Cited by 1,598Cancer-related Molecular PathwaysCancer Genomics and DiagnosticsGenomics and Rare Diseases

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Impact of mutant p53 functional properties on TP53 mutation patterns and tumor phenotype: lessons from recent developments in the IARC TP53 database

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Petitjean, Audrey, Mathe, Ewy, Kato, Shunsuke, Ishioka, Chikashi, Tavtigian, Sean V., Hainaut, Pierre, Olivier, Magali·2007·Human Mutation

DOI 10.1002/humu.20495

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Abstract

The tumor suppressor gene TP53 is frequently mutated in human cancers. More than 75% of all mutations are missense substitutions that have been extensively analyzed in various yeast and human cell assays. The International Agency for Research on Cancer (IARC) TP53 database (www-p53.iarc.fr) compiles all genetic variations that have been reported in TP53. Here, we present recent database developments that include new annotations on the functional properties of mutant proteins, and we perform a systematic analysis of the database to determine the functional properties that contribute to the occurrence of mutational "hotspots" in different cancer types and to the phenotype of tumors. This analysis showed that loss of transactivation capacity is a key factor for the selection of missense mutations, and that difference in mutation frequencies is closely related to nucleotide substitution rates along TP53 coding sequence. An interesting new finding is that in patients with an inherited missense mutation, the age at onset of tumors was related to the functional severity of the mutation, mutations with total loss of transactivation activity being associated with earlier cancer onset compared to mutations that retain partial transactivation capacity. Furthermore, 80% of the most common mutants show a capacity to exert dominant-negative effect (DNE) over wild-type p53, compared to only 45% of the less frequent mutants studied, suggesting that DNE may play a role in shaping mutation patterns. These results provide new insights into the factors that shape mutation patterns and influence mutation phenotype, which may have clinical interest.

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Surfing the p53 network
Vogelstein, B., Lane, D., & Levine, A. J. (2000) · Nature · doi:10.1038/35042675 · Cited by 6,607 · cited 1×
“The tumor suppressor gene TP53 (OMIM ]191117) encodes a transcription factor that responds to several forms of cellular stress and exerts multiple, antiproliferative functions [Vogelstein et al., 2000].”
Background
Germ Line p53 Mutations in a Familial Syndrome of Breast Cancer, Sarcomas, and Other Neoplasms
Malkin, D., Li, F. P., Strong, L. C., Fraumeni, J. F., Nelson, C. E., Kim, D. H., Kassel, J., Gryka, M. A., Bischoff, F. Z., Tainsky, M. A., et al. (1990) · Science · doi:10.1126/science.1978757 · Cited by 3,765 · cited 1×
“Inherited TP53 mutations predispose to a wide spectrum of early-onset cancers and are associated with Li-Fraumeni and Li-Fraumeni-like syndrome (LFS and LFL, respectively) [Malkin et al., 1990].”
Background
Preferential Formation of Benzo[ a ]pyrene Adducts at Lung Cancer Mutational Hotspots in P53
Denissenko, M. F., Pao, A., Tang, M.-S., & Pfeifer, G. P. (1996) · Science · doi:10.1126/science.274.5286.430 · Cited by 1,650 · cited 1×
“In lung cancers, V157F, R158L, R248L, and R273L hotspots are due to G4T transversions that have been shown to be caused by the presence of benzo(a)-pyrene diol epoxide (BPDE) adducts on guanines at these codons [Denissenko et al., 1996].”
Background
Mutant p53 gain of function in two mouse models of Li-Fraumeni syndrome
Olive, K. P., Tuveson, D. A., Ruhe, Z. C., Yin, B., Willis, N. A., Bronson, R. T., Crowley, D., & Jacks, T. (2004) · Cell · doi:10.1016/j.cell.2004.11.004 · Cited by 1,308 · cited 1×
“Studies in mouse models of LFS have reported evidence of GOF for R175H and R273H mutants [Lang et al., 2004; Olive et al., 2004].”
Background
The IARC TP53 database: new online mutation analysis and recommendations to users
Olivier, M., Eeles, R., Hollstein, M., Khan, M. A., Harris, C. C., & Hainaut, P. (2002) · Human Mutation · doi:10.1002/humu.10081 · Cited by 1,248 · cited 1×
“It contains annotations related to the clinical and pathological characteristics of tumors, as well as the demographics and carcinogen exposure of patients [Olivier et al., 2002].”
Background
Gain of function of a p53 hot spot mutation in a mouse model of Li-Fraumeni syndrome
Lang, G. A., Iwakuma, T., Suh, Y.-A., Liu, G., Rao, V. A., Parant, J. M., Valentin-Vega, Y. A., Terzian, T., Caldwell, L. C., Strong, L. C., et al. (2004) · Cell · doi:10.1016/j.cell.2004.11.006 · Cited by 1,069 · cited 1×
“Studies in mouse models of LFS have reported evidence of GOF for R175H and R273H mutants [Lang et al., 2004; Olive et al., 2004].”
