ArticleScientific reports2019
Rapid and reversible suppression of ALT by DAXX in osteosarcoma cells.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 45 citations in OpenAlex.
- SMARCAL1 is a candidate therapeutic target for ALT-positive tumors.Genes & development · 2026Article
- SMARCAL1 is a targetable synthetic lethal therapeutic vulnerability in ATRX-deficient gliomas that use alternative lengthening of telomeres.Neuro-oncology · 2026Article
- SFPQ directs histone H3.3 deposition to R-loops in DNA repeats to protect genome stability.Nature communications · 2026Article
- ATRX: From Chromatin Remodeling to Disease.Genesis (New York, N.Y. : 2000) · 2025Review
- Telomerase and alternative lengthening of telomeres coexist in the regenerating zebrafish caudal fins.EMBO reports · 2025Article
- Emerging roles and therapeutic potential of non-coding RNA in osteosarcoma: a review.Medical oncology (Northwood, London, England) · 2025Review
- Distinct mechanisms underlying extrachromosomal telomere DNA generation in ALT cancers.Nucleic acids research · 2025Article
- Telomere interactions and structural variants in ALT cells revealed with TelSPRITE.bioRxiv : the preprint server for biology · 2024Article
- Article
- Impacts of radiation exposure, hindlimb unloading, and recovery on murine skeletal muscle cell telomere length.NPJ microgravity · 2023Article
- Hyperextended telomeres promote formation of C-circle DNA in telomerase positive human cells.The Journal of biological chemistry · 2023Article
- Histone demethylase KDM2A is a selective vulnerability of cancers relying on alternative telomere maintenance.Nature communications · 2023Article
- Review
- Hyperextended telomeres promote C-circle formation in telomerase positive human cells.bioRxiv : the preprint server for biology · 2023Article
- Alternative Lengthening of Telomeres (ALT) and Telomerase Reverse Transcriptase Promoter Methylation in Recurrent Adult and Primary Pediatric Pituitary Neuroendocrine Tumors.Endocrine pathology · 2022Article
- Article
- DAXX-ATRX regulation of p53 chromatin binding and DNA damage response.Nature communications · 2022Article
- New twists to the ALTernative endings at telomeres.DNA repair · 2022Review
- Knowledge atlas and emerging trends on ncRNAs of osteosarcoma: A bibliometric analysis.Frontiers in endocrinology · 2022Article
- Proteome-wide mapping of short-lived proteins in human cells.Molecular cell · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 2 countries.
Funding
Abstract
Many tumors maintain chromosome-ends through a telomerase-independent, DNA-templated mechanism called alternative lengthening of telomeres (ALT). While ALT occurs in only a subset of tumors, it is strongly associated with mutations in the genes ATRX and DAXX, which encode components of an H3.3 histone chaperone complex. The role of ATRX and DAXX mutations in potentiating the mechanism of ALT remains incompletely understood. Here we characterize an osteosarcoma cell line, G292, with wild-type ATRX but a unique chromosome translocation resulting in loss of DAXX function. While ATRX and DAXX form a complex in G292, this complex fails to localize to nuclear PML bodies. We demonstrate that introduction of wild type DAXX suppresses the ALT phenotype and restores the localization of ATRX/DAXX to PML bodies. Using an inducible system, we show that ALT-associated PML bodies are disrupted rapidly following DAXX induction and that ALT is again restored following withdrawal of DAXX.
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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.