The UMD TP53 database and website: update and revisions
Abstract
Mutation of the p53 gene is the most frequent genetic alteration found in human cancer, but it is also the most frequently reported with more than 22,000 mutations published in 2,000 papers. In 1991, we developed a database and software to handle and analyze all this information. The database has been widely used for clinical analysis and molecular epidemiology. We have expanded the scope of the database by integrating structural, phylogenetic and biological information on wild-type (wt) and mutant TP53. Integration of the TP53 mutant activity database provides unique information that will be useful to both clinicians and scientists. All of this information is available from a new website (www.umd.be:2072/) that will generate a detailed informative page for every TP53 mutant in the database. New tools to check TP53 mutations and minimize errors found in the literature are also available.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
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 Hamroun, et al., 2006
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 Hamroun, et al., 2006
Cites
Vogelstein, B., Lane, D., & Levine, A. J. (2000) · Nature · doi:10.1038/35042675 · Cited by 6,607 · see citing works
Mutations in the p53 tumor suppressor gene: clues to cancer etiology and molecular pathogenesis.
Greenblatt, M. S., Bennett, W. P., Hollstein, M., & Harris, C. C. (1994) · PubMed · Cited by 3,463 · see citing works
Live or let die: the cell's response to p53
Vousden, K. H., & Lü, X. (2002) · Nature reviews. Cancer · doi:10.1038/nrc864 · Cited by 3,177 · see citing works
Crystal Structure of a p53 Tumor Suppressor-DNA Complex: Understanding Tumorigenic Mutations
Cho, Y., Gorina, S., Jeffrey, P. D., & Pavletich, N. P. (1994) · Science · doi:10.1126/science.8023157 · Cited by 2,559 · cited 2× · see citing works
“Two classes of mutations have been distinguished on the basis of various in vitro assays and the three-dimensional structure of the protein [Cho et al., 1994]: class I mutations, exemplified by mutants at codon 248 (7.”
BackgroundStructure of the MDM2 Oncoprotein Bound to the p53 Tumor Suppressor Transactivation Domain
Kussie, P. H., Gorina, S., Marechal, V., Elenbaas, B., Moreau, J., Levine, A. J., & Pavletich, N. P. (1996) · Science · doi:10.1126/science.274.5289.948 · Cited by 2,206 · see citing works
Definition of a consensus binding site for p53
El-Deiry, W. S., Kern, S. E., Pietenpol, J. A., Kinzler, K. W., & Vogelstein, B. (1992) · Nature Genetics · doi:10.1038/ng0492-45 · Cited by 1,985 · see citing works
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 · see citing works
Post-translational modification of p53 in tumorigenesis
Bode, A. M., & Dong, Z. (2004) · Nature Reviews Cancer · doi:10.1038/nrc1455 · Cited by 1,270 · see citing works
Decision making by p53: life, death and cancer
Oren, M. (2003) · Cell Death and Differentiation · doi:10.1038/sj.cdd.4401183 · Cited by 1,063 · see citing works
Gannon, J., Greaves, R. F., Iggo, R. D., & Lane, D. P. (1990) · The EMBO Journal · doi:10.1002/j.1460-2075.1990.tb08279.x · Cited by 970 · see citing works
Gain of function mutations in p53
Dittmer, D., Pati, S., Zambetti, G., Chu, S., Teresky, A. K., Moore, M., Finlay, C., & Levine, A. J. (1993) · Nature Genetics · doi:10.1038/ng0593-42 · Cited by 894 · see citing works
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 877 · see citing works
Self-citationp53: oncogene or anti-oncogene?Preprint
Lane, D. P., & Benchimol, S. (1990) · Genes & Development · doi:10.1101/gad.4.1.1 · Cited by 796 · see citing works
Assessing TP53 status in human tumours to evaluate clinical outcome
Soussi, T., & Béroud, C. (2001) · Nature reviews. Cancer · doi:10.1038/35106009 · Cited by 659 · see citing works
Self-citationStructure of the p53 Tumor Suppressor Bound to the Ankyrin and SH3 Domains of 53BP2
Gorina, S. S., & Pavletich, N. P. (1996) · Science · doi:10.1126/science.274.5289.1001 · Cited by 571 · see citing works
Rescuing the function of mutant p53
Bullock, A. N., & Fersht, A. R. (2001) · Nature reviews. Cancer · doi:10.1038/35094077 · Cited by 565 · see citing works
Bullock, A. N., Henckel, J., & Fersht, A. R. (2000) · Oncogene · doi:10.1038/sj.onc.1203434 · Cited by 435 · see citing works
Hinds, P. W., Finlay, C. A., Quartin, R. S., Baker, S. J., Fearon, E. R., Vogelstein, B., & Levine, A. J. (1990) · PubMed · Cited by 408 · see citing works
Liu, G., Parant, J. M., Lang, G., Chau, P., Chavez-Reyes, A., El-Naggar, A. K., Multani, A., Chang, S., & Lozano, G. (2004) · Nature Genetics · doi:10.1038/ng1282 · Cited by 325 · see citing works
Specific loss of apoptotic but not cell‐cycle arrest function in a human tumor derived p53 mutant.
