ReviewNature reviews. Cancer2020
p53: 800 million years of evolution and 40 years of discovery.
Review in Nature reviews. Cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 493 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
493 citing papers in PubMed, 1 synthesis or guideline pooled it, 801 citations in OpenAlex.
- Roles of hypoxia inducible factors in viral infection: Are they a potential therapeutic target?Virulence · 2025Pooled it
- Comparative efficacy and long-term survival of CD19/22 versus CD19 CAR-T immunotherapy in Relapsed/Refractory B-ALL with TP53 alterations.Journal of translational medicine · 2026Trial
- Osimertinib plus chemotherapy versus osimertinib for patients with advanced NSCLC with concomitant EGFR and TP53 mutations: a prospective cohort study.Scientific reports · 2025Trial
- Switches in alternatively spliced isoforms impact protein and drug interactions in melanoma, ovarian cancer, and acute myeloid leukemia.British journal of cancer · 2026Article
- ERG Orchestrates a Dedifferentiation-Senescence-Inflammation Triad in Prostate Cancer.Molecular cancer research : MCR · 2026Article
- TP53 mutation-biased CD8British journal of cancer · 2026Article
- Article
- Mutant p53Molecular oncology · 2026Article
- Opportunities in cancer gene therapy: inhibiting MDM2 and restoring p14ARF as a means to activate p53.Molecular and cellular biochemistry · 2026Review
- Cytotoxic and Apoptotic Effects of Sultamicillin and Cefuroxime Axetil and Their Potential Transformation Products in RTG-2 Fish Gonad Cells.Cell biochemistry and biophysics · 2026Article
- Cancers modulate processing and presentation of p53 neoantigens to evade T cell detection.Immunity · 2026Article
- TM6SF2 overexpression suppresses the proliferation and promotes apoptosis of human hepatocellular carcinoma cells.Oncology reports · 2026Article
- The TP53 gene contains a diversity box that makes it more than a tumor suppressor.Cell death and differentiation · 2026Review
- Lipid droplet-associated gene signatures classify metabolic subtypes and identify PLIN3 as a key driver in hepatocellular carcinoma.Genes & diseases · 2026Article
- Pathway potency in methylation altered network reveals lung cancer branching evolution and hallmarks.iScience · 2026Article
- Genome-wide CRISPR screen reveals CGS-15943 induced heme-dependent cell death mediated by aryl hydrocarbon receptor in lung cancer cells.Apoptosis : an international journal on programmed cell death · 2026Article
- Rewiring of the Apoptotic Rheostat in HTLV-1 Infection and Adult T-Cell Leukemia/Lymphoma.Cancers · 2026Review
- Longitudinally cultured precision cut lung slices as a predictiveNanomedicine (London, England) · 2026Article
- Associative memory plays a role in ER-1α positive breast cancers.Cell death and differentiation · 2026Review
- PTP4A2 promotes leukemogenesis through inhibiting the p53 tumor suppressor signaling pathway in leukemia-initiating cells.Blood advances · 2026Article
433 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 at 1 institution in 1 country.
Funding
Abstract
The evolutionarily conserved p53 protein and its cellular pathways mediate tumour suppression through an informed, regulated and integrated set of responses to environmental perturbations resulting in either cellular death or the maintenance of cellular homeostasis. The p53 and MDM2 proteins form a central hub in this pathway that receives stressful inputs via MDM2 and respond via p53 by informing and altering a great many other pathways and functions in the cell. The MDM2-p53 hub is one of the hubs most highly connected to other signalling pathways in the cell, and this may be why TP53 is the most commonly mutated gene in human cancers. Initial or truncal TP53 gene mutations (the first mutations in a stem cell) are selected for early in cancer development inectodermal and mesodermal-derived tissue-specific stem and progenitor cells and then, following additional mutations, produce tumours from those tissue types. In endodermal-derived tissue-specific stem or progenitor cells, TP53 mutations are functionally selected as late mutations transitioning the mutated cell into a malignant tumour. The order in which oncogenes or tumour suppressor genes are functionally selected for in a stem cell impacts the timing and development of a tumour.
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.