ReviewNature cell biology2013
p53 mutations in cancer.
Review in Nature cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 991 papers, 4 of them syntheses 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
991 citing papers in PubMed, 4 syntheses or guidelines pooled it.
- Genetic drivers of etiologic heterogeneity in thyroid cancer.Nature communications · 2026Pooled it
- Impact of TP53 somatic mutations on prognosis in endometrial cancer: a systematic review and meta-analysis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Pooled it
- Rationale for Testing TP53 Mutations in Thyroid Cancer-Original Data and Meta-Analysis.International journal of molecular sciences · 2025Pooled it
- Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023Pooled it
- Restoration of p53 function via hybrid strontium sulfite nanoparticles modified LNP improves the antitumor efficacy in breast cancers.Cancer gene therapy · 2026Article
- Mutant p53Molecular oncology · 2026Article
- Mutant p53-R280K hijacks SREBP1 to promote fatty acid synthesis and breast cancer progression via FASN.Molecular biology reports · 2026Article
- Nanocarrier-based delivery of Pt(IV) compounds for chemoimmunotherapy and theranostics: Advances, challenges, and prospects.Acta pharmaceutica Sinica. B · 2026Review
- Article
- Clinical significance of TP53 mutations in patients with acute myeloid leukemia: the HM-SCREEN-JAPAN 01/02 study.International journal of hematology · 2026Article
- Review
- Investigating the anticancer activity of eravacycline in pancreatic cancer via target-based deep learning and experimental validation.Briefings in bioinformatics · 2026Article
- SPPIDER-seq: sequence-based partner-aware predictor of protein-protein interaction sites.Bioinformatics (Oxford, England) · 2026Article
- p53 mutation-associated prognosis across cancer types underlines hematological malignancy as an applicable cancer type to p53-rescue therapy.Fundamental research · 2026Article
- Unraveling the intricate molecular mechanisms of sex hormones' roles in breast cancer pathogenesis: A review.Medicine · 2026Review
- Flavonoids as Modulators of the p53-Bcl-2 Axis in Cancer: Molecular Mechanisms and Therapeutic Implications.Pharmaceutics · 2026Review
- The p53 Isoforms as Potential Biomarkers in Different Cancer Entities.International journal of molecular sciences · 2026Review
- Lipid transfer proteins and PI4KIIα initiate nuclear p53-phosphoinositide signaling.The Journal of biological chemistry · 2026Article
- Reactivation ofInternational journal of molecular sciences · 2026Article
- Cancer-linked aggregation of p53 is driven by sequence-encoded frustration, solvation, and hydrophobic gating absent in its paralogs.Communications chemistry · 2026Article
931 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
2 authors.
Funding
Abstract
In the past fifteen years, it has become apparent that tumour-associated p53 mutations can provoke activities that are different to those resulting from simply loss of wild-type tumour-suppressing p53 function. Many of these mutant p53 proteins acquire oncogenic properties that enable them to promote invasion, metastasis, proliferation and cell survival. Here we highlight some of the emerging molecular mechanisms through which mutant p53 proteins can exert these oncogenic functions.
Indexed as
Identifiers
23263379What 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.