ArticleCancer discovery2025
Mutant p53 Gain of Function: Why Many See It, Why Some Do Not.
Article in Cancer discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed.
- Mutant p53Molecular oncology · 2026Article
- Special Issue "p53-Oncogene, Tumor Suppressor Gene, Guardian of the Genome and the Cell".International journal of molecular sciences · 2026Article
- Mutant p53 gains RNA-binding activity to reprogram translation and mitochondrial function.Cell reports · 2026Article
- Modulation ofInternational journal of molecular sciences · 2026Article
- LFPM inhibition of RING1-mediated p53Cell death and differentiation · 2026Article
- Genetics and Molecular Mechanisms in Oral Squamous Cell Carcinoma: A Narrative Review.Medicina (Kaunas, Lithuania) · 2026Review
- Molecular Characterization ofCancers · 2026Article
- Low-penetrance TP53 variants are mainly hypomorphic: an underestimated issue with high clinical significance.NPJ genomic medicine · 2026Article
- Targeting mutant p53 in cancer: from mechanistic insights to therapeutic strategies.Cellular & molecular biology letters · 2026Review
- Elucidating cooperative genetic events in DCIS progression in mutantProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Article
- KCTD10 as a selective cancer dependency from transcription-replication conflicts (TRCs).Ageing and cancer research & treatment · 2026Article
- Mice carrying nonsense mutant p53 develop frequent multicentric or metastatic tumors.Cell death & disease · 2025Article
- Mutant p53 binds RNA to drive mitochondrial dysfunction.bioRxiv : the preprint server for biology · 2025Article
- Mutant p53 regulates cancer cell invasion in complex three-dimensional environments through mevalonate pathway-dependent Rho/ROCK signaling.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Mutant p53 as a Therapeutic Target: The Report of Its Death Was an Exaggeration.International journal of molecular sciences · 2025Review
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
Mutations in the TP53 tumor-suppressor gene in human cancer are unique in that 60% to 70% are of the missense variety, resulting in a full-length protein that is often highly expressed in patients' tumors. These missense mutant proteins often exhibit pro-oncogenic activities (referred to as gain of function) in mouse models and human cell lines and correlate with poor cancer prognosis in some cases.
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.