Background
p53 and Human Cancer: The First Ten Thousand Mutations
Hainaut, P. L., & Hollstein, M. C. (1999) · Advances in cancer research · doi:10.1016/s0065-230x(08)60785-x · Cited by 999 · cited 1×
“Somatic TP53 gene alterations are frequent in most human cancers [Hainaut and Hollstein, 2000], ranging from 5 to 80% depending on the type, stage, and etiology of tumors.”
BackgroundSelf-citation
Understanding the function–structure and function–mutation relationships of p53 tumor suppressor protein by high-resolution missense mutation analysis
Kato, S., Han, S., Liu, W., Otsuka, K., Shibata, H., Kanamaru, R., & Ishioka, C. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1431692100 · Cited by 895 · cited 2×
“…2007 WILEY-LISS, INC. and a single study has performed a systematic analysis of the activity of all possible missense mutations produced by singlenucleotide substitution in the entire sequence of TP53 (2,314 mutations) on eight different p53-RE in yeast cells [Kato et al., 2003].”
BackgroundSelf-citation
The clinical value of somatic TP53 gene mutations in 1,794 patients with breast cancer.
Olivier, M., Langer√∏d, A., Carrieri, P., Bergh, J. C. S., Klaar, S., Eyfjord, J. E., Theillet, C. G., Rodríguez, C., Lidereau, R., Bièche, I., et al. (2006) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-05-1029 · Cited by 590 · cited 1×
“However, in a recent study on a large series of patients with breast cancer, we found that TP53 mutations were an independent factor of poor prognosis [Olivier et al., 2006], but that TA did not accurately predict differences in survival among patients with TP53 mutations.”
ResultSelf-citation
Li-Fraumeni and related syndromes: correlation between tumor type, family structure, and TP53 genotype.
Olivier, M., Goldgar, D. E., Sodha, N., Ohgaki, H., Kleihues, P., Hainaut, P. L., & Eeles, R. A. (2003) · PubMed · Cited by 480
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“These mutations all occur in the DNA binding domain of p53, altering its ability to bind to p53 response elements and induce transcription of many proteins [27, 52], possibly including IGFBP-3.”
Background
Detection of TP53 dysfunction in chronic lymphocytic leukemia by an in vitro functional assay based on TP53 activation by the non-genotoxic drug Nutlin-3: a proposal for clinical application
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“Mutations were confirmed on both strands on independent amplimers and validated by the IARC TP53 Mutation Database R15 [31].”
ResultInfluential
Childhood adrenocortical carcinoma as a sentinel cancer for detecting families with germline TP53 mutations
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“Although more than 500 families with TP53 mutations have been reported in the literature, only 15 are in continental Asia (China: 4, India: 4, Korea: 4, Malaysia: 2, Singapore: 1) and none in Africa (9).”
Background
Novel tools for extraction and validation of disease-related mutations applied to fabry disease
Kuipers, R. K. P., van den Bergh, T., Joosten, H., Deprez, R. H. L., Mannens, M. M. A. M., & Schaap, P. J. (2010) · Human Mutation · doi:10.1002/humu.21317 · Cited by 22
“Examples of such mutation databases are the IARC TP53 Mutation database [Petitjean et al., 2007] and UMD p53 database for the tumor repressor gene TP53 [Olivier et al., 2002].”
Method
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“Single nucleotide variations (SNVs) were scanned in the IARC-TP53-Database for detection of validated single nucleotide polymorphisms (SNPs) [35, 47], and excluded.”
BackgroundMethodInfluential
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“Especially, the p53 DNA-binding domain is frequently mutated in cancer cells (15).”
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“Remarkably, a total of four different TP53 mutations were identified, all of which are recurrent, functionally-significant cancer-associated alleles (19).”
Background
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“For example, the tumor suppressor P53 is mutated in many breast carcinomas [67].”
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“4, the pattern of (±)-anti-BPDE chemoselectivity within the selected 14-mer oligonucleotide did not correlate with the mutational spectra in the p53 gene reported for lung cancer[27].”
