The DOI matches its Crossref record; 108 of the 118 references it cites were found in a registry or an index.
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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“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]
Experimental — accuracy not yet measuredIn the citing paper
“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
In the citing paper
“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]
In the citing paper
“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
In the citing paper
“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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Citations
Cites
p53 Mutations in Human Cancers
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Self-citationp53, the cellular gatekeeper for growth and division
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Germ Line p53 Mutations in a Familial Syndrome of Breast Cancer, Sarcomas, and Other Neoplasms
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Somatic mutations affect key pathways in lung adenocarcinoma
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“The p53 DBD is made of an immunoglobulinlike b-sandwich of two antiparallel b-sheets, providing a scaffold for a flexible DNA-binding surface (Cho et al. 1994).”
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Flagged first, then by citations
10 of the 118 references couldn’t be matched to a known paper.
Cited by
Sorted by citations
Signatures of mutational processes in human cancer
Initiative, A. P. C. G., Alexandrov, L. B., ICGC Breast Cancer Consortium, ICGC MMML-Seq Consortium, PedBrain, I., Nik-Zainal, S., Wedge, D. C., Aparicio, S. A. J. R., Behjati, S., Biankin, A. V., et al. (2013) · Nature · doi:10.1038/nature12477 · Cited by 9,660
Pan-cancer analysis of whole genomes
The ICGC/TCGA Pan-Cancer Analysis of Whole Genomes Consortium, Aaltonen, L. A., Abascal, F., Abeshouse, A., Aburatani, H., Adams, D. J., Agrawal, N., Ahn, K. S., Ahn, S.-M., Aikata, H., et al. (2020) · Nature · doi:10.1038/s41586-020-1969-6 · Cited by 3,064
Kastenhuber, E. R., & Lowe, S. W. (2017) · Cell · doi:10.1016/j.cell.2017.08.028 · Cited by 1,906
Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype
Kumari, R., & Jat, P. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.645593 · Cited by 1,622
Endogenous DNA damage as a source of genomic instability in cancer
Tubbs, A., & Nussenzweig, A. (2017) · Cell · doi:10.1016/j.cell.2017.01.002 · Cited by 1,452
Metadata
- 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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