ArticleOncotarget2018
Human cancer cells utilize mitotic DNA synthesis to resist replication stress at telomeres regardless of their telomere maintenance mechanism.
Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
What it found
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Who cites it
67 citing papers in PubMed, 88 citations in OpenAlex.
- Beyond End Protection: Shelterin, POT1 Dysfunction, and Telomere Replication Stress in Cancer.Biomolecules · 2026Review
- ATR activity regulates DNA replication and RNA polymerase II transcription during S-phase.iScience · 2026Article
- Mitotic microhomology-mediated break-induced replication promotes chromoanasynthesis.Nature communications · 2026Article
- NPM1 phosphorylation-mediated telomere maintenance via stabilization of POLD3 in ALT-positive osteosarcoma: unraveling mechanisms and therapeutic opportunities.Theranostics · 2026Article
- The alternative lengthening of telomeres pathway through a DNA repair lens: mechanism and therapeutic opportunities.NAR cancer · 2025Review
- DNA double-strand break end resection factors and WRN facilitate mitotic DNA synthesis in human cells.Nature communications · 2025Article
- Biomolecular Condensates in Telomere Maintenance of ALT Cancer Cells.Journal of molecular biology · 2025Review
- RAD52 and ERCC6L/PICH have a compensatory relationship for genome stability in mitosis.PLoS genetics · 2024Article
- Polyubiquitinated PCNA triggers SLX4-mediated break-induced replication in alternative lengthening of telomeres (ALT) cancer cells.Nucleic acids research · 2024Article
- LAP2α orchestrates alternative lengthening of telomeres suppression through telomeric heterochromatin regulation with HDAC1: unveiling a potential therapeutic target.Cell death & disease · 2024Article
- Ancestral aneuploidy and stable chromosomal duplication resulting in differential genome structure and gene expression control in trypanosomatid parasites.Genome research · 2024Article
- PARP2 promotes Break Induced Replication-mediated telomere fragility in response to replication stress.Nature communications · 2024Article
- MutSβ protects common fragile sites by facilitating homology-directed repair at DNA double-strand breaks with secondary structures.Nucleic acids research · 2024Article
- Distinct modes of telomere synthesis and extension contribute to Alternative Lengthening of Telomeres.iScience · 2024Article
- Genome maintenance meets mechanobiology.Chromosoma · 2024Review
- Mitotic DNA Synthesis in Untransformed Human Cells Preserves Common Fragile Site Stability via a FANCD2-Driven Mechanism That Requires HELQ.Journal of molecular biology · 2023Article
- The DHX9 helicase interacts with human DNA polymerase δ4 and stimulates its activity in D-loop extension synthesis.DNA repair · 2023Article
- Pathway choice in the alternative telomere lengthening in neoplasia is dictated by replication fork processing mediated by EXD2's nuclease activity.Nature communications · 2023Article
- Homology directed telomere clustering, ultrabright telomere formation and nuclear envelope rupture in cells lacking TRF2Nature communications · 2023Article
- Review
7 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 resemble common fragile sites (CFSs) in that they are difficult-to-replicate and exhibit fragility in mitosis in response to DNA replication stress. At CFSs, this fragility is associated with a delay in the completion of DNA replication until early mitosis, whereupon cells are proposed to switch to a RAD52-dependent form of break-induced replication. Here, we show that this mitotic DNA synthesis (MiDAS) is also a feature of human telomeres. Telomeric MiDAS is not restricted to those telomeres displaying overt fragility, and is a feature of a wide range of cell lines irrespective of whether their telomeres are maintained by telomerase or by the alternative lengthening of telomeres (ALT) mechanism. MiDAS at telomeres requires RAD52, and is mechanistically similar to CFS-associated MiDAS, with the notable exception that telomeric MiDAS does not require the MUS81-EME1 endonuclease. We propose a model whereby replication stress initiates a RAD52-dependent form of break-induced replication that bypasses a requirement for MUS81-EME1 to complete DNA synthesis in mitosis.
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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.