Background
Identification of a novel TP53 germline mutation E285V in a rare case of paediatric adrenocortical carcinoma and choroid plexus carcinoma
Russell-Swetek, A., West, A. N., Mintern, J. E., Jenkins, J., Galindo, C. R., Ribeiro, R. C., & Zambetti, G. P. (2008) · Journal of Medical Genetics · doi:10.1136/jmg.2008.059568 · Cited by 21
“fr), it has been infrequently observed in sporadic tumours of the liver, bladder, lung, ovary, brain, colon, blood and skin.(11)”
Li-Fraumeni Syndrome: The Genetics and Treatment Considerations for the Sarcoma and Associated Neoplasms
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Inactivation of the ATMIN/ATM pathway protects against glioblastoma formation
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“Precancerous lesions in which the DNA damage response is activated are under selective pressure to lose or mutate TP53, and loss of TP53 is known to cooperate with several genes to accelerate tumorigenesis (as summarized in the IARC database [Petitjean et al., 2007]).”
Background
Germline TP53 Mutation and Clinical Characteristics of Korean Patients With Li-Fraumeni Syndrome
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“Although the IARC database provided essential information pertaining to the mutation distribution and cancer spectrum in LFS, the majority of data originated from Caucasian populations [7].”
BackgroundMethod
TP53 and CDKN1A mutation analysis in families with Li–Fraumeni and Li–Fraumeni like syndromes
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“rhabdomyosarcoma at age 3, and was found to carry the TP53 I195N mutation, which has not been previously reported in the germline [17].”
Background
Exome sequencing identifies new somatic alterations and mutation patterns of tongue squamous cell carcinoma in a Chinese population
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“All missense mutations in our study were located in this region and the hotspot mutations were reported to have oncogenic activities (gain of function) in addition to loss of transactivation [21].”
Background
p53 mutations in classic and pleomorphic invasive lobular carcinoma of the breast
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“Recently, Das et al.showed that soft tissue sarcomas might have a higher prevalence of TP53 exon 4 mutations than previously thought (29).Accordingly, the possibility of mutations outside the classical core-binding domain of TP53 could not be completely excluded in malignant D-TSGCTs (27, 28, 30 ).”
Background
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“C176F is specific to esophagus SCC, R249S is specific to hepatocellular carcinoma, and H179Y is dominant in skin basal cell carcinoma [41].”
Background
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“Base substitution data were retrieved for the entire TP53 gene from the IARC TP53 database (33) for lung cancer designated smokers or non-smokers with no other known exposure.”
BackgroundMethodInfluential
The potential of molecular markers to improve interventions through the natural history of oesophageal squamous cell carcinoma
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Human variation databases
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“This review is meant to provide an overview on the current status of mutation data in public ..................................................................................................................................................................................................................................…”
BackgroundInfluential
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“Expression of mutant p53 is connected with abolishment of tumor suppressor functions [29].”
Background
On the Role of Flexibility in Protein–Ligand Interactions: the Example of p53 Tetramerization Domain
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“fr/) was used for comparing different TP53 mutational patterns [2].”
MethodResult
The Gain of Function of p53 Mutant p53S in Promoting Tumorigenesis by Cross-talking with H-RasV12
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“base (version R14, November 2009) [1] shows that human p53N239S (or p.”
BackgroundInfluential
Solar-UV-signature mutation prefers TCG to CCG: extrapolative consideration from UVA1-induced mutation spectra in mouse skin
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Key MicroRNA’s and Their Targetome in Adrenocortical Cancer
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“9% of all human tumors harboring germline TP53 mutations, after breast, soft-tissue, and brain tumors [28].”
Background
Estrogen-related receptor alpha directly binds to p53 and cooperatively controls colon cancer growth through the regulation of mitochondrial biogenesis and function
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“TP53 is known to be the most frequently altered gene in human cancer [33, 34].”
Background
TP53 mutations, human papilloma virus DNA and inflammation markers in esophageal squamous cell carcinoma from the Rift Valley, a high-incidence area in Kenya
Patel, K. T., Mining, S. K., Wakhisi, J., Gheit, T., Tommasino, M., Martel-Planche, G., Hainaut, P. L., & Abedi‐Ardekani, B. (2011) · BMC Research Notes · doi:10.1186/1756-0500-4-469 · Cited by 19
“Furthermore, the mutations identified, both in the present study and in Transkei, differ from the average mutation patterns of most cancers which are dominated by transition mutations at “hotspot” codons within CpG sites [34].”
BackgroundSelf-citation
Genotoxicity evaluation of individual cigarette smoke toxicants using the in vitro γH2AX assay by High Content Screening
Garcia‐Canton, C., Anadón, A., & Meredith, C. (2013) · Toxicology Letters · doi:10.1016/j.toxlet.2013.08.024 · Cited by 19
Correlation of telomere length shortening with TP53 somatic mutations, polymorphisms and allelic loss in breast tumors and esophageal cancer
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“TP53 is a tumor-suppressor gene, whose mutations and loss of heterozygosity (LOH) are hallmarks of most human cancers (11,12).”
