ReviewCancers2019
p53-Mediated Tumor Suppression: DNA-Damage Response and Alternative Mechanisms.
Review in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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
54 citing papers in PubMed, 87 citations in OpenAlex.
- SUMOylation inhibitor TAK-981 suppresses proliferation and induces apoptosis in SK-UT-1B uterine leiomyosarcoma cells.Oncology letters · 2026Article
- Malignant epithelial tumors associated with Felis catus papilloma virus type 3 and type 4 infections at distinct anatomical sites in a domestic cat.The Journal of veterinary medical science · 2026Article
- Identification of novel protein markers and therapeutic targets for common urological cancers by integrating large-scale human plasma proteome with the genome.Scientific reports · 2026Article
- Article
- Characterization of Oncogenic and Immunogenic Profiling in Patients with Breast Cancer Tumors After Radiation Therapy.International journal of molecular sciences · 2026Article
- Article
- Article
- Radiotherapy enhances M1 macrophage immunogenic activity through IFNs induction and stimulation in TP53-wild type tumors.Cancer immunology, immunotherapy : CII · 2026Article
- Bioactive glass nanoparticles induce intrinsic p53-dependent apoptosis and promote genomic instability via ROS overproduction and mitochondrial depolarization in triple-negative breast cancer cells.Scientific reports · 2026Article
- DNA-damaging chemotherapy reshapes cardiac-resident macrophage composition and function.Science immunology · 2026Article
- Ataxia-telangiectasia mutated activation mediates transforming growth factor beta signaling in acetaminophen-induced liver injury in mice.Physiological reports · 2025Article
- Claspin and Cancer: Where Are We Now?International journal of molecular sciences · 2025Review
- Role of hydrogen peroxide preconditioning in mesenchymal stem cell-mediated heart regeneration: Molecular insights.World journal of cardiology · 2025Review
- Targeting p53-p21 signaling to enhance mesenchymal stem cell regenerative potential.Regenerative therapy · 2025Review
- Review
- Review
- Sodium Butyrate: A Multifaceted Modulator in Colorectal Cancer Therapy.Medicina (Kaunas, Lithuania) · 2025Article
- Premature renal epithelial cell senescence promoted by LXN/Rps3/p53 signaling pathway activation increases calcium oxalate crystal deposition by altering macrophage polarization.Frontiers in immunology · 2025Article
- Chronic kidney disease and aging: dissecting the p53/p21 pathway as a therapeutic target.Biogerontology · 2024Review
- Chemical Implications of apo-8, 6' Carotendial versus Intact Lycopene on Mechanism of Enhanced Cell-cell Communication and Apoptosis Induction in Breast Cancer Cells.Cell biochemistry and biophysics · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 5 institutions in 3 countries.
Funding
Abstract
The tumor suppressor p53 regulates different cellular pathways involved in cell survival, DNA repair, apoptosis, and senescence. However, according to an increasing number of studies, the p53-mediated canonical DNA damage response is dispensable for tumor suppression. p53 is involved in mechanisms regulating many other cellular processes, including metabolism, autophagy, and cell migration and invasion, and these pathways might crucially contribute to its tumor suppressor function. In this review we summarize the canonical and non-canonical functions of p53 in an attempt to provide an overview of the potentially crucial aspects related to its tumor suppressor activity.
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.