ReviewCell death and differentiation2025
TP53: the unluckiest of genes?
Review in Cell death and differentiation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed.
- Article
- Revisiting tumor immunogenicity through the lens of mutant p53: Implications for cancer immunotherapy.Apoptosis : an international journal on programmed cell death · 2026Review
- Article
- Splice-altering TP53 missense mutations as drivers of dysfunction and targets for RNA-based therapy.Stem cell research & therapy · 2026Article
- Lactate metabolism and lactylation in cancer: from pathogenesis to therapeutic advances.Signal transduction and targeted therapy · 2026Review
- Protein lactylation: a metabolic signal driving cancer therapy resistance.Cell death discovery · 2026Review
- CBC3T-3: a novel patient-derived cisplatin-resistant distal cholangiocarcinoma cell line harboring multiple TP53 missense mutations.Human cell · 2026Article
- Targeting mutant p53 in cancer: from mechanistic insights to therapeutic strategies.Cellular & molecular biology letters · 2026Review
- The protein kinase DYRK1B is a p53 target gene and functions as a negative feedback regulator of the transcription factor RFX7.Cell death & disease · 2026Article
- Evaluation of non-canonical p53 functions in DNA replication and recombination for variant classification.Cell death & disease · 2026Article
- Targeting the p53 cancer mutants Y220C, Y220N, and Y220S with the small-molecule stabilizer rezatapopt.Cell death & disease · 2026Article
- Understanding Cancer Health Disparities.Cancers · 2026Review
- Lung-molGPA may stratify the prognostic impact of TP53 co-mutation in EGFR-mutant lung adenocarcinoma with brain metastases: a multi-center retrospective analysis.Therapeutic advances in medical oncology · 2026Article
- A prognostic lncRNA signature associated with ribonucleotide reductase predicts overall survival and immune landscape in hepatocellular carcinoma.Frontiers in cell and developmental biology · 2026Article
- [p53-SOAT1 Axis: A Novel Target for Tumor Lipid Metabolism and Therapy].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2025Review
- Understanding Functional Evolution in Orthologs and Paralogs.Journal of molecular evolution · 2025Review
- Whole genome characterization of patient-derived lung cancer organoids.Translational lung cancer research · 2025Article
- Multi-hit TP53 confers the poorest survival in multiple myeloma in the era of novel therapies.Molecular medicine (Cambridge, Mass.) · 2025Article
- Dissecting cross-lineage tumourigenesis under p53 inactivation through single-cell multi-omics and spatial transcriptomics.Clinical and translational medicine · 2025Article
- Correlation ofCurrent oncology (Toronto, Ont.) · 2025Article
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.
Funding
Abstract
The transcription factor p53 plays a key role in the cellular defense against cancer development. It is inactivated in virtually every tumor, and in every second tumor this inactivation is due to a mutation in the TP53 gene. In this perspective, we show that this diverse mutational spectrum is unique among all other cancer-associated proteins and discuss what drives the selection of TP53 mutations in cancer. We highlight that several factors conspire to make the p53 protein particularly vulnerable to inactivation by the mutations that constantly plague our genome. It appears that the TP53 gene has emerged as a victim of its own evolutionary past that shaped its structure and function towards a pluripotent tumor suppressor, but came with an increased structural fragility of its DNA-binding domain. TP53 loss of function - with associated dominant-negative effects - is the main mechanism that will impair TP53 tumor suppressive function, regardless of whether a neomorphic phenotype is associated with some of these variants.
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.