ArticleThe EMBO journal2012
Oncogene-induced telomere dysfunction enforces cellular senescence in human cancer precursor lesions.
Article in The EMBO journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 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.
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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.
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Who cites it
142 citing papers in PubMed, 222 citations in OpenAlex.
- Immunocyte senescence: A new perspective on the remodeling of the ovarian cancer microenvironment and therapeutic intervention.Journal of pharmaceutical analysis · 2026Review
- Replicative senescence induction in single cells is not predicted by telomere length, dysfunction, or oxidation.iScience · 2026Article
- Harnessing Natural Extracellular Vesicles to Combat Age-Related Diseases: From Aging Drivers to Therapeutic Opportunities.International journal of nanomedicine · 2026Review
- R-2-hydroxyglutarate-mediated inhibition of KDM4A compromises telomere integrity.Nucleic acids research · 2025Article
- From telomeres and senescence to integrated longevity medicine: redefining the path to extended healthspan.Biogerontology · 2025Review
- The relationship between telomere length and aging-related diseases.Clinical and experimental medicine · 2025Review
- Detecting Telomeric DNA Damage by Immuno-Telo FISH.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Review
- Senescent cell-derived vaccines: a new concept towards an immune response against cancer and aging?Aging · 2024Review
- Replication stress as a driver of cellular senescence and aging.Communications biology · 2024Review
- A Review of the Repair of DNA Double Strand Breaks in the Development of Oral Cancer.International journal of molecular sciences · 2024Review
- A novel machine learning algorithm selects proteome signature to specifically identify cancer exosomes.eLife · 2024Article
- Application of mesenchymal stem cells for anti-senescence and clinical challenges.Stem cell research & therapy · 2023Review
- Dyskeratosis Congenita Links Telomere Attrition to Age-Related Systemic Energetics.The journals of gerontology. Series A, Biological sciences and medical sciences · 2023Article
- Senescence-associated transcriptional derepression in subtelomeres is determined in a chromosome-end-specific manner.Aging cell · 2023Article
- Escape from oncogene-induced senescence is controlled by POU2F2 and memorized by chromatin scars.Cell genomics · 2023Article
- Review
- UV light-induced dual promoter mutations dismantle the telomeric guardrails in melanoma.DNA repair · 2023Review
- Review
- Escape from Cellular Senescence Is Associated with Chromosomal Instability in Oral Pre-Malignancy.Biology · 2023Review
82 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
Abstract
In normal human somatic cells, telomere dysfunction causes cellular senescence, a stable proliferative arrest with tumour suppressing properties. Whether telomere dysfunction-induced senescence (TDIS) suppresses cancer growth in humans, however, is unknown. Here, we demonstrate that multiple and distinct human cancer precursor lesions, but not corresponding malignant cancers, are comprised of cells that display hallmarks of TDIS. Furthermore, we demonstrate that oncogenic signalling, frequently associated with initiating cancer growth in humans, dramatically affected telomere structure and function by causing telomeric replication stress, rapid and stochastic telomere attrition, and consequently telomere dysfunction in cells that lack hTERT activity. DNA replication stress induced by drugs also resulted in telomere dysfunction and cellular senescence in normal human cells, demonstrating that telomeric repeats indeed are hypersensitive to DNA replication stress. Our data reveal that TDIS, accelerated by oncogene-induced DNA replication stress, is a biological response of cells in human cancer precursor lesions and provide strong evidence that TDIS is a critical tumour suppressing mechanism in humans.
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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.