ReviewGenes2016
The Role of ATRX in the Alternative Lengthening of Telomeres (ALT) Phenotype.
Review in Genes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.
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
61 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.
- Genetic aetiology of global developmental delay and intellectual disability in Africa: a scoping review.Frontiers in genetics · 2026Pooled it
- Genetic Determinants of Telomere Length and Their Role in Human Disease: Molecular Mechanisms and Underrepresented Populations' Perspectives.Biomedicines · 2026Review
- SMARCAL1 is a targetable synthetic lethal therapeutic vulnerability in ATRX-deficient gliomas that use alternative lengthening of telomeres.Neuro-oncology · 2026Article
- Telomere-driven dysfunctional changes in gynecological cancers: mechanistic insights, biomarker potential, and therapeutic targeting.Frontiers in cell and developmental biology · 2026Review
- Telomerase and alternative lengthening of telomeres coexist in the regenerating zebrafish caudal fins.EMBO reports · 2025Article
- Decoding Pancreatic Neuroendocrine Tumors: Molecular Profiles, Biomarkers, and Pathways to Personalized Therapy.International journal of molecular sciences · 2025Review
- High-Throughput Targeted Drug Screening for NF1-associated High-Grade Gliomas with ATRX Deficiency.bioRxiv : the preprint server for biology · 2025Article
- Daxx and HIRA go viral - How chromatin remodeling complexes affect DNA virus infection.Tumour virus research · 2025Review
- Biomolecular Condensates in Telomere Maintenance of ALT Cancer Cells.Journal of molecular biology · 2025Review
- LAP2α orchestrates alternative lengthening of telomeres suppression through telomeric heterochromatin regulation with HDAC1: unveiling a potential therapeutic target.Cell death & disease · 2024Article
- The Future of Targeted Therapy for Leiomyosarcoma.Cancers · 2024Review
- Mutant ATRX: pathogenesis of ATRX syndrome and cancer.Frontiers in molecular biosciences · 2024Review
- Telomere Maintenance Mechanisms in a Cohort of High-Risk Neuroblastoma Tumors and Its Relation to Genomic Variants in theCancers · 2023Article
- Liquid biopsy: creating opportunities in brain space.British journal of cancer · 2023Review
- Impacts of radiation exposure, hindlimb unloading, and recovery on murine skeletal muscle cell telomere length.NPJ microgravity · 2023Article
- Article
- Potential effects of assisted reproductive technology on telomere length and telomerase activity in human oocytes and early embryos.Journal of ovarian research · 2023Review
- Article
- Oncohistones and disrupted development in pediatric-type diffuse high-grade glioma.Cancer metastasis reviews · 2023Review
- Cell Immortalization: In Vivo Molecular Bases and In Vitro Techniques for Obtention.Biotech (Basel (Switzerland)) · 2023Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Telomeres are responsible for protecting chromosome ends in order to prevent the loss of coding DNA. Their maintenance is required for achieving immortality by neoplastic cells and can occur by upregulation of the telomerase enzyme or through a homologous recombination-associated process, the alternative lengthening of telomeres (ALT). The precise mechanisms that govern the activation of ALT or telomerase in tumor cells are not fully understood, although cellular origin may favor one of the other mechanisms that have been found thus far in mutual exclusivity. Specific mutational events influence ALT activation and maintenance: a unifying frequent feature of tumors that acquire this phenotype are the recurrent mutations of the Alpha Thalassemia/Mental Retardation Syndrome X-Linked (ATRX) or Death-Domain Associated Protein (DAXX) genes. This review summarizes the established criteria about this phenotype: its prevalence, theoretical molecular mechanisms and relation with ATRX, DAXX and other proteins (directly or indirectly interacting and resulting in the ALT phenotype).
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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.