Unambiguous Detection of Multiple TP53 Gene Mutations in AAN-Associated Urothelial Cancer in Belgium Using Laser Capture Microdissection
Aydın, S., Dekairelle, A., Ambroise, J., Durant, J.-F., Heusterspreute, M., Guiot, Y., Cosyns, J., & Gala, J. (2014) · PLoS ONE · doi:10.1371/journal.pone.0106301 · Cited by 19
“T transversion was significantly and consistently higher than in the IARC database [27].”
Result
The interplay of mutations and electronic properties in disease-related genes
Shih, C.-T., Wells, S. A., Hsu, C.-L., Cheng, Y.-Y., & Römer, R. A. (2012) · Scientific Reports · doi:10.1038/srep00272 · Cited by 19
CpG methylation of ubiquitin carboxyl-terminal hydrolase 1 (UCHL1) and P53 mutation pattern in sporadic colorectal cancer
Abdelmaksoud‐Dammak, R., Saadallah-Kallel, A., Miladi-Abdennadher, I., Ayedi, L., Khabir, A., Sallemi-Boudawara, T., Frikha, M., Daoud, J., & Mokdad‐Gargouri, R. (2015) · Tumor Biology · doi:10.1007/s13277-015-3902-4 · Cited by 19
“The P53 gene is mutated in about half of human cancers, and in CRC, somatic mutations are found in 40 to 50 % of samples [24, 25].”
Background
The case for aflatoxins in the causal chain of gallbladder cancer
Foerster, C., Koshiol, J. E., Guerrero, A. R., Kogan, M. J., & Catterina Ferreccio, R. (2015) · Medical Hypotheses · doi:10.1016/j.mehy.2015.11.026 · Cited by 19
“According to the IARC TP53 database, 39% of the HCC is associated to this transvertion followed by transitions GC to AT [9].”
Method
Control of Nucleotide Metabolism Enables Mutant p53’s Oncogenic Gain-of-Function Activity
Schmidt, V. A., Nagar, R., & Martinez, L. A. (2017) · International Journal of Molecular Sciences · doi:10.3390/ijms18122759 · Cited by 20
“While these missense mutations have been detected in more than 250 codons of TP53, resulting in over 1800 different amino acid substitutions, they occur most frequently within the region encoding the DNA-binding domain of the p53 protein [7].”
Background
Identification of Kinases and Interactors of p53 Using Kinase-Catalyzed Cross-Linking and Immunoprecipitation
Garre, S., Gamage, A. K., Faner, T. R., Arachchige, P. D., & Pflum, M. K. H. (2018) · Journal of the American Chemical Society · doi:10.1021/jacs.8b10160 · Cited by 20
p53 Mutation at Serine 249 and Its Gain of Function Are Highly Related to Hepatocellular Carcinoma after Smoking Exposure
Wang, H., Lu, C., Zhou, T., Zhang, Z., & Zeng, C. (2021) · Public Health Genomics · doi:10.1159/000516598 · Cited by 19
New experimental data linking secondhand smoke exposure to lung cancer in nonsmokers
Kim, S., Yoon, J., Tommasi, S., & Nia, A. B. (2012) · The FASEB Journal · doi:10.1096/fj.11-199984 · Cited by 19
Prognostic Role of Cell Cycle and Proliferative Markers in Clear Cell Renal Cell Carcinoma
Krabbe, L., Margulis, V., & Lotan, Y. (2015) · Urologic Clinics of North America · doi:10.1016/j.ucl.2015.08.010 · Cited by 19
Age-related function of tumor suppressor gene TP53:contribution to cancer risk and progression.
Чердынцева, Н. В., Анатольевна, Г. П., Litvyakov, N. V., Mn, S., Aa, P., Ay, D., Denisov, E. V., Белявская, В. А., & Choĭnzonov, E. L. (2010) · PubMed · Cited by 18
Human Telomerase Reverse Transcriptase Promotes the Epithelial to Mesenchymal Transition in Lung Cancer Cells by Enhancing c-MET Upregulation
Prasad, R. R., Mishra, D. K., Kumar, M., & Yadava, P. K. (2021) · Heliyon · doi:10.1016/j.heliyon.2021.e08673 · Cited by 19
“However, p53 mutant exerts a dominant-negative effect over wild-type p53 [52]; mutant p53 acquires oncogenic potential and promotes the expression of c-MET [53].”
