ReviewInternational journal of molecular medicine2025
TP53 mutations in cancer: Molecular features and therapeutic opportunities (Review).
Review in International journal of molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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
70 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Disentangling the inverse relationship between cancer and Alzheimer's or Parkinson's disease: A systematic review on Mendelian randomization studies.Neurobiology of disease · 2025Pooled it
- VCP at the crossroads of UPS and autophagy in cancer.Genes & diseases · 2027Review
- Citron Kinase, a mitotic kinase with increasing significance in cancer.Cell cycle (Georgetown, Tex.) · 2026Review
- Article
- Opportunities in cancer gene therapy: inhibiting MDM2 and restoring p14ARF as a means to activate p53.Molecular and cellular biochemistry · 2026Review
- Special Issue "p53-Oncogene, Tumor Suppressor Gene, Guardian of the Genome and the Cell".International journal of molecular sciences · 2026Article
- Covalent Targeting and Thermostabilization of Oncogenic R280K and R273H Mutants p53 by Small Molecule RVJB59.ChemMedChem · 2026Article
- Construction and evaluation of an independently generated transgenic mouse model carrying mutated human HRAS genes for short-term carcinogenicity assessment.Transgenic research · 2026Article
- Article
- Multi-Site Aggregation of p53: Insights from Self- and Co-Aggregation of Multiple Aggregation-Prone Regions.ACS omega · 2026Article
- Comprehensive bioinformatics analysis of NCAPH expression and its clinical importance in endometrial cancer.Oncology letters · 2026Article
- Review
- ATR inhibition enhances radiosensitivity in p53-deficient colorectal cancer cells.Discover oncology · 2026Article
- Modulation ofInternational journal of molecular sciences · 2026Article
- Correlation of P53 expression and TP53 mutation in stage I lung adenocarcinoma and the predictive value for postoperative recurrence within 5 years.Diagnostic pathology · 2026Article
- Exploring the Impact of Multiple Gene Mutations on Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor Response in Asian Nonsmall Cell Lung Cancer Patients.ACS pharmacology & translational science · 2026Review
- Nuclear adenosine metabolism defines a metabolic vulnerability unmasked by TP53 loss.bioRxiv : the preprint server for biology · 2026Article
- SDC1 Knockdown Suppresses Malignant Phenotypes of Breast Cancer by Modulating the MAPK Signaling Pathway.Cancer medicine · 2026Article
- Dysregulated KIF2A correlates with p53 expression pattern in breast cancer.Molecular and cellular biochemistry · 2026Article
- Fundamentals and emerging frontiers in p53-targeted drug development.Biochemistry and biophysics reports · 2026Review
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumour suppressor factor p53 plays an essential role in regulating numerous cellular processes, including the cell cycle, DNA repair, apoptosis, autophagy, cell metabolism and immune response. TP53 is the most commonly mutated gene in human cancers. These mutations are primarily non‑synonymous changes that produce mutant p53 proteins characterized by loss of function, a dominant negative effect on p53 tetramerisation and gain of function (GOF). GOF mutations not only disrupt the tumour‑suppressive activities of p53 but also endow the mutant proteins with new oncogenic properties. Recent studies analysing different pathogenic features of mutant p53 in cancer‑derived cell lines have demonstrated that restoring wild‑type p53, rather than removing GOF mutations, reduces cancer cell growth. These findings suggest that therapeutic strategies for reactivating wild‑type p53 function in cancer cells may bring a greater benefit than approaches halting mutant p53. This approach could involve the use of small molecules, gene therapy and other methods to re‑establish wild‑type p53 activity. This review describes the complexity of the biological activities of different p53 mutants and summarizes the current therapeutic approaches to restore p53 function.
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.