumors exhibit a better response to radiotherapy compared with those with wild-type (WT) IDH1. In the present study, the potential mechanism of radiosensitization mediated by IDH1-R132H was investigated by overexpressing IDH1-R132H in U87MG glioma cells. The results demonstrated decreased clonogenic capacity of IDH1-R132H-expressing cells, as well as delayed repair of DNA double-strand breaks compared with IDH1-WT. Data from The Cancer Genome Atlas were analyzed, which demonstrated that the expression of TP53-induced glycolysis and apoptosis regulator (TIGAR) was lower in patients with glioma harboring IDH1 mutations compared with that in patients with IDH1-WT. TIGAR-knockdown increases the radiosensitivity of glioma cells; in U87MG cells, IDH1-R132H suppressed TIGAR expression. Chromatin immunoprecipitation assays revealed increased levels of repressive H3K9me3 markers at the TIGAR promoter in IDH1-R132H compared with IDH1-WT. These data indicated that IDH1-R132H may overcome radioresistance in glioma cells through epigenetic suppression of TIGAR expression. However, these favorable effects were not observed in U87MG glioma stem-like cells. The results of the present study provide an improved understanding of the functionality of IDH1 mutations in glioma cells, which may improve the therapeutic efficacy of radiotherapy.
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.