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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
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Background
Germ Line p53 Mutations in a Familial Syndrome of Breast Cancer, Sarcomas, and Other Neoplasms
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“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
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Background
Mutant p53 gain of function in two mouse models of Li-Fraumeni syndrome
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Background
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Background
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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×
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Background
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“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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Ancestry of the Brazilian TP53 c.1010G>A (p.Arg337His, R337H) Founder Mutation: Clues from Haplotyping of Short Tandem Repeats on Chromosome 17p
Paskulin, D. D., Giacomazzi, J., Achatz, M. I., Costa, S., Reis, R. M., Hainaut, P. L., dos Santos, S. E. B., & Ashton‐Prolla, P. (2015) · PLoS ONE · doi:10.1371/journal.pone.0143262 · Cited by 25
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Ubiquitin in Cell-Cycle Regulation and Dysregulation in Cancer
Borg, N. A., & Dixit, V. M. (2017) · Annual Review of Cancer Biology · doi:10.1146/annurev-cancerbio-040716-075607 · Cited by 26
“The importance of the p53 tumor suppressor is exemplified by its functional inactivation or negative regulation in most human cancers (Hollstein et al. 1991, Petitjean et al. 2007).”
Background
Current Prognostic and Predictive Biomarkers for Endometrial Cancer in Clinical Practice: Recommendations/Proposal from the Italian Study Group
Zannoni, G. F., Bragantini, E., Castiglione, F., Fassan, M., Troncone, G., Inzani, F. S., Pesci, A., Santoro, A., & Fraggetta, F. (2022) · Frontiers in Oncology · doi:10.3389/fonc.2022.805613 · Cited by 25
“Dysfunction of p53 has been observed in many malignant tumors (53, 54), mainly due to the inactivation of p53 protein by binding proteins or TP53 mutations.”
Background
Enhanced anti‐tumour effects of V inca alkaloids given separately from cytostatic therapies
Ehrhardt, H., Pannert, L., Pfeiffer, S., Wachter, F., Amtmann, E., & Jeremias, I. (2012) · British Journal of Pharmacology · doi:10.1111/bph.12068 · Cited by 25
“Within its pleiotropic functions, p53 is known to mediate cell cycle arrest, and all the cell lines studied express functionally active p53 (Zhou and Elledge, 2000; Yu and Zhang, 2005; Petitjean et al., 2007; Rozan and El-Deiry, 2007).”
Background
Mutation or Loss of p53 Differentially Modifies TGFβ Action in Ovarian Cancer
hAinmhire, E. Ó., Quartuccio, S. M., Cheng, W., Ahmed, R. A., King, S. M., & Burdette, J. E. (2014) · PLoS ONE · doi:10.1371/journal.pone.0089553 · Cited by 25
“accounts for 8% of all p53 mutations [7].”
Background
Gene expression profiling of mouse p53-deficient epidermal carcinoma defines molecular determinants of human cancer malignancy
García‐Escudero, R., Martínez‐Cruz, A. B., Santos, M., Lorz, C., Segrelles, C., Garaulet, G., Sáiz-Ladera, C., Costa, C., Buitrago-Pérez, Á., Dueñas, M., et al. (2010) · Molecular Cancer · doi:10.1186/1476-4598-9-193 · Cited by 26
“The overlapping of the tumor signature of p53-deficient mouse with genes differentially expressed in human aggressive tumors suggests that this signature could be predictive of malignant progression, in agreement with the observation that TP53 mutations have been associated with poor prognosis in human cancer [9, 11].”