Background
HERC5/IFI16/p53 signaling mediates breast cancer cell proliferation and migration
Liu, C., Li, L., Hou, G., Lu, Y., Gao, M., & Zhang, L. (2022) · Life Sciences · doi:10.1016/j.lfs.2022.120692 · Cited by 19
Concurrent TP53 mutations predict a poor prognosis of EGFR‑mutant NSCLCs treated with TKIs: An updated systematic review and meta‑analysis
Lan, B., Zhao, N., Du, K., & Leng, B. (2022) · Oncology Letters · doi:10.3892/ol.2022.13504 · Cited by 22
TP53 Aberrations in Chronic Lymphocytic Leukemia
Trbušek, M., & Malčíková, J. (2013) · Advances in experimental medicine and biology · doi:10.1007/978-1-4614-8051-8_5 · Cited by 19
“Currently, both experimental data and clinical observations recognize the p53 as the most important tumor-suppressor protein: (a) TP53 / mice invariably develop tumors [7], (b) heterozygous inherited mutations predispose to the Li-Fraumeni cancer-prone syndrome in humans [8], and (c) somatic mutations are frequent in…”
Background
Predicting the combined effect of multiple genetic variants
Liu, M., Watson, L. T., & Zhang, L. (2015) · Human Genomics · doi:10.1186/s40246-015-0040-4 · Cited by 18
Ethical Issues in Presymptomatic Genetic Testing for Minors: A dilemma in Li‐Fraumeni Syndrome
Fresneau, B. C., Brugières, L., Caron, O., & Moutel, G. (2012) · Journal of Genetic Counseling · doi:10.1007/s10897-012-9556-0 · Cited by 18
Identification and characterization of a novel germline p53 mutation in a patient with glioblastoma and colon cancer
Yamada, H., Shinmura, K., Yamamura, Y., Kurachi, K., Nakamura, T., Tsuneyoshi, T., Yokota, N., Maekawa, M., & Sugimura, H. (2009) · International Journal of Cancer · doi:10.1002/ijc.24432 · Cited by 18
Small Molecules Targeting Mutant P53: A Promising Approach for Cancer Treatment
Lopes, E. A., Gomes, S., Saraiva, L., & Santos, M. M. M. (2018) · Current Medicinal Chemistry · doi:10.2174/0929867325666181116124308 · Cited by 19
Diverse and cancer type‑specific roles of the p53 R248Q gain‑of‑function mutation in cancer migration and invasiveness
Olszewski, M. B., Pruszko, M., Snaar-Jagalska, E. B., Żylicz, M., & Żylicz, M. (2019) · International Journal of Oncology · doi:10.3892/ijo.2019.4723 · Cited by 18
“TCF8/ZEB1 is a pleiotropic suppressor of epithelial features and inducer of EMT, whose importance in cancer metastasis is well recognized (62-64).”
BackgroundMethodInfluential
BCL-W is dispensable for the sustained survival of select Burkitt lymphoma and diffuse large B-cell lymphoma cell lines
Diepstraten, S. T., Chang, C. W. T., Tai, L., Gong, J., Lan, P., Dowell, A. C., Taylor, G. S., Strasser, A., & Kelly, G. L. (2020) · Blood Advances · doi:10.1182/bloodadvances.2019000541 · Cited by 18
“Results Characterization of human B-cell lymphoma lines Six human B-cell lymphoma-derived cell lines were analyzed for expression of the prosurvival proteins BCL-W, BCL-2, BCL-XL, BFL-1, and MCL-1, along with proapoptotic BIM that is frequently epigenetically silenced in BLs,(9) and the tumor suppressor TP53, which is…”
Background
Identification of molecular and functional patterns of p53 alterations in chronic lymphocytic leukemia patients in different phases of the disease
Marinelli, M., Peragine, N., Maio, V. D., Chiaretti, S., Propris, M. S. D., Raponi, S., Tavolaro, S., Mauro, F. R., Giudice, I. D., Guarini, A., et al. (2012) · Haematologica · doi:10.3324/haematol.2012.069906 · Cited by 18
Effects of CpG Methylation on Recognition of DNA by the Tumour Suppressor p53
Petrovich, M., & Veprintsev, D. B. (2008) · Journal of Molecular Biology · doi:10.1016/j.jmb.2008.11.054 · Cited by 18
The cyclin-dependent kinase inhibitor 5, 6-dichloro-1-beta-D-ribofuranosylbenzimidazole induces nongenotoxic, DNA replication-independent apoptosis of normal and leukemic cells, regardless of their p53 status
Turinetto, V., Porcedda, P., Orlando, L., Marchi, M., Amoroso, A., & Giachino, C. (2009) · BMC Cancer · doi:10.1186/1471-2407-9-281 · Cited by 17
“Moreover, it is becoming clear that a high percentage of resistant and recurrent tumours carry de novo p53 mutations [2,4,6,10].”
Background
Multiple Effects of Bracken Fern under in vivo and in vitro Conditions
Tourchi-Roudsari, M. (2014) · Asian Pacific Journal of Cancer Prevention · doi:10.7314/apjcp.2014.15.18.7505 · Cited by 18
“Because p53 gene usually suppresses tumors in human (Petitjean et al., 2007), researchers evaluated mutations in exons 2-4 in treated mice.”
