Assessing TP53 status in human tumours to evaluate clinical outcome

Soussi, Thierry; Béroud, Christophe

doi:10.1038/35106009

Cited by 659Cancer-related Molecular PathwaysHead and Neck Cancer StudiesCancer Genomics and Diagnostics

Assessing TP53 status in human tumours to evaluate clinical outcome

Soussi, Thierry, Béroud, Christophe·2001·Nature reviews. Cancer

DOI 10.1038/35106009

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Abstract

TP53 is probably the most extensively studied tumour-suppressor gene, and patients with TP53 mutations are known to have a poor outcome. However, inconsistencies in the analysis of TP53 status, and failure to realize that different mutations behave in different ways, prevent us from effectively applying our vast knowledge of this protein in clinical practice. What simple steps can be taken to ensure that patients benefit from our understanding of TP53?

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p53 is mutated in approximately 50% of all cancers.
“It is estimated that p53 is mutated in approximately 50% of all cancers with 60% of TNBCs bearing mutations in p53 (14, 15);”
From Potentiation of carboplatin-mediated DNA damage by the Mdm2 modulator Nutlin-3a in a humanized orthotopic breast-to-lung metastatic model (2015) · cites this paper as [14]
60% of triple-negative breast cancers bear mutations in p53.
“It is estimated that p53 is mutated in approximately 50% of all cancers with 60% of TNBCs bearing mutations in p53 (14, 15);”
From Potentiation of carboplatin-mediated DNA damage by the Mdm2 modulator Nutlin-3a in a humanized orthotopic breast-to-lung metastatic model (2015) · cites this paper as [14]
p73 is rarely mutated in cancers.
“in contrast, p73 is rarely mutated in cancers (14, 16).”
From Potentiation of carboplatin-mediated DNA damage by the Mdm2 modulator Nutlin-3a in a humanized orthotopic breast-to-lung metastatic model (2015) · cites this paper as [14]

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Stolzenberg, M., Brugières, L., Gardes, M., Dessarps-Freichey, F., Chompret, A., Paillerets, B. B., Lenoir, G., Bonaïti‐Pellié, C., Lemerle, J., & Feunteun, J. (1994) · PubMed · Cited by 13 · see citing works

