The DOI matches its Crossref record; 103 of the 105 references it cites were found in a registry or an index.
Reactivation of mutant p53: molecular mechanisms and therapeutic potential
Abstract
The p53 tumor suppressor gene is the most frequently mutated gene in cancer. Most p53 mutations are missense point mutations that cluster in the DNA-binding core domain. This results in distortion of core domain folding and disruption of DNA binding and transcriptional transactivation of p53 target genes. Structural studies have demonstrated that mutant p53 core domain unfolding is not irreversible. Mutant p53 is expressed at high levels in many tumors. Therefore, mutant p53 is a promising target for novel cancer therapy. Mutant p53 reactivation will restore p53-dependent apoptosis, resulting in efficient removal of tumor cells. A number of strategies for targeting mutant p53 have been designed, including peptides and small molecules that restore the active conformation and DNA binding to mutant p53 and induce p53-dependent suppression of tumor cell growth in vitro and in vivo. This opens possibilities for the clinical application of mutant p53 reactivation in the treatment of cancer.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
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?
In the citing paper
“since many of the deleterious side effects of genotoxic chemotherapies could actually result from chemoresistance arising from p53 mutations [50].”
From Ligand dependent restoration of human TLR3 signaling and death in p53 mutant cells (2016) · cites this paper as [50]
Citations
Cites
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 3,231
The Consensus Coding Sequences of Human Breast and Colorectal Cancers
Sjöblom, T., Jones, S., Wood, L. D., Parsons, D. W., Lin, J., Barber, T. D., Mandelker, D. L., Leary, R. J., Ptak, J., Silliman, N., et al. (2006) · Science · doi:10.1126/science.1133427 · Cited by 3,161
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×
“…more recent nuclear magnetic resonance (NMR) and X-ray studies on tumor-derived core domain mutants have revealed the structural impact of amino-acid residues that are most frequently mutated in human cancers (Cho et al., 1994; Wong et al., 1999; Joerger et al., 2004, 2005a, b; Ang et al., 2006).”
BackgroundThe 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
Restoration of the tumor suppressor function to mutant p53 by a low-molecular-weight compound
Bykov, V. J. N., Issaeva, N., Shilov, A., Hultcrantz, M., Pugacheva, E., Chumakov, P., Bergman, J., Wiman, K. G., & Selivanova, G. (2002) · Nature Medicine · doi:10.1038/nm0302-282 · Cited by 1,067
Self-citationGannon, 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
Nevins, J. R. (2001) · Human Molecular Genetics · doi:10.1093/hmg/10.7.699 · Cited by 939
Pharmacological Rescue of Mutant p53 Conformation and Function
Foster, B. A., Coffey, H. A., Morin, M. J., & Rastinejad, F. (1999) · Science · doi:10.1126/science.286.5449.2507 · Cited by 802
Presence of a Potent Transcription Activating Sequence in the p53 Protein
Fields, S., & Jang, S. K. (1990) · Science · doi:10.1126/science.2144363 · Cited by 790
Cited by
Sorted by citations
The senescence-associated secretory phenotype: the dark side of tumor suppression
Coppé, J.-P., Desprez, P.-Y., Krtolica, A., & Campisi, J. (2010) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev-pathol-121808-102144 · Cited by 5,206
Blinded by the Light: The Growing Complexity of p53
Vousden, K. H., & Prives, C. (2009) · Cell · doi:10.1016/j.cell.2009.04.037 · Cited by 3,163
Principles of cancer therapy: oncogene and non-oncogene addiction
Luo, J., Solimini, N. L., & Elledge, S. J. (2009) · Cell · doi:10.1016/j.cell.2009.02.024 · Cited by 1,765
Encyclopedia of Inorganic and Bioinorganic Chemistry
Casini, A., Miller, J. J., Gomes, L. M. F., & Storr, T. (2011) · Wiley eBooks · doi:10.1002/9781119951438 · Cited by 1,617
Principles of Protein−Protein Interactions: What are the Preferred Ways For Proteins To Interact?
Keskin, O., Gursoy, A., Ma, B., & Nussinov, R. (2008) · Chemical Reviews · doi:10.1021/cr040409x · Cited by 697
Metadata
- Authors
- Selivanova, G., & Wiman, K. G.
- Affiliations
- Karolinska Institutet (SE)
- Corresponding author
- Wiman, K G
- Venue
- Oncogene
- Published
- 2007-04-02
- Volume
- 26
- Issue
- 15
- Pages
- 2243-2254
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- OpenAlex
- W2025977492
- Cited by
- 186
- References
- 105
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 3 · 2023: 7 · 2022: 6 · 2021: 9 · 2020: 8 · 2019: 6 · 2018: 9 · 2017: 7 · 2016: 16 · 2015: 11 · 2014: 9 · 2013: 11 · 2012: 7
- FWCI
- 1.98
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Oncogene (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Cancerfonden
- Karolinska Institutet
- Cancerföreningen i Stockholm
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heat shock proteins research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Structure and Dynamics
- Keywords
- mutant p53, p53 reactivation, p53 tumor suppressor, missense mutations, protein unfolding, p53-dependent apoptosis, transcriptional activation, cancer therapy
- MeSH terms
- Humans, Mutation, Neoplasms, Protein Conformation, Tumor Suppressor Protein p53
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
