ReviewCell2017
Putting p53 in Context.
Review in Cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,210 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
1,210 citing papers in PubMed.
- VCP at the crossroads of UPS and autophagy in cancer.Genes & diseases · 2027Review
- Host chromatin architecture in HPV-driven cervical cancer: molecular mechanisms and therapeutic resistance.Medical oncology (Northwood, London, England) · 2026Review
- Switches in alternatively spliced isoforms impact protein and drug interactions in melanoma, ovarian cancer, and acute myeloid leukemia.British journal of cancer · 2026Article
- Role of the MDM2/p53 axis in regulating cisplatin response in tumor cells.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Mutant p53Molecular oncology · 2026Article
- Special Issue "p53-Oncogene, Tumor Suppressor Gene, Guardian of the Genome and the Cell".International journal of molecular sciences · 2026Article
- Review
- Article
- Enhancing the efficacy of B7-H3-targeting antibody-drug conjugate DS-7300a in TP53-deficient tumors by inducing ferroptosis.Oncogene · 2026Article
- Dual contributions of Xrp1 to genome integrity through the DNA damage response and cell competition.PLoS genetics · 2026Article
- DNA-Peptide Crosslinks Placed at Codon 249 of the p53 Tumor Suppressor Gene Induce G to A Transitions in Human Cells.Chembiochem : a European journal of chemical biology · 2026Article
- Multi-Site Aggregation of p53: Insights from Self- and Co-Aggregation of Multiple Aggregation-Prone Regions.ACS omega · 2026Article
- PhiKan 083 Inhibits MYCN Expression in Liver Cancer Cells Independent of p53 Pathways.ACS pharmacology & translational science · 2026Article
- DNA-damage-targeting copper nanoparticles induce cuproptosis for enhanced cancer radiotherapy.Materials today. Bio · 2026Article
- Longitudinally cultured precision cut lung slices as a predictiveNanomedicine (London, England) · 2026Article
- Proteomic Analysis of TCGA Data Reveals Limited Prognostic Value of p53 but Suggests BAX as a Potential Survival Marker in Cervical Carcinoma.International journal of molecular sciences · 2026Article
- Modern Concepts in Precision Targeting of Acute Myeloid Leukemia Based on Principles of Molecular Oncology.Cancers · 2026Review
- SPPIDER-seq: sequence-based partner-aware predictor of protein-protein interaction sites.Bioinformatics (Oxford, England) · 2026Article
- TP53 mutation at codon 179 metabolically reprograms cancer cells to promote invasion.Cancer gene therapy · 2026Article
- The Mutational Landscape of Acute Myeloid Leukemia and Its Impact.International journal of molecular sciences · 2026Review
1,150 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
TP53 is the most frequently mutated gene in human cancer. Functionally, p53 is activated by a host of stress stimuli and, in turn, governs an exquisitely complex anti-proliferative transcriptional program that touches upon a bewildering array of biological responses. Despite the many unveiled facets of the p53 network, a clear appreciation of how and in what contexts p53 exerts its diverse effects remains unclear. How can we interpret p53's disparate activities and the consequences of its dysfunction to understand how cell type, mutation profile, and epigenetic cell state dictate outcomes, and how might we restore its tumor-suppressive activities in cancer?
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.