Mutant p53 in Cancer: New Functions and Therapeutic Opportunities
Open accessAbstract
Many different types of cancer show a high incidence of TP53 mutations, leading to the expression of mutant p53 proteins. There is growing evidence that these mutant p53s have both lost wild-type p53 tumor suppressor activity and gained functions that help to contribute to malignant progression. Understanding the functions of mutant p53 will help in the development of new therapeutic approaches that may be useful in a broad range of cancer types.
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Various strategies have been explored to induce/reactivate wild type p53 or inhibit GOF mut-p53 in a wide range of cancer types, including glioblastoma.
“Various strategies have been explored to induce/reactivate wt-p53 or inhibit GOF mut-p53 in a wide range of cancer types, including GBM [113].”
From The p53 Pathway in Glioblastoma (2018) · cites this paper as [113]
The section “Therapeutic Strategies to Restore Wild-Type Activity to Mutant p53” describes several approaches to reactivate p53, and “Targeting Mutant p53 Regulated Pathways” describes an approach to block mutant p53’s oncogenic effects. The GBM-specific example in “Future Directions” is a computational search for potential synthetic-lethal targets using GBM project data; it does not show that p53-reactivation or GOF-inhibition strategies were explored as treatments in GBM. Page numbers are not available in our copy. (LLM, conf=0.86)
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Cites
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- Authors
- Muller, P. A. J., & Vousden, K. H.
- Affiliations
- Medical Research Council (GB)
- Cancer Research UK Scotland Institute (GB)
- Corresponding author
- Muller, Patricia A.J.
- Vousden, Karen H.
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2014-03
- Volume
- 25
- Issue
- 3
- Pages
- 304-317
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC3970583
- OpenAlex
- W1995068068
- Cited by
- 1,545
- References
- 14
- Citations by year
- 2026: 69 · 2025: 74 · 2024: 90 · 2023: 113 · 2022: 139 · 2021: 140 · 2020: 166 · 2019: 145 · 2018: 176 · 2017: 157 · 2016: 126 · 2015: 108 · 2014: 38 · 2012: 1
- FWCI
- 16.30
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Cancer Cell (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Durham Research Online (Durham University) (submittedVersion, cc-by)
- Research Explorer (The University of Manchester) (submittedVersion)
- Funders
- Cancer Research Society
- Wellcome Trust (101242)
- Cancer Research UK (18274)
- Royal Society
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Keywords
- mutant p53, TP53 mutation, gain-of-function p53, malignant progression, cancer therapy
- MeSH terms
- Animals, Humans, Mutation, Neoplasms, Signal Transduction, Gene Expression Regulation, Neoplastic, Tumor Suppressor Protein p53, Apoptosis, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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