ArticleScientific reports2015
Quantifying replicative senescence as a tumor suppressor pathway and a target for cancer therapy.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 24 citations in OpenAlex.
- Cellular Senescence in Health, Disease, and Lens Aging.Pharmaceuticals (Basel, Switzerland) · 2025Review
- The Role of Senescence, its Therapeutic Relevance and Clinical Implications in the Tumor Microenvironment.Theranostics · 2025Review
- Extended lifespan and improved genome stability in HepaRG-derived cell lines through reprogramming by high-density stress.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Review
- TERT promoter alterations could provide a solution for Peto's paradox in rodents.Scientific reports · 2020Article
- A dynamical systems model for the measurement of cellular senescence.Journal of the Royal Society, Interface · 2019Article
- The role of telomere shortening in carcinogenesis: A hybrid stochastic-deterministic approach.Journal of theoretical biology · 2019Article
- Capn4 regulates migration and invasion of ovarian carcinoma cells via targeting osteopontin-mediated PI3K/AKT signaling pathway.Oncology letters · 2019Article
- Variation of mutational burden in healthy human tissues suggests non-random strand segregation and allows measuring somatic mutation rates.PLoS computational biology · 2018Article
- Unlocking the chromatin of adenoid cystic carcinomas using HDAC inhibitors sensitize cancer stem cells to cisplatin and induces tumor senescence.Stem cell research · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To study quantitatively replicative senescence as a tumor suppressor mechanism, we investigate the distribution of a growing clonal cell population restricted by Hayflick's limit. We find that in the biologically relevant range of parameters, if the imbalance between cell division and death is moderate or low (high death-to-birth ratio), senescence offers significant protection against cancer by halting abnormal cell proliferation at early pre-diagnostic stages of tumor development. We also find that by the time tumors are typically detected, there is a high probability that telomerase is activated, even if the cell of origin was telomerase negative. Hence, the fact that most cancers are positive for telomerase is not necessarily an indication that cancer originated in a telomerase positive cell. Finally, we discuss how the population dynamics of cells can determine the outcomes of anti-telomerase cancer therapies, and provide guidelines on how the model could potentially be applied to develop clinically useful tools to predict the response to treatment by telomerase inhibitors in individual patients.
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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.