ArticleJournal of aging research2010
Cellular senescence as a target in cancer control.
Article in Journal of aging research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
25 citing papers in PubMed, 45 citations in OpenAlex.
- Environmental Carcinogenesis as a Stochastic Evolutionary Failure of Senescence-Control Systems.Cells · 2026Review
- A Darwinian Perspective on Tumor Evolution.International journal of biological sciences · 2026Review
- Further characterisation of immortalised human lymphatic endothelial cells to explore their transcriptomic profile and VEGFC response.Scientific reports · 2025Article
- Molecular Regulation of SASP in Cellular Senescence: Therapeutic Implications and Translational Challenges.Cells · 2025Review
- Petroleum ether extract of3 Biotech · 2025Article
- Therapy-induced senescence in breast cancer: an overview.Exploration of targeted anti-tumor therapy · 2024Review
- Fitting parameters and therapies of ODE tumor models with senescence and immune system.Journal of mathematical biology · 2023Article
- Review
- Distinct mechanisms mediating therapy-induced cellular senescence in prostate cancer.Cell & bioscience · 2022Review
- Cellular senescence in cancers: relationship between bone marrow cancer and cellular senescence.Molecular biology reports · 2022Review
- Role of Senescence in Tumorigenesis and Anticancer Therapy.Journal of oncology · 2022Review
- Role of Bioactive Constituents ofFrontiers in pharmacology · 2021Review
- Differential Gene Expression Analysis Reveals Global LMTK2 Regulatory Network and Its Role in TGF-β1 Signaling.Frontiers in oncology · 2021Article
- Mechanisms and significance of therapy-induced and spontaneous senescence of cancer cells.Cellular and molecular life sciences : CMLS · 2020Review
- RAC3 more than a nuclear receptor coactivator: a key inhibitor of senescence that is downregulated in aging.Cell death & disease · 2015Article
- Mitotic Stress Is an Integral Part of the Oncogene-Induced Senescence Program that Promotes Multinucleation and Cell Cycle Arrest.Cell reports · 2015Article
- Disruptive chemicals, senescence and immortality.Carcinogenesis · 2015Review
- Integrin-linked kinase regulates senescence in an Rb-dependent manner in cancer cell lines.Cell cycle (Georgetown, Tex.) · 2015Article
- Id4 promotes senescence and sensitivity to doxorubicin-induced apoptosis in DU145 prostate cancer cells.Anticancer research · 2013Article
- Tumor regression by phenethyl isothiocyanate involves DDB2.Cancer biology & therapy · 2013Article
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 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Somatic cells show a spontaneous decline in growth rate in continuous culture. This is not related to elapsed time but to an increasing number of population doublings, eventually terminating in a quiescent but viable state termed replicative senescence. These cells are commonly multinucleated and do not respond to mitogens or apoptotic stimuli. Cells displaying characteristics of senescent cells can also be observed in response to other stimuli, such as oncogenic stress, DNA damage, or cytotoxic drugs and have been reported to be found in vivo. Most tumors show unlimited replicative potential, leading to the hypothesis that cellular senescence is a natural antitumor program. Recent findings suggest that cellular senescence is a natural mechanism to prevent undesired oncogenic stress in somatic cells that has been lost in malignant tumors. Given that the ultimate goal of cancer research is to find the definitive cure for as many tumor types as possible, exploration of cellular senescence to drive towards antitumor therapies may decisively influence the outcome of new drugs. In the present paper, we will review the potential of cellular senescence to be used as target for anticancer therapy.
Identifiers
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.