BackgroundInfluential
The importance of codon context for understanding the Ig-like somatic hypermutation strand-biased patterns in TP53 mutations in breast cancer
Lindley, R. A. (2013) · Cancer Genetics · doi:10.1016/j.cancergen.2013.05.016 · Cited by 25
Prevalence of germline TP53 mutations and history of Li–Fraumeni syndrome in families with childhood adrenocortical tumors, choroid plexus tumors, and rhabdomyosarcoma: A population‐based survey
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Rare germline variant (rs78378222) in the TP53 3' UTR: Evidence for a new mechanism of cancer predisposition in Li-Fraumeni syndrome
Macedo, G. S., Vieira, I. A., Brandalize, A. P. C., Giacomazzi, J., Palmero, E. I., Volc, S. M., Paixão‐Côrtes, V. R., Caleffi, M. M., Alves, M. S., Achatz, M. I., et al. (2016) · Cancer Genetics · doi:10.1016/j.cancergen.2015.12.012 · Cited by 25
Self-citation
Classification of TP53 mutations and HPV predict survival in advanced larynx cancer
Scheel, A., Bellile, E. L., McHugh, J. B., Walline, H. M., Prince, M. E., Urba, S. G., Wolf, G. T., Eisbruch, A., Worden, F. P., Carey, T. E., et al. (2016) · The Laryngoscope · doi:10.1002/lary.25915 · Cited by 25
“of 76%–140%), partially functional (median TA of 21%–75%), and nonfunctional (median TA below or equal 20%).(15,28)”
Background
The HDM2 (MDM2) Inhibitor NVP-CGM097 Inhibits Tumor Cell Proliferation and Shows Additive Effects with 5-Fluorouracil on the p53-p21-Rb-E2F1 Cascade in the p53wild type Neuroendocrine Tumor Cell Line GOT1
Reuther, C., Heinzle, V., Nölting, S., Herterich, S., Hahner, S., Halilovic, E., Jeay, S., Wuerthner, J., Prada, E. T. A., Spöttl, G., et al. (2016) · Neuroendocrinology · doi:10.1159/000453369 · Cited by 25
JAK2V617F and p53 mutations coexist in erythroleukemia and megakaryoblastic leukemic cell lines
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“Interestingly, mutations of p53 are the most common in solid tumors but relatively rare in blood cell malignancies such as leukemia [7,9].”
BackgroundInfluential
TP53 rs1625895 is Related to Breast Cancer Incidence and Early Death in Iranian Population
Samani, L. A., Javadirad, S.-M., Parsafar, S., Tabatabaeian, H., Ghaedi, K., & Azadeh, M. (2018) · Indian Journal of Clinical Biochemistry · doi:10.1007/s12291-018-0774-6 · Cited by 24
Cancer-Associated Mutations Perturb the Disordered Ensemble and Interactions of the Intrinsically Disordered p53 Transactivation Domain
Schrag, L. G., Liu, X., Thevarajan, I., Prakash, O., Žółkiewski, M., & Chen, J. (2021) · Journal of Molecular Biology · doi:10.1016/j.jmb.2021.167048 · Cited by 26
Li–Fraumeni Syndrome–Associated Dimer-Forming Mutant p53 Promotes Transactivation-Independent Mitochondrial Cell Death
Choe, J. H., Kawase, T., Xu, A., Guzman, A., Obradović, A., Low-Calle, A. M., Alaghebandan, B., Raghavan, A., Long, K., Hwang, P. M., et al. (2023) · Cancer Discovery · doi:10.1158/2159-8290.cd-22-0882 · Cited by 25
Zoledronic Acid Produces Antitumor Effects on Mesothelioma Through Apoptosis and S-Phase Arrest in p53-Independent and Ras prenylation-Independent Manners
Okamoto, S., Kawamura, K., Li, Q., Yamanaka, M., Yang, S., Fukamachi, T., Tada, Y., Tatsumi, K., Shimada, H., Hiroshima, K., et al. (2012) · Journal of Thoracic Oncology · doi:10.1097/jto.0b013e31824c7d43 · Cited by 24
“to a frequent mutation site within the DNA-binding region.(18) The cell lines were as sensitive to ZoL as the other p53 WT mesothelioma cells (Fig.”
