ArticlePloS one2018
ATRX loss induces multiple hallmarks of the alternative lengthening of telomeres (ALT) phenotype in human glioma cell lines in a cell line-specific manner.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
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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
49 citing papers in PubMed, 68 citations in OpenAlex.
- Review
- Explainable incremental-value analysis of apparent diffusion coefficient and arterial spin labeling radiomics for ATRX status prediction in glioblastoma.Frontiers in oncology · 2026Article
- Alternative Lengthening of Telomeres: The Need forInternational journal of molecular sciences · 2025Article
- High-Throughput Targeted Drug Screening for NF1-associated High-Grade Gliomas with ATRX Deficiency.bioRxiv : the preprint server for biology · 2025Article
- Combined inhibition of de novo glutathione and nucleotide biosynthesis is synthetically lethal in glioblastoma.Cell reports · 2025Article
- Loss of function ofiScience · 2025Article
- Telomere Maintenance Pathways in Lower-Grade Gliomas: Insights from Genetic Subtypes and Telomere Length Dynamics.International journal of molecular sciences · 2025Article
- Loss of DAXX/ATRX Protein Expression Results in Ischemia Resistance and Radiation Sensitivity in Pancreatic Neuroendocrine Tumor Cells and Is Associated with Improved Response to Trans-Arterial Radioembolization.Neuroendocrinology · 2025Article
- Fructose-1,6-bisphosphatase 1 dephosphorylates and inhibits TERT for tumor suppression.Nature chemical biology · 2024Article
- The TERT Promoter is Polycomb-Repressed in Neuroblastoma Cells with Long Telomeres.Cancer research communications · 2024Article
- Mechanisms of telomere maintenance and associated therapeutic vulnerabilities in malignant gliomas.Neuro-oncology · 2024Review
- BLM helicase unwinds lagging strand substrates to assemble the ALT telomere damage response.Molecular cell · 2024Article
- Targeting ATR in patients with cancer.Nature reviews. Clinical oncology · 2024Review
- DAXX promotes centromeric stability independently of ATRX by preventing the accumulation of R-loop-induced DNA double-stranded breaks.Nucleic acids research · 2024Article
- Telomere Maintenance Mechanisms in a Cohort of High-Risk Neuroblastoma Tumors and Its Relation to Genomic Variants in theCancers · 2023Article
- Induction of the alternative lengthening of telomeres pathway by trapping of proteins on DNA.Nucleic acids research · 2023Article
- Article
- Alternative Lengthening of Telomeres in Pediatric High-Grade Glioma and Therapeutic Implications.Cancers · 2023Article
- A non-genetic switch triggers alternative telomere lengthening and cellular immortalization in ATRX deficient cells.Nature communications · 2023Article
- Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Cancers must maintain their telomeres at lengths sufficient for cell survival. In several cancer subtypes, a recombination-like mechanism termed alternative lengthening of telomeres (ALT), is frequently used for telomere length maintenance. Cancers utilizing ALT often have lost functional ATRX, a chromatin remodeling protein, through mutation or deletion, thereby strongly implicating ATRX as an ALT suppressor. Herein, we have generated functional ATRX knockouts in four telomerase-positive, ALT-negative human glioma cell lines: MOG-G-UVW, SF188, U-251 and UW479. After loss of ATRX, two of the four cell lines (U-251 and UW479) show multiple characteristics of ALT-positive cells, including ultrabright telomeric DNA foci, ALT-associated PML bodies, and c-circles. However, telomerase activity and overall telomere length heterogeneity are unaffected after ATRX loss, regardless of cellular context. The two cell lines that showed ALT hallmarks after complete ATRX loss also did so upon ATRX depletion via shRNA-mediated knockdown. These results suggest that other genomic or epigenetic events, in addition to ATRX loss, are necessary for the induction of ALT in human cancer.
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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.