ReviewNucleus (Austin, Tex.)
PML body meets telomere: the beginning of an ALTernate ending?
Review in Nucleus (Austin, Tex.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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
56 citing papers in PubMed, 100 citations in OpenAlex.
- Discovery of novel murine PML isoforms.Nucleus (Austin, Tex.) · 2026Article
- Membrane curvature elastic stress triggers recruitment of PML-II onto the inner nuclear membrane.Molecular biology of the cell · 2026Article
- Telomeric SUMO level influences the choices of APB formation pathways and ALT efficiency.The Journal of cell biology · 2025Article
- RNF4 and USP7 coordinate spatial regulation of SLX4 stability within the PML nuclear bodies.Nucleic acids research · 2025Article
- Epitalon increases telomere length in human cell lines through telomerase upregulation or ALT activity.Biogerontology · 2025Article
- The Dynamic Regulation of Daxx-Mediated Transcriptional Inhibition by SUMO and PML NBs.International journal of molecular sciences · 2025Review
- Biomolecular Condensates in Telomere Maintenance of ALT Cancer Cells.Journal of molecular biology · 2025Review
- Locking the gates of immortality: targeting alternative lengthening of telomeres (ALT) pathways.Medical oncology (Northwood, London, England) · 2025Review
- Orphan nuclear receptors-induced ALT-associated PML bodies are targets for ALT inhibition.Nucleic acids research · 2024Article
- The interactions between PML nuclear bodies and small and medium size DNA viruses.Virology journal · 2023Review
- The Molecular Mechanisms and Therapeutic Prospects of Alternative Lengthening of Telomeres (ALT).Cancers · 2023Review
- Signalling mechanisms and cellular functions of SUMO.Nature reviews. Molecular cell biology · 2022Review
- XPF activates break-induced telomere synthesis.Nature communications · 2022Article
- Shelterin Components Modulate Nucleic Acids Condensation and Phase Separation in the Context of Telomeric DNA.Journal of molecular biology · 2022Article
- Article
- Running 'LAPS' Around nLD: Nuclear Lipid Droplet Form and Function.Frontiers in cell and developmental biology · 2022Review
- Identification of proximal SUMO-dependent interactors using SUMO-ID.Nature communications · 2021Article
- SLX4IP N-terminus dictates telomeric localization in ALT-like castration-resistant prostate cancer cell lines.The Prostate · 2021Article
- Alternative Lengthening of Telomeres: Lessons to Be Learned from Telomeric DNA Double-Strand Break Repair.Genes · 2021Review
- Genetic Determinants of Paget's Disease of Bone.Current osteoporosis reports · 2021Review
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The unlimited proliferation potential of cancer cells requires the maintenance of their telomeres. This is frequently accomplished by reactivation of telomerase. However, in a significant fraction of tumors an alternative lengthening of telomeres (ALT) mechanism is active. The molecular mechanism of the ALT pathway remains elusive. In particular, the role of characteristic complexes of promyelocytic leukemia nuclear bodies (PML-NBs) with telomeres, the ALT-associated PML-NBs (APBs), is currently under investigation. Here, we review recent findings on the assembly, structure and functions of APBs. It is discussed how genomic aberrations in ALT-positive cancer cells could result in the formation of APBs and in ALT activity. We conclude that they are important functional intermediates in what is considered the canonical ALT pathway and discuss deregulations of cellular pathways that contribute to the emergence of 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.