Background
Molecular Biomarkers in Colorectal Carcinoma
Puerta-García, E., Cañadas‐Garre, M., & Calleja‐Hernández, M. Á. (2015) · Pharmacogenomics · doi:10.2217/pgs.15.63 · Cited by 21
Expression ofSESN1, UHRF1BP1, and miR-377-3p as prognostic markers in mutatedTP53squamous cell carcinoma of the head and neck
Baroudi, M. E., Machiels, J., & Schmitz, S. (2017) · Cancer Biology & Therapy · doi:10.1080/15384047.2017.1373212 · Cited by 18
“regulation of target genes and thus allow TP53 mutants to exert oncogenic activities.(12-15) Fifty of these have been classified as hotspot mutations(16) due to their high prevalence in cancer.”
Background
A case study of an integrative genomic and experimental therapeutic approach for rare tumors: identification of vulnerabilities in a pediatric poorly differentiated carcinoma
Cruz, F. S. D., Diolaiti, D., Turk, A. T., Rainey, A. R., Ambesi‐Impiombato, A., Andrews, S. J., MANSUKHANI, M. M., Nagy, P. L., Alvarez, M. J., Califano, A., et al. (2016) · Genome Medicine · doi:10.1186/s13073-016-0366-0 · Cited by 18
“The identified TP53 (p.R248Q) mutation is a previously described gain-of-function mutation which is associated with early-onset development of many tumor types [30 – 32].”
Pan-cancer Analysis of Tumor Mutational Burden and Homologous Recombination DNA Damage Repair Using Targeted Next-Generation Sequencing
Wang, H., Deng, L., Li, Y.-Q., Zhang, X., Long, Y., Zhang, X., Feng, Y., He, Y. M., Tang, T., Yang, X., et al. (2021) · Cancer Research and Treatment · doi:10.4143/crt.2020.798 · Cited by 17
“mutation, copy number loss, and epigenetic silencing are very common in cancer and can be associated with increased mutation frequency [30].”
Potential of rescue and reactivation of tumor suppressor p53 for cancer therapy
Hibino, E., & Hiroaki, H. (2022) · Biophysical Reviews · doi:10.1007/s12551-021-00915-5 · Cited by 17
Quantitative prediction of the effect of genetic variation using hidden Markov models
Liu, M., Watson, L. T., & Zhang, L. (2014) · BMC Bioinformatics · doi:10.1186/1471-2105-15-5 · Cited by 17
“This section addresses whether the HMMvar score can reflect the degree of mutation effects on two extensively studied disease related proteins, TP53 and CFTR. TP53 (known as tumor protein 53) acts as a tumor suppressor, and regulates cell division by keeping cells from growing and dividing too fast or in an uncontroll…”
MethodInfluential
Feasibility of a randomized controlled trial of vitamin D vs. placebo in women with recently diagnosed breast cancer
Cescon, D. W., Ganz, P. A., Beddows, S., Ennis, M., Kahn-Mills, B. A., & Goodwin, P. J. (2012) · Breast Cancer Research and Treatment · doi:10.1007/s10549-012-2120-7 · Cited by 17
Serine 312 phosphorylation is dispensable for wild-type p53 functions in vivo
Lee, M. K., Tong, W., Wang, Z. Q., & Sabapathy, K. (2010) · Cell Death and Differentiation · doi:10.1038/cdd.2010.90 · Cited by 17
Ad-p53 enhances the sensitivity of triple-negative breast cancer MDA-MB-468 cells to the EGFR inhibitor gefitinib
Wang, X., SONG, H., Yu, Q., Liu, Q., Wang, L., Liu, Z., & Yu, Z. (2014) · Oncology Reports · doi:10.3892/or.2014.3665 · Cited by 17
“Its mutation has been related to the poor prognosis and drug resistance of cancer cells (14,15).”