Rowan, S., Ludwig, R., Haupt, Y., Bates, S., Lü, X., Oren, M., & Vousden, K. H. (1996) · The EMBO Journal · doi:10.1002/j.1460-2075.1996.tb00418.x · Cited by 300 · see citing works
A Mutant p53 That Discriminates between p53-Responsive Genes Cannot Induce Apoptosis
Friedlander, P. A., Haupt, Y., Prives, C. L., & Oren, M. (1996) · Molecular and Cellular Biology · doi:10.1128/mcb.16.9.4961 · Cited by 275 · see citing works
p53 point mutation and survival in colorectal cancer patients.
Goh, H. S., Yao, J. T. D., & Smith, D. R. (1995) · PubMed · Cited by 238 · see citing works
Ory, K., Legros, Y., Auguin, C., & Soussi, T. (1994) · The EMBO Journal · doi:10.1002/j.1460-2075.1994.tb06656.x · Cited by 229 · see citing works
Self-citationHot-spot mutants of p53 core domain evince characteristic local structural changes
Wong, K., DeDecker, B. S., Freund, S. M. V., Proctor, M. R., Bycroft, M., & Fersht, A. R. (1999) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.96.15.8438 · Cited by 219 · see citing works
Børresen, A., Andersen, T. I., Eyfjord, J. E., et al. (1995) · Genes Chromosomes and Cancer · doi:10.1002/gcc.2870140113 · Cited by 181 · see citing works
Resnick, M. A., & Inga, A. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1633803100 · Cited by 149 · see citing works
Locus-specific mutation databases: pitfalls and good practice based on the p53 experience
Soussi, T., Ishioka, C., Claustres, M., & Béroud, C. (2006) · Nature reviews. Cancer · doi:10.1038/nrc1783 · Cited by 144 · see citing works
Self-citationBørresen‐Dale, A., Lothe, R. A., Meling, G. I., Hainaut, P. L., Rognum, T. O., & Skovlund, E. (1998) · PubMed · Cited by 119 · see citing works
UMD (Universal Mutation Database): 2005 update
Béroud, C., Hamroun, D., Collod‐Béroud, G., Boileau, C., Soussi, T., & Claustres, M. (2005) · Human Mutation · doi:10.1002/humu.20210 · Cited by 116 · see citing works
Self-citationBerns, E., van Staveren, I., Look, M., et al. (1998) · British Journal of Cancer · doi:10.1038/bjc.1998.187 · Cited by 97 · see citing works
Flexibility: the key to p53 function?
Milner, J. (1995) · Trends in Biochemical Sciences · doi:10.1016/s0968-0004(00)88954-9 · Cited by 88 · see citing works
Hussain, S. P., Hollstein, M., & Harris, C. C. (2000) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2000.tb06870.x · Cited by 80 · see citing works
Soussi, T., Asselain, B. J. R., Hamroun, D., Kato, S., Ishioka, C., Claustres, M., & Béroud, C. (2006) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-05-0413 · Cited by 80 · see citing works
Self-citationLegros, Y., Meyer, A., Ory, K., et al. (1994) · PubMed · Cited by 72 · see citing works
The p53 tumour suppressor gene: a model for molecular epidemiology of human cancer
Soussi, T. (1996) · Molecular Medicine Today · doi:10.1016/1357-4310(96)88756-9 · Cited by 56 · see citing works
Self-citationKučera, E., Speiser, P., Gnant, M., Szabo, L., Samonigg, H., Hausmaninger, H., Mittlböck, M., Fridrik, M., Seifert, M., Kubista, E., et al. (1999) · European Journal of Cancer · doi:10.1016/s0959-8049(98)00400-6 · Cited by 37 · see citing works
p53 mutations and resistance to chemotherapy: A stab in the back for p73
Soussi, T. (2003) · Cancer Cell · doi:10.1016/s1535-6108(03)00081-3 · Cited by 28 · see citing works
Self-citation
Flagged first, then by citations
Cited by
Sorted by citations
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-citationThe Mdm network and its regulation of p53 activities: a rheostat of cancer risk
Eischen, C. M., & Lozano, G. (2014) · Human Mutation · doi:10.1002/humu.22524 · Cited by 79 · see citing works
- Authors
- Hamroun, D., Kato, S., Ishioka, C., Claustres, M., Béroud, C., & Soussi, T.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- Tohoku University (JP)
- Karolinska Institutet (SE)
- Corresponding author
- Soussi, Thierry
- ORCID
- Venue
- Human Mutation
- Publisher
- Hindawi Limited
- Published
- 2006-01
- Volume
- 27
- Issue
- 1
- Pages
- 14-20
- ISSN
- 1059-7794 (ISSN-L)
- 1098-1004
- OpenAlex
- W2058701056
- Cited by
- 140
- References
- 37
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 2 · 2023: 8 · 2022: 6 · 2021: 4 · 2020: 1 · 2019: 9 · 2018: 8 · 2017: 2 · 2016: 5 · 2015: 4 · 2014: 8 · 2013: 8 · 2012: 8
- FWCI
- 5.13
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Human Mutation (publishedVersion)
- PubMed (publishedVersion)
- HAL Portal Artxiker (Hindustan Aeronautics Limited (India)) (submittedVersion)
- HAL (submittedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genomics and Rare Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Keywords
- TP53, TP53 mutation, wild-type p53, cancer genetics, molecular epidemiology
- MeSH terms
- DNA Mutational Analysis, Humans, Mutation, Phylogeny, Tumor Suppressor Protein p53, Internet, Databases, Genetic
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