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When mutants gain new powers: News from the mutant p53 field
Brosh, R., & Rotter, V. (2009) · Nature Reviews Cancer · doi:10.1038/nrc2693 · Cited by 1,132 · see citing works
Potential Predictive Value of <i>TP53</i> and <i>KRAS</i> Mutation Status for Response to PD-1 Blockade Immunotherapy in Lung Adenocarcinoma
Dong, Z.-Y., Zhong, W.-Z., Zhang, X.-C., Su, J., Xie, Z., Liu, S.-Y., Tu, H.-Y., Chen, H.-J., Sun, Y.-L., Zhou, Q., et al. (2017) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-16-2554 · Cited by 959 · see citing works
p53 controls cancer cell invasion by inducing the MDM2-mediated degradation of Slug
Wang, S.-P., Wang, W.-L., Chang, Y.-L., Wu, C.-T., Chao, Y.-C., Kao, S.-H., Yuan, A., Lin, C.-W., Yang, S.-C., Chan, W.-K., et al. (2009) · Nature Cell Biology · doi:10.1038/ncb1875 · Cited by 493 · see citing works
Mutant p53 Drives Pancreatic Cancer Metastasis through Cell-Autonomous PDGF Receptor β Signaling
Weissmueller, S., Manchado, E., Saborowski, M., Morris, J. P., Wagenblast, E., Davis, C. A., Moon, S.-H., Pfister, N. T., Tschaharganeh, D. F., Kitzing, T., et al. (2014) · Cell · doi:10.1016/j.cell.2014.01.066 · Cited by 466 · see citing works
“Accordingly, human tumors with mutant p53 are associated with poor patient prognosis (Soussi and Béroud, 2001) and drug resistance (Masciarelli et al., 2013).”
Molecular Mechanisms of Radiation-Induced Cancer Cell Death: A Primer
Sia, J., Szmyd, R., Hau, E., & Gee, H. E. (2020) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2020.00041 · Cited by 378 · see citing works
Analysis of P53 mutations and their expression in 56 colorectal cancer cell lines
Liu, Y., & Bodmer, W. F. (2006) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0510146103 · Cited by 257 · see citing works
The TP53 website: An integrative resource centre for the TP53 mutation database and TP53 mutant analysis
Leroy, B., Fournier, J. L., Ishioka, C., Monti, P., Inga, A., Fronza, G., & Soussi, T. (2013) · Nucleic Acids Research · doi:10.1093/nar/gks1033 · Cited by 185 · see citing works
Self-citation
The UMD TP53 database and website: update and revisions
Hamroun, D., Kato, S., Ishioka, C., Claustres, M., Béroud, C., & Soussi, T. (2006) · Human Mutation · doi:10.1002/humu.20269 · Cited by 140 · see citing works
Self-citation
ATM Phosphorylation of Mdm2 Ser394 Regulates the Amplitude and Duration of the DNA Damage Response in Mice
Gannon, H. S., Woda, B. A., & Jones, S. N. (2012) · Cancer Cell · doi:10.1016/j.ccr.2012.04.011 · Cited by 105 · see citing works
Mdm2–p53 signaling regulates epidermal stem cell senescence and premature aging phenotypes in mouse skin
Gannon, H. S., Donehower, L. A., Lyle, S., & Jones, S. N. (2011) · Developmental Biology · doi:10.1016/j.ydbio.2011.02.007 · Cited by 87 · see citing works
Potentiation of carboplatin-mediated DNA damage by the Mdm2 modulator Nutlin-3a in a humanized orthotopic breast-to-lung metastatic model
Tonsing-Carter, E., Bailey, B. J., Saadatzadeh, M. R., Ding, J., Wang, H., Sinn, A. L., Peterman, K. M., Spragins, T. K., Silver, J. M., Sprouse, A. A., et al. (2015) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-15-0237 · Cited by 42 · see citing works
MdmX regulates transformation and chromosomal stability in p53-deficient cells
Matijasevic, Z., Krzywicka-Racka, A., Sluder, G., & Jones, S. N. (2008) · Cell Cycle · doi:10.4161/cc.7.19.6797 · Cited by 34 · see citing works

Authors: Soussi, T., & Béroud, C.
Affiliations: Université Pierre-et-Marie-Curie (FR)
Hôpital Necker-Enfants Malades (FR)
Corresponding author: Soussi, Thierry
ORCID: Soussi, Thierry
Béroud, Christophe
Venue: Nature reviews. Cancer
Publisher: Springer Science and Business Media LLC
Published: 2001-12
Volume: 1
Issue: 3
Pages: 233-239
ISSN: 1474-175X (ISSN-L)
1474-1768
DOI: 10.1038/35106009
OpenAlex: W2049137769
Cited by: 659
References: 84
Citations by year: 2026: 11 · 2025: 8 · 2024: 14 · 2023: 13 · 2022: 13 · 2021: 10 · 2020: 21 · 2019: 22 · 2018: 26 · 2017: 15 · 2016: 37 · 2015: 23 · 2014: 43 · 2013: 31 · 2012: 29
FWCI: 2.58
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Nature reviews. Cancer (publishedVersion)
PubMed (publishedVersion)
Funders: National Cancer Institute
Topics: Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Health Sciences › Medicine › Otorhinolaryngology › Head and Neck Cancer Studies
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
Keywords: TP53, tumor suppressor, TP53 mutation, clinical outcomes, prognostic factors, mutation analysis, cancer genomics
MeSH terms: Tumor Protein p73, DNA-Binding Proteins, Humans, Membrane Proteins, Mutation, Neoplasms, Nuclear Proteins, Phosphoproteins, Polymorphism, Genetic, Prognosis, Structure-Activity Relationship, Transcription Factors, Transcriptional Activation, Trans-Activators, Genes, Tumor Suppressor, Genes, p53, Tumor Suppressor Protein p53, Li-Fraumeni Syndrome, Treatment Outcome, Gene Deletion, Point Mutation, Loss of Heterozygosity, Amino Acid Substitution, Mutation, Missense, RNA Splice Sites, Tumor Suppressor Proteins

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Assessing TP53 status in human tumours to evaluate clinical outcome

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