Background
p53-independent Epigenetic Repression of the p21WAF1 Gene in T-cell Acute Lymphoblastic Leukemia
Davies, C. H., Hogarth, L., Dietrich, P. A., Bachmann, P. S., MacKenzie, K. L., Hall, A. G., & Lock, R. B. (2011) · Journal of Biological Chemistry · doi:10.1074/jbc.m111.272336 · Cited by 27
Early occurrence of lung adenocarcinoma and breast cancer after radiotherapy of a chest wall sarcoma in a patient with a de novo germline mutation in TP53
Ferrarini, A., Auteri-Kaczmarek, A., Pica, A., Boesch, N., Heinimann, K., Schäfer, S. C., Mégalo, S. V., Cina, V., Beckmann, J. S., & Monnerat, C. (2011) · Familial Cancer · doi:10.1007/s10689-010-9415-9 · Cited by 24
EFGR-mutant lung adenocarcinoma and Li-Fraumeni syndrome: Report of two cases and review of the literature
Ricordel, C., Tiercin, M., Lespagnol, A., Kerjouan, M., Dugast, C., Mosser, J., Desrues, B., & Léna, H. (2014) · Lung Cancer · doi:10.1016/j.lungcan.2014.11.005 · Cited by 24
“[8] Petitjean A, Mathe E, Kato S, Ishioka C, Tavtigian SV, Hainaut P, et al.”
Background
SV40 TAg mouse models of cancer
Colvin, E. K., Weir, C., Ikin, R. J., & Hudson, A. L. (2014) · Seminars in Cell and Developmental Biology · doi:10.1016/j.semcdb.2014.02.004 · Cited by 26
Screening for germline BRCA1, BRCA2, TP53 and CHEK2 mutations in families at-risk for hereditary breast cancer identified in a population-based study from Southern Brazil
Palmero, E., Alemar, B., Schuler-faccini, L., Hainaut, P., Moreira-Filho, C., Ewald, I., dos Santos, P. K., Ribeiro, P. L., de Oliveira, C. D., Calvez-Kelm, F. L., et al. (2016) · Genetics and Molecular Biology · doi:10.1590/1678-4685-gmb-2014-0363 · Cited by 21
“Sequence variations were classified according to data submitted to the TP53 database at the International Agency for Research on Cancer - IARC version R17 (Petitjean et al., 2007).”
MethodSelf-citation
Combined Expression of c-jun, c-fos, and p53 Improves Estimation of Prognosis in Oral Squamous Cell Carcinoma
Wang, S., Xu, X. Y., Xu, F., Meng, Y., Sun, C., Shi, L., & Zhao, E. (2016) · Cancer Investigation · doi:10.1080/07357907.2016.1217422 · Cited by 24
“Mutational inactivation of p53 has been reported in nearly half of the oral cancer population (22, 23).”
Background
p53, stem cell biology and childhood blastomas
Oh, L., Hafsi, H., Hainaut, P. L., & Ariffin, H. (2019) · Current Opinion in Oncology · doi:10.1097/cco.0000000000000504 · Cited by 23
Self-citation
Virtual screening of p53 mutants reveals Y220S as an additional rescue drug target for PhiKan083 with higher binding characteristics
Raghavan, V., Agrahari, M., & Gowda, D. K. (2019) · Computational Biology and Chemistry · doi:10.1016/j.compbiolchem.2019.05.005 · Cited by 24
A novel hotspot and rare somatic mutation p.A138V, at TP53 is associated with poor survival of pancreatic ductal and periampullary adenocarcinoma patients
Saha, G., Singh, R., Mandal, A., Das, S. K., Chattopadhyay, E., Panja, P., Roy, P., Sarkar, N. D., Gulati, S., Ghatak, S., et al. (2020) · Molecular Medicine · doi:10.1186/s10020-020-00183-1 · Cited by 23
Estrogens, regulation of p53 and breast cancer risk: a balancing act
Jerry, D. J., Dunphy, K. A., & Hagen, M. J. (2010) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-009-0244-7 · Cited by 23
“Mutation of TP53 is common in sporadic breast cancers [17] and appears to be a necessary”
Background
Loss of heterozygosity on chromosome 10q in glioblastomas, and its association with other genetic alterations and survival in Indian patients
Suri, V. S., Kakkar, A., Jha, P., Srivastava, A., Sharma, V., Pathak, P., Sharma, M. C., Sharma, M., Kale, S., Chosdol, K., et al. (2011) · Neurology India · doi:10.4103/0028-3886.79139 · Cited by 24
Differential expression of senescence tumour markers and its implications on survival outcomes of breast cancer patients
Pare, R., Soon, P. S., Shah, A., & Lee, C. S. (2019) · PLOS ONE · doi:10.1371/journal.pone.0214604 · Cited by 23
Etoposide-induced dna damage is increased in p53 mutants: identification of atr and other genes that influence effects of p53 mutations on top2-induced cytotoxicity
Menendez, D., Anand, J. R., Murphy, C. C., Bell, W. J., Fu, J., Slepushkina, N., Buehler, E., Martin, S. E., Lal-Nag, M., Nitiss, J. L., et al. (2022) · Oncotarget · doi:10.18632/oncotarget.28195 · Cited by 22
“In HCT116 p53−/− cells stably expressing mutant p53R273H, a commonly occurring cancer mutation [16], etoposide treatment induced accumulation of p53 protein, indicating that this mutant p53 can be stabilized as well as its WT counterpart after exposure to DNA damaging agents.”
