ReviewTrends in biochemical sciences2022
Consequences of telomere replication failure: the other end-replication problem.
Review in Trends in biochemical sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 33 citations in OpenAlex.
- Chromosomal instability in cancer: sources, consequences and new therapeutic opportunities.Signal transduction and targeted therapy · 2026Review
- Beyond End Protection: Shelterin, POT1 Dysfunction, and Telomere Replication Stress in Cancer.Biomolecules · 2026Review
- Selective killing of ALT-cancer cells by Withaferin-A involves destabilization of Rad51 and disruption of DNA repair.Cell death & disease · 2026Article
- Quantifying telomere length: from bulk assays to single-molecule resolution.Biophysics reports · 2026Article
- Vascular Aging and Atherosclerosis: The Modulatory Impact of Selenium-A Comprehensive Review.Cells · 2026Review
- Conditional deletion of human STN1 leads to telomere dysfunction, genome instability and proliferation defects.Journal of cell science · 2026Article
- Cancer-associated TRF1 mutations alter PARP1 interaction dynamics: an in silico study.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- A mechanism for telomere-specific telomere length regulation.Nucleic acids research · 2026Article
- Cellular adaptations impact the biological activity of naphthalene diimide G-quadruplex ligands in ALT-positive osteosarcoma cells.Cell death & disease · 2025Article
- A mechanism for telomere-specific telomere length regulation.bioRxiv : the preprint server for biology · 2025Article
- Oxidative Stress and DNA Damage at Telomeres.Cold Spring Harbor perspectives in biology · 2025Review
- The DNA damage tolerance factor Rad5 and telomere replication.Current genetics · 2025Review
- Multiple functions of the ALT favorite helicase, BLM.Cell & bioscience · 2025Review
- Telomerase in cancer- ongoing quest and future discoveries.Molecular biology reports · 2025Review
- Inherited Predispositions to Myeloid Neoplasms: Pathogenesis and Clinical Implications.Annual review of pathology · 2025Review
- Ustilago maydis Trf2 ensures genome stability by antagonizing Blm-mediated telomere recombination: Fine-tuning DNA repair factor activity at telomeres through opposing regulations.PLoS genetics · 2024Article
- POLD3 as Controller of Replicative DNA Repair.International journal of molecular sciences · 2024Review
- Article
- Guardians of the Genome: How the Single-Stranded DNA-Binding Proteins RPA and CST Facilitate Telomere Replication.Biomolecules · 2024Review
- Oxidative guanine base damage plays a dual role in regulating productive ALT-associated homology-directed repair.Cell reports · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Telomeres are chromosome-capping structures that protect ends of the linear genome from DNA damage sensors. However, these structures present obstacles during DNA replication. Incomplete telomere replication accelerates telomere shortening and limits replicative lifespan. Therefore, continued proliferation under conditions of replication stress requires a means of telomere repair, particularly in the absence of telomerase. It was recently revealed that replication stress triggers break-induced replication (BIR) and mitotic DNA synthesis (MiDAS) at mammalian telomeres; however, these mechanisms are error prone and primarily utilized in tumorigenic contexts. In this review article, we discuss the consequences of replication stress at telomeres and how use of available repair pathways contributes to genomic instability. Current research suggests that fragile telomeres are ultimately tumor-suppressive and thus may be better left unrepaired.
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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.