ReviewCold Spring Harbor perspectives in medicine2017
The Regulation of Cellular Functions by the p53 Protein: Cellular Senescence.
Review in Cold Spring Harbor perspectives in medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.
- Association between TP53 gene codon72 polymorphism and prostate cancer risk: A systematic review and meta-analysis.Medicine · 2019Pooled it
- TMEM72 Inhibits the proliferation by promoting cellular senescence through the activation of the P38/MAPK signaling pathway in renal cell carcinoma.Translational oncology · 2026Article
- HMGA2 identified via m6A-senescence multi-omics in laryngeal squamous cell carcinoma.Scientific reports · 2026Article
- Translational Geroscience Strategies for Delaying Multimorbidity.ACS pharmacology & translational science · 2026Review
- Oxidative stress and antioxidants in breast cancer: a double-edged sword.Frontiers in oncology · 2026Review
- Molecular and Biochemical Evidence of Edaravone's Impact on Dasatinib-induced AGS Cell Senescence: A Promising Strategy for Gastric Cancer Therapy.Current medicinal chemistry · 2026Article
- The Impact of Senescence-Associated Secretory Phenotype (SASP) on Head and Neck Cancers: From Biology to Therapy.Cancers · 2025Review
- Balancing Decidualization, Autophagy, and Cellular Senescence for Reproductive Success in Endometriosis Biology.International journal of molecular sciences · 2025Review
- Vital Role of Visceral Adipose Tissue in Maintaining Cognitive Functions.International journal of molecular sciences · 2025Review
- Addressing osteoblast senescence: Molecular pathways and the frontier of anti-ageing treatments.Clinical and translational medicine · 2025Review
- TP53 -Mutated Myeloid Neoplasms: 2024 Update on Diagnosis, Risk-Stratification, and Management.American journal of hematology · 2025Review
- Targeting p53-p21 signaling to enhance mesenchymal stem cell regenerative potential.Regenerative therapy · 2025Review
- Nuclear AGO2 supports influenza A virus replication through type-I interferon regulation.Nucleic acids research · 2025Article
- Functional circuits of LYL1 controlled by supraphysiological androgen in prostate cancer cells to regulate cell senescence.Cell communication and signaling : CCS · 2024Article
- Nrf2 Signaling in Renal Cell Carcinoma: A Potential Candidate for the Development of Novel Therapeutic Strategies.International journal of molecular sciences · 2024Review
- Therapeutic approaches targeting aging and cellular senescence in Huntington's disease.CNS neuroscience & therapeutics · 2024Review
- Public neoantigens in breast cancer immunotherapy (Review).International journal of molecular medicine · 2024Review
- APR-246 as a radiosensitization strategy for mutant p53 cancers treated with alpha-particles-based radiotherapy.Cell death & disease · 2024Article
- The Role of Sensory Nerves in Dental Pulp Homeostasis: Histological Changes and Cellular Consequences after Sensory Denervation.International journal of molecular sciences · 2024Article
- Article
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 at 2 institutions in 1 country.
Funding
Abstract
Transformed cells have properties that allow them to survive and proliferate inappropriately. These characteristics often arise as a result of mutations caused by DNA damage. p53 suppresses transformation by removing the proliferative or survival capacity of cells with DNA damage or inappropriate cell-cycle progression. Cellular senescence, marked by morphological and gene expression changes, is a critical component of p53-mediated tumor suppression. In response to stress, p53 can facilitate an arrest and senescence program in cells exposed to stresses such as DNA damage and oncogene activation, preventing transformation. Senescent cells are evident in precancerous adenoma-type lesions, whereas proliferating, malignant tumors have bypassed senescence, either by p53 mutation or inactivation of the p53 pathway by other means. Tumors that have retained wild-type p53 often show a p53-mediated senescence response to chemotherapy. This response is actually detrimental in some tumor types, as senescent cells can drive relapse by persisting and producing cytokines and chemokines through an acquired secretory phenotype.
Indexed as
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.