Background
Inauhzin Sensitizes p53-Dependent Cytotoxicity and Tumor Suppression of Chemotherapeutic Agents
Zhang, Y., Zhang, Q., Zeng, S. X., Hao, Q., & Lu, H. (2013) · Neoplasia · doi:10.1593/neo.13142 · Cited by 23
“[15] Petitjean A, Mathe E, Kato S, Ishioka C, Tavtigian SV, Hainaut P, and Olivier M”
Background
Targeted next-generation sequencing of dedifferentiated chondrosarcoma in the skull base reveals combined TP53 and PTEN mutations with increased proliferation index, an implication for pathogenesis
Gao, L., Hong, X., Guo, X., Cao, D., Gao, X., DeLaney, T. F., Gong, X., Chen, R., Ni, J., Yao, Y., et al. (2016) · Oncotarget · doi:10.18632/oncotarget.9618 · Cited by 23
“The International Agency for Research on Cancer (IARC) database for TP53 was investigated, and the codons close to this mutation were frequently mutated in various types of cancer [17].”
Background
Inhibition of p53 and/or AKT as a new therapeutic approach specifically targeting ALT cancers
Ge, Y., Wu, S., Zhang, Z., Li, X., Li, F., Yan, S., Liu, H., Huang, J., & Zhao, Y. B. (2019) · Protein & Cell · doi:10.1007/s13238-019-0634-z · Cited by 24
A p53-JAK-STAT connection involved in myeloproliferative neoplasm pathogenesis and progression to secondary acute myeloid leukemia
Goyal, H., Chachoua, I., Pecquet, C., Vainchenker, W., & Constantinescu, S. N. (2020) · Blood Reviews · doi:10.1016/j.blre.2020.100712 · Cited by 24
Estrogen receptor α as a predictive biomarker for survival in human papillomavirus-positive oropharyngeal squamous cell carcinoma
Kwon, S., Ahn, S.-H., Jeong, W., Jung, Y. H., Bae, Y. J., Paik, J. H., Chung, J.-H., & Kim, H. (2020) · Journal of Translational Medicine · doi:10.1186/s12967-020-02396-8 · Cited by 23
TP53 R273C Mutation Is Associated With Poor Prognosis in LGG Patients
Zhang, J., Liu, M., Fang, Y., Li, J., Chen, Y., & Jiao, S. (2022) · Frontiers in Genetics · doi:10.3389/fgene.2022.720651 · Cited by 23
Anticancer Therapeutic Strategies Targeting p53 Aggregation
Ferretti, G. D. S., Quarti, J., dos Santos, G., Rangel, L. P., & Silva, J. L. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms231911023 · Cited by 23
Nucleolar GTP-binding Protein-1 (NGP-1) Promotes G1 to S Phase Transition by Activating Cyclin-dependent Kinase Inhibitor p21Cip1/Waf1
Datta, D., Kumaraswamy, A., Suryaraja, R., Priya, R. S., Desai, P., & Mahalingam, S. (2015) · Journal of Biological Chemistry · doi:10.1074/jbc.m115.637280 · Cited by 23
“Elevated p53 in cancer is usually mutated (35–39) and fails to regulate cell cycle progression (40) or acquires oncogenic properties (41– 43), hence promoting tumorigenesis.”
