The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.
Mutant p53 in cell-cell interactions
Abstract
p53 is an important tumor suppressor, and the complexities of p53 function in regulating cancer cell behaviour are well established. Many cancers lose or express mutant forms of p53, with evidence that the type of alteration affecting p53 may differentially impact cancer development and progression. It is also clear that in addition to cell-autonomous functions, p53 status also affects the way cancer cells interact with each other. In this review, we briefly examine the impact of different p53 mutations and focus on how heterogeneity of p53 status can affect relationships between cells within a tumor.
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“Mutant p53 can interact with transcription factors and cofactors to regulate multiple gene expression programs that promote cell proliferation, survival, invasion, and drug resistance.493”
From p53: from understanding its structure to advances in therapeutic targeting (2026) · cites this paper as [493]
In the citing paper
“Mutant p53 may not only lose the tumor suppressor function of wild-type p53 but also acquire new tumor-promoting functions, such as promoting tumor invasion, metastasis, and drug resistance.”
From p53: from understanding its structure to advances in therapeutic targeting (2026) · cites this paper as [493]
In the citing paper
“mutant p53 GOF activities, including the facilitation of cell proliferation, invasion, survival, cancer-promoting metabolism, protumorigenic inflammation, and drug resistance, have been observed in a series of experimental models, and multiple GOF mechanisms have been proposed.140,493,494”
From p53: from understanding its structure to advances in therapeutic targeting (2026) · cites this paper as [493]
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Citations
Cites
Tumorigenic conversion of primary embryo fibroblasts requires at least two cooperating oncogenes
Land, H., Parada, L. F., & Weinberg, R. A. (1983) · Nature · doi:10.1038/304596a0 · Cited by 2,804
Tracking the Evolution of Non–Small-Cell Lung Cancer
Jamal-Hanjani, M., Wilson, G. A., McGranahan, N., Birkbak, N. J., Watkins, T. B. K., Veeriah, S., Shafi, S., Johnson, D. H., Mitter, R., Rosenthal, R., et al. (2017) · New England Journal of Medicine · doi:10.1056/nejmoa1616288 · Cited by 2,349
High burden and pervasive positive selection of somatic mutations in normal human skin
Martincorena, I., Roshan, A., Gerstung, M., Ellis, P., Van Loo, P., McLaren, S., Wedge, D. C., Fullam, A., Alexandrov, L. B., Tubio, J. M., et al. (2015) · Science · doi:10.1126/science.aaa6806 · Cited by 1,770
Mutant p53 in Cancer: New Functions and Therapeutic Opportunities
Muller, P. A. J., & Vousden, K. H. (2014) · Cancer Cell · doi:10.1016/j.ccr.2014.01.021 · Cited by 1,545
Self-citationSomatic mutation in cancer and normal cells
Martincorena, I., & Campbell, P. J. (2015) · Science · doi:10.1126/science.aab4082 · Cited by 1,396
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
P53 in survival, death and metabolic health: a lifeguard with a licence to kill.
Kruiswijk, F., Labuschagne, C. F., & Vousden, K. H. (2015) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm4007 · Cited by 1,080
Self-citationTargeting mutant p53 for efficient cancer therapy
Bykov, V. J. N., Eriksson, S. E., Bianchi, J., & Wiman, K. G. (2018) · Nature Reviews Cancer · doi:10.1038/nrc.2017.109 · Cited by 889 · cited 1×
“However, APR-246 and its related compounds also show a variety of p53-independent activities that could underlie therapeutic efficacy (Bykov et al. 2018; Eriksson et al. 2019).”
BackgroundMetabolic Interactions in the Tumor Microenvironment
Lyssiotis, C. A., & Kimmelman, A. C. (2017) · Trends in Cell Biology · doi:10.1016/j.tcb.2017.06.003 · Cited by 853 · cited 1×
“This composition has led to the description of tumors as “pseudoorgans” (Lyssiotis and Kimmelman 2017).”
BackgroundNon-Cell-Autonomous Tumor Suppression by p53
Lujambio, A., Akkari, L., Simon, J., Grace, D., Tschaharganeh, D. F., Bolden, J. E., Zhao, Z., Thapar, V., Joyce, J. A., Krizhanovsky, V., et al. (2013) · Cell · doi:10.1016/j.cell.2013.03.020 · Cited by 766 · cited 2×
“…tissue by suppressing the expression of SDF-1/CXCL12, a chemokine that increases cell invasiveness (Moskovits et al. 2006) and the release of factors from p53-expressing hepatic stellate cells that promote macrophage polarization toward the tumor-suppressive M1 type (Lujambio et al. 2013).”
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Cited by
p53: from understanding its structure to advances in therapeutic targeting
Wang, W., Liu, X., Liu, H., Abolhassani, H., Yan, H., Zhang, H., & Wang, X. (2026) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-025-02549-5 · Cited by 30
Metadata
- Authors
- Pilley, S., Rodriguez, T. A., & Vousden, K. H.
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2021-04-01
- Volume
- 35
- Issue
- 7-8
- Pages
- 433-448
- ISSN
- 0890-9369
- 1549-5477
- Cited by
- 53
- References
- 31
- Language
- en
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