ReviewCancer science2009
Cellular senescence: its role in tumor suppression and aging.
Review in Cancer science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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
58 citing papers in PubMed.
- Identification of E3 Ubiquitin Ligases Associated with Survival in Soft Tissue Sarcomas.International journal of molecular sciences · 2026Article
- Human adipose-derived mesenchymal stromal cells in vitro expansion for regenerative applications: tracking small genetic variants reveals dynamic changes within a genetically stable framework.Stem cell research & therapy · 2026Article
- Prognostic significance of fibroblast senescence and senescence-associated secretory phenotype factor expression in the tumor microenvironment of pancreatic ductal adenocarcinoma.Oncology reports · 2026Article
- Development of Cells Repository ofAnimals : an open access journal from MDPI · 2026Article
- Targeting cancer hallmarks using resveratrol: isolation, formulation, and mechanisms of action.Frontiers in nutrition · 2026Review
- Machine learning-driven multi-omics integration uncovers a senescence associated molecular axis in HCC.Frontiers in immunology · 2026Article
- Targeting Musashi-2 to counteract senescence and resistance in chronic myeloid leukemia: enhancing the efficacy of imatinib therapy.BMC cancer · 2025Article
- The Converging Roles of Nucleases and Helicases in Genome Maintenance and the Aging Process.Life (Basel, Switzerland) · 2025Review
- Review
- Downregulating FGGY carbohydrate kinase domain containing promotes cell senescence by activating the p53/p21 signaling pathway in colorectal cancer.International journal of molecular medicine · 2025Article
- Comparing Length and Telomere Expression at Oral Precancerous and Cancerous Stages.Iranian journal of pathology · 2024Article
- How to make full use of dental pulp stem cells: an optimized cell culture method based on explant technology.Frontiers in bioengineering and biotechnology · 2024Article
- P16INK4A-More Than a Senescence Marker.Life (Basel, Switzerland) · 2022Review
- The Senescence Markers p16INK4A, p14ARF/p19ARF, and p21 in Organ Development and Homeostasis.Cells · 2022Review
- Article
- Characterization of an active LINE-1 in the naked mole-rat genome.Scientific reports · 2021Article
- Genomic destabilization and its associated mutagenesis increase with senescence-associated phenotype expression.Cancer science · 2021Review
- Human colorectal cancer derived-MSCs promote tumor cells escape from senescence via P53/P21 pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020Article
- C/EBPα deficiency in podocytes aggravates podocyte senescence and kidney injury in aging mice.Cell death & disease · 2019Article
- CALB1 enhances the interaction between p53 and MDM2, and inhibits the senescence of ovarian cancer cells.Molecular medicine reports · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
In normal tissue, cell division is carefully regulated to maintain the correct proliferative balance. Abnormal cell division underlies many hypoproliferative and hyperproliferative disorders, including cancer, and a better understanding of the mechanisms involved could lead to new strategies for treatment and prevention. Cellular senescence, a state of irreversible growth arrest, was first described as a limit to the replicative life span of somatic cells after serial cultivation in vitro. Recently, however, it has also been shown to be triggered prematurely by potentially oncogenic stimuli such as oncogene expression, oxidative stress, and DNA damage in cell culture studies. These data suggest that cellular senescence is therefore acting as a tumor-protective fail-safe mechanism. However, the significance of cellular senescence has remained an issue of debate over the years, with the possibility that it might be a cell culture-related artifact. Recent reports on oncogene-induced senescence detected in premalignant tumors have provided evidence to validate its role as a physiological response to prevent oncogenesis in vivo. In this review, we discuss the mechanisms for cellular senescence and its roles in vivo.
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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.