Background
Original article Mutations in the exon 7 of Trp53 gene and the level of p53 protein in double transgenic mouse model of Alzheimer’s disease
Dorszewska, J., Oczkowska, A., Suwalska, M., Różycka, A., Florczak‐Wyspianska, J., Dezor, M., Lianeri, M., Jagodziński, P. P., Kowalczyk, M. J., Prendecki, M., et al. (2014) · Folia Neuropathologica · doi:10.5114/fn.2014.41742 · Cited by 17
“Due to the overwhelming sequence similarity between human and murine p53, especially within the DNA-binding core domain, we tried to estimate the potential influence of these four mutations on the protein activity with the use of the human IARC TP53 database that compiles TP53 variations identified in human population…”
Method
PIGN gene expression aberration is associated with genomic instability and leukemic progression in acute myeloid leukemia with myelodysplastic features
Teye, E. K., Sido, A., Xin, P., Finnberg, N. K., Gokare, P. R., Kawasawa, Y. I., Salzberg, A. C., Shimko, S., Bayerl, M. G., Ehmann, W. C., et al. (2017) · Oncotarget · doi:10.18632/oncotarget.15136 · Cited by 17
Molecular characterization of AML with RUNX1‐RUNX1T1 at diagnosis and relapse reveals net loss of co‐mutations
Höllein, A., Nadarajah, N., Meggendorfer, M., Jeromin, S., Kern, W., Haferlach, C., & Haferlach, T. (2019) · HemaSphere · doi:10.1097/hs9.0000000000000178 · Cited by 17
Identification of the Germline Mutation Profile in Esophageal Squamous Cell Carcinoma by Whole Exome Sequencing
Deng, J., Weng, X., Ye, J., Zhou, D., Liu, Y., & Zhao, K. (2019) · Frontiers in Genetics · doi:10.3389/fgene.2019.00047 · Cited by 17
Chemopreventive effects of pterostilbene through p53 and cell cycle in mouse lung of squamous cell carcinoma model
Surien, O., Ghazali, A. R., & Masre, S. F. (2021) · Scientific Reports · doi:10.1038/s41598-021-94508-7 · Cited by 18
Regulation of miRNAs Expression by Mutant p53 Gain of Function in Cancer
Madrigal, T., Hernández‐Monge, J., Herrera, L. A., la Rosa, C. H. G.-D., Domínguez-Gómez, G., Candelaria, M., Luna-Maldonado, F., Calderón-González, K. G., & Díaz‐Chávez, J. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.695723 · Cited by 18
“Besides, the mutant p53 protein can, in many cases, lose its functions and may exert a dominant negative regulation on any remaining p53 wt (Petitjean et al., 2007).”
Background
Emerging Targets in the Bioactivity of Ellipticines and Derivatives
O’Sullivan, E. C., Miller, C. M., Deane, F. M., & McCarthy, F. O. (2013) · Studies in natural products chemistry · doi:10.1016/b978-0-444-62615-8.00006-0 · Cited by 17
Association of germline or somatic TP53 missense mutation with oncogene amplification in tumors developed in patients with Li‐Fraumeni or Li‐Fraumeni‐like syndrome
Sugawara, W., Arai, Y., Kasai, F., Fujiwara, Y., Haruta, M., Hosaka, R., 西田, 一., 黒住昌史, Kobayashi, Y., Akagi, K., et al. (2011) · Genes Chromosomes and Cancer · doi:10.1002/gcc.20878 · Cited by 17
Specific Genomic Aberrations Predict Survival, But Low Mutation Rate in Cancer Hot Spots, in Clear Cell Renal Cell Carcinoma
Köhn, L., Svenson, U., Ljungberg, B., & Roos, G. (2014) · Applied immunohistochemistry & molecular morphology · doi:10.1097/pai.0000000000000087 · Cited by 17
“5 (0-127) Tumor diameter (mm) 80 (16-180) TNM stage I 23 II 10 III 16 IV 25 Grade 1 3 2 27 3 34 4 10”
5-FU resistance abrogates the amplified cytotoxic effects induced by inhibiting checkpoint kinase 1 in p53-mutated colon cancer cells
Akasaka, T., Tsujii, M., Kondo, J., Hayashi, Y., YING, J., Lu, Y., Kato, M., Yamada, T., Yamamoto, S., Inoue, T., et al. (2014) · International Journal of Oncology · doi:10.3892/ijo.2014.2693 · Cited by 17
CMPD: cancer mutant proteome database
Huang, P.-J., Lee, C., Tan, B. C., Yeh, Y., Chu, L. J., Chen, T.-W., Chang, K., Lee, C., Gan, R.-C., Liu, H., et al. (2014) · Nucleic Acids Research · doi:10.1093/nar/gku1182 · Cited by 17
“Supplementary Figure S1 is a Venn diagram illustrating the overlapping of protein-altering mutations between CMPD and widely accepted resources such as UniProt (11), COSMIC (8) and IARC TP53 (9).”
Background
The contribution of molecular epidemiology to the identification of human carcinogens: current status and future perspectives
Boffetta, P., & Islami, F. (2012) · Annals of Oncology · doi:10.1093/annonc/mds543 · Cited by 17
“The frequency of alterations (5%–80%) depends on the type, stage, and etiology of tumors [45].”
