ReviewOncogene2007
Are interactions with p63 and p73 involved in mutant p53 gain of oncogenic function?
Review in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 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
105 citing papers in PubMed, 1 synthesis or guideline pooled it, 172 citations in OpenAlex.
- Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023Pooled it
- Multi-hit TP53 confers the poorest survival in multiple myeloma in the era of novel therapies.Molecular medicine (Cambridge, Mass.) · 2025Article
- Valemetostat-SAHA-Driven Acetylation of p53 via SET/TAF-Iβ Displacement and p300 Activation Modulates Cell Cycle Regulators in Pancreatic Cancer Cells.Biomedicines · 2025Article
- Mutant p53 Gain of Function: Why Many See It, Why Some Do Not.Cancer discovery · 2025Article
- TP53: the unluckiest of genes?Cell death and differentiation · 2025Review
- p63: A Master Regulator at the Crossroads Between Development, Senescence, Aging, and Cancer.Cells · 2025Review
- microRNA-205 represses breast cancer metastasis by perturbing the rab coupling protein [RCP]-mediated integrin β1 recycling on the membrane.Apoptosis : an international journal on programmed cell death · 2024Article
- Mutant p53 gains oncogenic functions through a chromosomal instability-induced cytosolic DNA response.Nature communications · 2024Article
- Metabolomic Analysis of Phytochemical Compounds from Ethanolic Extract of Lime (Molecules (Basel, Switzerland) · 2023Article
- Targeting mutant p53 stabilization for cancer therapy.Frontiers in pharmacology · 2023Review
- PRIMA-1 inhibits Y220C p53 amyloid aggregation and synergizes with cisplatin in hepatocellular carcinoma.Frontiers in molecular biosciences · 2023Article
- Effects of USP7 on radiation sensitivity through p53 pathway in laryngeal squamous cell carcinoma.Translational oncology · 2022Article
- Review
- Regulation of p53 Function by Formation of Non-Nuclear Heterologous Protein Complexes.Biomolecules · 2022Review
- Regulation of P53 signaling in breast cancer by the E3 ubiquitin ligase RNF187.Cell death & disease · 2022Article
- Targeting mutant p53-R248W reactivates WT p53 function and alters the onco-metabolic profile.Frontiers in oncology · 2022Article
- APR-246 induces apoptosis and enhances chemo-sensitivity via activation of ROS and TAp73-Noxa signal in oesophageal squamous cell cancer with TP53 missense mutation.British journal of cancer · 2021Article
- p53, A Victim of the Prion Fashion.Cancers · 2021Review
- Mechanisms of Functional Pleiotropy of p73 in Cancer and Beyond.Frontiers in cell and developmental biology · 2021Review
- Review
45 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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although still controversial, the presence of mutant p53 in cancer cells may result in more aggressive tumors and correspondingly worse outcomes. The means by which mutant p53 exerts such pro-oncogenic activity are currently under extensive investigation and different models have been proposed. We focus here on a proposed mechanism by which a subset of tumor-derived p53 mutants physically interact with p53 family members, p63 and p73, and negatively regulate their proapoptotic function. Both cell-based assays and knock-in mice expressing mutant forms of p53 support this model. As more than half of human tumors harbor mutant forms of p53 protein, approaches aimed at disrupting the pathological interactions among p53 family members might be of clinical value.
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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.