Background
NOXA as critical mediator for drug combinations in polychemotherapy
Ehrhardt, H., Höfig, I., Wachter, F., Obexer, P., Fulda, S., Terziyska, N., & Jeremias, I. (2012) · Cell Death and Disease · doi:10.1038/cddis.2012.53 · Cited by 23
“This can be explained by the complex network of p53 signal transduction described, where different p53-activating stimuli induce upregulation of different p53 target genes.(22,23,31) The data are in line with our recent results that demonstrated drugspecific regulation of common p53 target genes.”
BackgroundResult
Variations in p53-like cDNA sequence are correlated with mussel haemic neoplasia: A potential molecular-level tool for biomonitoring
Vassilenko, E. I., Muttray, A. F., Schulte, P. M., & Baldwin, S. A. (2010) · Mutation Research/Genetic Toxicology and Environmental Mutagenesis · doi:10.1016/j.mrgentox.2010.06.001 · Cited by 23
Molecular, histopathological, and genomic variants of glioblastoma
Karsy, M. J. (2014) · Frontiers in bioscience · doi:10.2741/4268 · Cited by 23
Analysis of the DNA-binding activity of p53 mutants using functional protein microarrays and its relationship to transcriptional activation
Malčíková, J., Tichý, B., Damborský, J., Kabáthová, J., Trbušek, M., Mayer, J., & Pospı́šilová, Š. (2010) · Biological Chemistry · doi:10.1515/bc.2010.027 · Cited by 23
“…of mutation R337C has been proven by its occurrence in 17 sporadic cancer cases and in 3 of 419 Li-Fraumeni and Li-Fraumeni-like families (Petitjean et al., 2007), where disease severity was not different from that of the family affected by completely inactive C-terminal mutation L344P…”
Background
Identification of p53 and Its Isoforms in Human Breast Carcinoma Cells
Milićević, Z., Bajić, V., Živković, L., Kasapović, J., Andjelković, U., & Spremo‐Potparević, B. (2014) · The Scientific World JOURNAL · doi:10.1155/2014/618698 · Cited by 26
Systematic investigation of cancer-associated somatic point mutations in SNP databases
Jung, H., Bleazard, T., Lee, J., & Hong, D. (2013) · Nature Biotechnology · doi:10.1038/nbt.2681 · Cited by 23
Expression of cell cycle regulators and frequency of TP53 mutations in high risk gastrointestinal stromal tumors prior to adjuvant imatinib treatment
Ihle, M. A., Huss, S., Jeske, W., Hartmann, W., Merkelbach‐Bruse, S., Schildhaus, H., Büttner, R., Sihto, H. J., Hall, K. S., Eriksson, M., et al. (2018) · PLoS ONE · doi:10.1371/journal.pone.0193048 · Cited by 23
“# According to the International Agency for Research on Cancer (IARC) TP53 database [29].”
BackgroundMethod
Dynamic perspectives into the mechanisms of mutation‐induced p53‐DNA binding loss and inactivation using active perturbation theory: Structural and molecular insights toward the design of potent reactivators in cancer therapy
Olotu, F. A., & Soliman, M. E. S. (2018) · Journal of Cellular Biochemistry · doi:10.1002/jcb.27458 · Cited by 23
Chk1 inhibition significantly potentiates activity of nucleoside analogs in TP53-mutated B-lymphoid cells
Zemanová, J., Hylse, O., Čolláková, J., Veselý, P., Oltová, A., Borský, M., Zápražná, K., Kasparkova, M., Janovská, P., Verner, J., et al. (2016) · Oncotarget · doi:10.18632/oncotarget.11388 · Cited by 23
“The mutations corresponded to database of the International Agency for Research on Cancer (IARC) [55] or to the literature data except REC1 cells reported as TP53-wt [56], but in fact harboring two mutations.”
Method
Long-lasting reduction in clonogenic potential of colorectal cancer cells by sequential treatments with 5-azanucleosides and topoisomerase inhibitors
Pawlak, A., Zioło, E., Fiedorowicz, A., Fidyt, K., Strządała, L., & Kałas, W. (2016) · BMC Cancer · doi:10.1186/s12885-016-2925-6 · Cited by 23

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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