ReviewSeminars in cell & developmental biology2014
Illuminating p53 function in cancer with genetically engineered mouse models.
Review in Seminars in cell & developmental biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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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
30 citing papers in PubMed, 59 citations in OpenAlex.
- Optimized Monothiol Thioredoxin Derivative (ORP100S) Protects In Vitro and In Vivo from Radiation and Chemotoxicity Without Promoting Tumor Proliferation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The TP53 tumor suppressor gene: From molecular biology to clinical investigations.Journal of internal medicine · 2025Review
- Article
- Inhibition of microRNA-30a alleviates vascular remodeling in pulmonary arterial hypertension.Molecular therapy. Nucleic acids · 2021Article
- Rely on Each Other: DNA Binding Cooperativity Shapes p53 Functions in Tumor Suppression and Cancer Therapy.Cancers · 2021Review
- Chaperones and Ubiquitin Ligases Balance Mutant p53 Protein Stability in Esophageal and Other Digestive Cancers.Cellular and molecular gastroenterology and hepatology · 2021Review
- HIF-1International journal of dentistry · 2021Article
- Regulating tumor suppressor genes: post-translational modifications.Signal transduction and targeted therapy · 2020Review
- Interplay between Endoplasmic Reticulum (ER) Stress and Autophagy Induces Mutant p53H273 Degradation.Biomolecules · 2020Article
- Phellinus gilvus‑derived protocatechualdehyde induces G0/G1 phase arrest and apoptosis in murine B16‑F10 cells.Molecular medicine reports · 2020Article
- Homologs of the Tumor Suppressor Protein p53: A Bioinformatics Study for Drug Design.MOJ proteomics & bioinformatics · 2020Article
- Article
- Mutant p53 and Cellular Stress Pathways: A Criminal Alliance That Promotes Cancer Progression.Cancers · 2019Review
- Dynamic role of the codon 72 p53 single-nucleotide polymorphism in mammary tumorigenesis in a humanized mouse model.Oncogene · 2019Article
- Combination therapy with atorvastatin and celecoxib delays tumor formation in a Fanconi anemia mouse model.Pediatric blood & cancer · 2019Article
- A mouse model of the Δ133p53 isoform: roles in cancer progression and inflammation.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- Tumor suppressive role for kinases phosphorylating p53 in DNA damage-induced apoptosis.Cancer science · 2018Review
- Deciphering p53 signaling in tumor suppression.Current opinion in cell biology · 2018Review
- Apoptosis and cell cycle aberrations in epithelial odontogenic lesions: An evidence by the expression of p53, Bcl-2 and Bax.Medicina oral, patologia oral y cirugia bucal · 2018Article
- Sustained protein synthesis and reduced eEF2K levels in TAp73Cell cycle (Georgetown, Tex.) · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The key role of the p53 protein in tumor suppression is highlighted by its frequent mutation in human cancers and by the completely penetrant cancer predisposition of p53 null mice. Beyond providing definitive evidence for the critical function of p53 in tumor suppression, genetically engineered mouse models have offered numerous additional insights into p53 function. p53 knock-in mice expressing tumor-derived p53 mutants have revealed that these mutants display gain-of-function activities that actively promote carcinogenesis. The generation of p53 knock-in mutants with alterations in different domains of p53 has helped further elucidate the cellular and biochemical activities of p53 that are most fundamental for tumor suppression. In addition, modulation of p53 post-translational modification (PTM) status by generating p53 knock-in mouse strains with mutations in p53 PTM sites has revealed a subtlety and complexity to p53 regulation. Analyses of mouse models perturbing upstream regulators of p53 have solidified the notion that the p53 pathway can be compromised by means other than direct p53 mutation. Finally, switchable p53 models that allow p53 reactivation in tumors have helped evaluate the potential of p53 restoration therapy for cancer treatment. Collectively, mouse models have greatly enhanced our understanding of physiological p53 function and will continue to provide new biological and clinical insights in future investigations.
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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.