Background
Upregulation of energy metabolism-related, p53-target TIGAR and SCO2 in HuH-7 cells with p53 mutation by geranylgeranoic acid treatment
Iwao, C., & Shidoji, Y. (2015) · Biomedical Research · doi:10.2220/biomedres.36.371 · Cited by 17
Expanding the reach of the p53 tumor suppressor network
Zambetti, G. P. (2014) · Cell Death and Differentiation · doi:10.1038/cdd.2014.13 · Cited by 17
dbGENVOC: database of GENomic Variants of Oral Cancer, with special reference to India
Pradhan, S., Das, S., Singh, A. K., Das, C., Basu, A., Majumder, P. P., & Biswas, N. K. (2021) · Database · doi:10.1093/database/baab034 · Cited by 16
Real-world routine diagnostic molecular analysis for TP53 mutational status is recommended over p53 immunohistochemistry in B-cell lymphomas
de Haan, L. M., de Groen, R. A. L., de Groot, F. A., Noordenbos, T., van Wezel, T., van Eijk, R., Ruano, D., Diepstra, A., Koens, L., Nicolae, A., et al. (2023) · Archiv für Pathologische Anatomie und Physiologie und für Klinische Medicin · doi:10.1007/s00428-023-03676-6 · Cited by 16
Facts, Dogmas, and Unknowns About Mitochondrial Reactive Oxygen Species in Cancer
Junco, M., Ventura, C., Valtierra, F. X. S., & Maldonado, E. N. (2024) · Antioxidants · doi:10.3390/antiox13121563 · Cited by 18
“Mutations in p53 result in the loss of wild-type function favoring angiogenesis, metastasis, therapy resistance, and inactivation of other p53 family members also involved in tumor suppression [255–257].”
Exploring response signals and targets in aggressive unresectable hepatocellular carcinoma: an analysis of targeted therapy phase 1 trials
Subbiah, I. M., Falchook, G. S., Kaseb, A. O., Hess, K. R., Tsimberidou, A. M., Fu, S., Subbiah, V., Hong, D. S., Naing, A., Piha-Paul, S. A., et al. (2015) · Oncotarget · doi:10.18632/oncotarget.4601 · Cited by 16
“Polymorphisms particularly in codon 72 of TP53 have been associated with increased risk for multiple solid malignancies including high-grade serous ovarian and pancreatic adenocarcinoma.[22, 23] In one series, TP53 mutations have been associated with recurrence of HCC; indeed, 16 of 33 cases (49%) of recurrent HCC wer…”
Background
Benzene-induced mutational pattern in the tumour suppressor gene TP53 analysed by use of a functional assay, the functional analysis of separated alleles in yeast, in human lung cells
Billet, S., Paget, V., Garçon, G., Heutte, N., André, V., Shirali, P., & Sichel, F. (2009) · Archives of Toxicology · doi:10.1007/s00204-009-0478-z · Cited by 16
“This value is approximately two fold the frequency of 10–12% observed in many cancers (e.g. oesophagus, liver, lung, or brain), except in AML where it reaches 19% (Petitjean et al. 2007b).”
Influential

Authors: Petitjean, A., Mathe, E., Kato, S., Ishioka, C., Tavtigian, S. V., Hainaut, P., & Olivier, M.
Affiliations: Centre international de recherche sur le cancer (FR)
Tohoku University (JP)
World Health Organization (CH)
Corresponding author: Hainaut, Pierre
ORCID: Petitjean, Audrey
Kato, Shunsuke
Ishioka, Chikashi
Tavtigian, Sean V.
Hainaut, Pierre
Olivier, Magali
Venue: Human Mutation
Publisher: Wiley
Published: 2007-06
Volume: 28
Issue: 6
Pages: 622-629
ISSN: 1059-7794 (ISSN-L)
1098-1004
DOI: 10.1002/humu.20495
OpenAlex: W1986076152
Cited by: 1,598
References: 26
Citations by year: 2026: 24 · 2025: 36 · 2024: 34 · 2023: 42 · 2022: 59 · 2021: 87 · 2020: 68 · 2019: 81 · 2018: 75 · 2017: 83 · 2016: 120 · 2015: 135 · 2014: 136 · 2013: 131 · 2012: 143
FWCI: 41.84
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: public-domain
doi.wiley.com/10.1002/tdm_license_1.1 (tdm, 3014 d)
Locations: Human Mutation (publishedVersion, public-domain)
PubMed (publishedVersion)
Funders: National Institutes of Health
National Institute of Environmental Health Sciences
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 › Genetics › Genomics and Rare Diseases
Keywords: TP53, TP53 mutation, missense mutations, mutational hotspots, dominant negative effect, tumor suppressor, nucleotide substitution rates, mutation patterns, tumor phenotype
MeSH terms: DNA Mutational Analysis, Humans, Mutation, Neoplasms, Phenotype, Transcriptional Activation, Tumor Suppressor Protein p53, Age of Onset, Germ-Line Mutation, Databases, Genetic

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Impact of mutant p53 functional properties on TP53 mutation patterns and tumor phenotype: lessons from recent developments in the IARC TP53 database

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