ArticlePloS one2012
Loss of wild-type ATRX expression in somatic cell hybrids segregates with activation of Alternative Lengthening of Telomeres.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 77 citations in OpenAlex.
- NPM1 phosphorylation-mediated telomere maintenance via stabilization of POLD3 in ALT-positive osteosarcoma: unraveling mechanisms and therapeutic opportunities.Theranostics · 2026Article
- Daxx and HIRA go viral - How chromatin remodeling complexes affect DNA virus infection.Tumour virus research · 2025Review
- Telomere interactions and structural variants in ALT cells revealed with TelSPRITE.bioRxiv : the preprint server for biology · 2024Article
- Changes inBiomedicines · 2024Article
- Orphan nuclear receptors-induced ALT-associated PML bodies are targets for ALT inhibition.Nucleic acids research · 2024Article
- Review
- Review
- A non-genetic switch triggers alternative telomere lengthening and cellular immortalization in ATRX deficient cells.Nature communications · 2023Article
- Review
- ATRX modulates the escape from a telomere crisis.PLoS genetics · 2022Article
- Telomeric replication stress: the beginning and the end for alternative lengthening of telomeres cancers.Open biology · 2022Review
- NHP2 downregulation counteracts hTR-mediated activation of the DNA damage response at ALT telomeres.The EMBO journal · 2021Article
- Low Protein Expression of bothInternational journal of molecular sciences · 2021Article
- A critical role of telomere chromatin compaction in ALT tumor cell growth.Nucleic acids research · 2020Article
- Targeting the DNA Damage Response for the Treatment of High Risk Neuroblastoma.Frontiers in oncology · 2020Review
- ATRX affects the repair of telomeric DSBs by promoting cohesion and a DAXX-dependent activity.PLoS biology · 2020Article
- Loss of atrx cooperates with p53-deficiency to promote the development of sarcomas and other malignancies.PLoS genetics · 2019Article
- Synthetic lethality of cytolytic HSV-1 in cancer cells with ATRX and PML deficiency.Journal of cell science · 2019Article
- Molecularly Targeted Therapy for Neuroblastoma.Children (Basel, Switzerland) · 2018Review
- Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alternative Lengthening of Telomeres (ALT) is a non-telomerase mechanism of telomere lengthening that occurs in about 10% of cancers overall and is particularly common in astrocytic brain tumors and specific types of sarcomas. Somatic cell hybridization analyses have previously shown that normal telomerase-negative fibroblasts and telomerase-positive immortalized cell lines contain repressors of ALT activity, indicating that activation of ALT results from loss of one or more unidentified repressors. More recently, ATRX or DAXX was shown to be mutated both in tumors with telomere lengths suggestive of ALT activity and in ALT cell lines. Here, an ALT cell line was separately fused to each of four telomerase-positive cell lines, and four or five independent hybrid lines from each fusion were examined for expression of ATRX and DAXX and for telomere lengthening mechanism. The hybrid lines expressed either telomerase or ALT, with the other mechanism being repressed. DAXX was expressed normally in all parental cell lines and in all of the hybrids. ATRX was expressed normally in each of the four telomerase-positive parental cell lines and in every telomerase-positive hybrid line, and was abnormal in the ALT parental cells and in all but one of the ALT hybrids. This correlation between ALT activity and loss of ATRX expression is consistent with ATRX being a repressor of ALT.
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