TP53 mutations in human cancers: origins, consequences, and clinical use.
Open accessAbstract
Somatic mutations in the TP53 gene are one of the most frequent alterations in human cancers, and germline mutations are the underlying cause of Li-Fraumeni syndrome, which predisposes to a wide spectrum of early-onset cancers. Most mutations are single-base substitutions distributed throughout the coding sequence. Their diverse types and positions may inform on the nature of mutagenic mechanisms involved in cancer etiology. TP53 mutations are also potential prognostic and predictive markers, as well as targets for pharmacological intervention. All mutations found in human cancers are compiled in the IARC TP53 Database (http://www-p53.iarc.fr/). A human TP53 knockin mouse model (Hupki mouse) provides an experimental model to study mutagenesis in the context of a human TP53 sequence. Here, we summarize current knowledge on TP53 gene variations observed in human cancers and populations, and current clinical applications derived from this knowledge.
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38-50% of human cancers carry inactivating alterations in TP53, 48-80% in CDKN2A and 14% in CIP1, while 15-20% and up to 8% harbour oncogenic mutations in RAS and BRAF, respectively.
“Of note, 38-50% of human cancers carry inactivating alterations in TP53 (ref. 132 ) , 48-80% in CDKN2A 133 and 14% in CIP1 (ref. 134 ) , while 15-20% and up to 8% harbour oncogenic mutations in RAS and BRAF , respectively 135,136 .”
From Senescence and cancer — role and therapeutic opportunities (2022) · cites this paper as [132]
The Somatic Mutations section (page not provided) reports TP53 mutation rates of 38–50% in several specified cancer types, but about 5% in others. It does not support applying the 38–50% figure to human cancers overall. The other genes have separate citations in the citing sentence and are not assessed here. (LLM, conf=0.88)
Experimental — accuracy not yet measuredActivated p53 regulates expression of a set of anti-proliferative genes.
“Activated p53 regulates expression of a set of anti-proliferative genes (Olivier et al., 2010; Kastenhuber and Lowe, 2017).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Olivier et al., 2010
About half of human cancers retain wild-type p53.
“As p53 remains wild type in $50% of human cancers, 6 reactivation of p53 by small molecules is an attractive therapeutic approach.”
From Mdm2 inhibitors synergize with topoisomerase II inhibitors to induce p53-independent pancreatic cancer cell death (2013) · cites this paper as [6]
Tumors use several routes to disable TP53, and the most frequent route is missense mutation of TP53, with some mutants acquiring gain-of-function activities.
“Tumors, which drastically deviate from these parameters, have evolved multiple mechanisms to inactivate TP53, the most prevalent of which is the emergence of TP53 missense mutations, some of which have gain-of function activities.”
From The Mdm network and its regulation of p53 activities: a rheostat of cancer risk (2014) · cites this paper as Olivier, et al., 2010
About 75% of TP53 mutations in cancer are missense mutations.
“In particular, missense mutations account for approximately 75% of all TP53 mutations in cancer (Hamroun, et al., 2006; Olivier, et al., 2010)”
From The Mdm network and its regulation of p53 activities: a rheostat of cancer risk (2014) · cites this paper as Olivier, et al., 2010
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- Authors
- Olivier, M., Hollstein, M., & Hainaut, P.
- Affiliations
- Centre international de recherche sur le cancer (FR)
- University of Leeds (GB)
- Venue
- Cold Spring Harbor Perspectives in Biology
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2009-11-11
- Volume
- 2
- Issue
- 1
- Pages
- a001008-a001008
- ISSN
- 1943-0264 (ISSN-L)
- PMC
- PMC2827900
- OpenAlex
- W2129769331
- Cited by
- 2,199
- References
- 118
- Citations by year
- 2026: 136 · 2025: 174 · 2024: 233 · 2023: 229 · 2022: 222 · 2021: 178 · 2020: 174 · 2019: 112 · 2018: 139 · 2017: 131 · 2016: 101 · 2015: 97 · 2014: 88 · 2013: 61 · 2012: 72
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cold Spring Harbor Perspectives in Biology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- TP53 mutation, somatic mutations, germline TP53 mutation, Li-Fraumeni syndrome, cancer susceptibility, mutagenesis mechanism, prognostic factors, predictive biomarkers, therapeutic target, cancer etiology
- MeSH terms
- Animals, Carcinogens, Humans, Mice, Transgenic, Models, Biological, Mutation, Neoplasms, Prognosis, Gene Expression Regulation, Neoplastic, Genes, p53, Mutagenesis, CpG Islands, Mice
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