ReviewJournal of internal medicine2025
The TP53 tumor suppressor gene: From molecular biology to clinical investigations.
Review in Journal of internal medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed.
- Network toxicology and molecular docking reveal the mechanistic basis of bisphenol A-mediated cholestatic liver injury.Toxicology reports · 2026Article
- Review
- Special Issue "p53-Oncogene, Tumor Suppressor Gene, Guardian of the Genome and the Cell".International journal of molecular sciences · 2026Article
- An Isogenic Yeast Model Reveals the Influence of Native Promoter G‑Quadruplex Forming Sequences on P53 and NF-κB Transactivation.ACS bio & med chem Au · 2026Article
- MDM2 binds and suppresses RNA polymerase III to restrain the innate immune response to cytosolic DNA.Cell death and differentiation · 2026Article
- GSH-Related Enzymes GPx4, Chac1, and GSTs and Redox Regulation of Ferroptosis in Cancer.International journal of molecular sciences · 2026Review
- Nuclear adenosine metabolism defines a metabolic vulnerability unmasked by TP53 loss.bioRxiv : the preprint server for biology · 2026Article
- Malignant craniopharyngiomas: Institutional experience and literature review.Brain pathology (Zurich, Switzerland) · 2026Review
- ComplexInternational journal of molecular sciences · 2026Review
- Cytogenetic alterations and coagulopathy in breast cancer patients: molecular mechanisms and clinical implications.Annals of medicine and surgery (2012) · 2026Review
- Genetic and Clinical Features in TP53-Mutated Patients With Myelodysplastic Neoplasms: A Retrospective Study Based on Next-Generation Sequencing Data.Cancer reports (Hoboken, N.J.) · 2026Article
- Review
- Brain Cancer: Molecular Alterations and Emerging Trends in Neuropharmacology.International journal of molecular sciences · 2026Review
- Pro-ATO/Allicin Liposomes for Dual-Pathway Targeting of p53-Mutant Tumors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Unveiling the Genomic Landscape of Yan Goose (Animals : an open access journal from MDPI · 2026Article
- Network Pharmacology, Molecular Docking and Dynamics Simulation Reveal the Anti-Colitis Mechanism ofClinical and experimental gastroenterology · 2026Article
- Biology of p53 protein isoforms and their significance in hematological malignancies.Frontiers in oncology · 2026Review
- Article
- Aberrant cohesin function in Saccharomyces cerevisiae activates Mcd1 degradation to promote cell lethality.PLoS genetics · 2025Article
- Targeted Therapies in Oral and Oropharyngeal Cancer: An Overview of Emerging and Repurposed Agents.Cancers · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Extensively studied over the past four decades, the TP53 gene has emerged as a pivotal watchman in cellular defense and a key factor in cancer biology. TP53 is the most frequently mutated gene in human malignancies, 50% of which carry alterations to it. Initially, the functions of p53 were thought to be restricted to cell-cycle arrest and apoptosis. With time, however, a growing number of functions have been discovered, illustrating p53's role as a master switch between any cellular stress and cellular or multicellular responses that contribute to its anti-tumor activity. Indeed, the peculiar landscape of TP53 mutations and its high heterogeneity are linked both to the structure of the protein and its ubiquitous function in regulating cellular homeostasis. Mutations in p53 are associated with poor response to therapy and shorter survival in most cancer types, and the diagnosis of p53 mutations is currently used to improve case management in some types of leukemia and lymphoma. Although TP53 has been defined as a tumor suppressor gene, overexpressed mutated p53 variants found in human tumors are defined as dominant oncogenes with a potential gain of function, which makes the gene a very attractive target for developing new cancer treatments. Beyond its role in cancer, our review also highlights TP53's significance in non-neoplastic conditions, such as bone marrow failure syndromes and certain developmental disorders, where chronic p53 activation plays a crucial role in cellular stress responses, demonstrating its broader biological importance.
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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.