The DOI matches its Crossref record; 18 of the 18 references it cites were found in a registry or an index.
Integrated Analysis of TP53 Gene and Pathway Alterations in The Cancer Genome Atlas
Open accessAbstract
The TP53 tumor suppressor gene is frequently mutated in human cancers. An analysis of five data platforms in 10,225 patient samples from 32 cancers reported by The Cancer Genome Atlas (TCGA) enables comprehensive assessment of p53 pathway involvement in these cancers. More than 91% of TP53-mutant cancers exhibit second allele loss by mutation, chromosomal deletion, or copy-neutral loss of heterozygosity. TP53 mutations are associated with enhanced chromosomal instability, including increased amplification of oncogenes and deep deletion of tumor suppressor genes. Tumors with TP53 mutations differ from their non-mutated counterparts in RNA, miRNA, and protein expression patterns, with mutant TP53 tumors displaying enhanced expression of cell cycle progression genes and proteins. A mutant TP53 RNA expression signature shows significant correlation with reduced survival in 11 cancer types. Thus, TP53 mutation has profound effects on tumor cell genomic structure, expression, and clinical outlook.
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In the citing paper
“TP53 is a negative regulator of cellular proliferation and is classed as a TSG, but it does not conform to this pattern; most mutational events in it are missense mutations dispersed across more than half of the protein (Fig. 1b,c) [6].”
From The TP53 tumor suppressor gene: From molecular biology to clinical investigations (2025) · cites this paper as [6]
In the citing paper
“TP53 is the most frequently mutated gene in human malignancies, 50% of which carry alterations to it.”
From The TP53 tumor suppressor gene: From molecular biology to clinical investigations (2025) · cites this paper as [6]
In the citing paper
“TP53 is the most frequently mutated gene in human malignancies, 50% of which carry alterations to it.”
From The TP53 tumor suppressor gene: From molecular biology to clinical investigations (2025) · cites this paper as [6]
In the citing paper
“most mutational events in it are missense mutations dispersed across more than half of the protein (Fig. 1b,c) [6].”
From The TP53 tumor suppressor gene: From molecular biology to clinical investigations (2025) · cites this paper as [6]
In the citing paper
“Situations involving different mutations in the two different alleles have also been observed, but they are very infrequent [6].”
From The TP53 tumor suppressor gene: From molecular biology to clinical investigations (2025) · cites this paper as [6]
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Cites
Subramanian, A., Tamayo, P., Mootha, V. K., Mukherjee, S., Ebert, B. L., Gillette, M. A., Paulovich, A., Pomeroy, S. L., Golub, T. R., Lander, E. S., et al. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0506580102 · Cited by 53,625
Cerami, E., Gao, J., Dogrusoz, U., Gross, B. E., Sumer, S. O., Aksoy, B. A., Jacobsen, A., Byrne, C. J., Heuer, M. L., Larsson, E., et al. (2012) · Cancer Discovery · doi:10.1158/2159-8290.cd-12-0095 · Cited by 17,455
Mootha, V. K., Lindgren, C. M., Eriksson, K.-F., Subramanian, A., Sihag, S., Lehar, J., Puigserver, P., Carlsson, E., Ridderstråle, M., Laurila, E., et al. (2003) · Nature Genetics · doi:10.1038/ng1180 · Cited by 10,197
Analysis of protein-coding genetic variation in 60,706 humans
Exome Aggregation Consortium, Lek, M., Karczewski, K. J., Minikel, E. V., Samocha, K. E., Banks, E., Fennell, T., O’Donnell-Luria, A. H., Ware, J. S., Hill, A. J., et al. (2016) · Nature · doi:10.1038/nature19057 · Cited by 9,587
The cancer genome atlas pan-cancer analysis project
The Cancer Genome Atlas Research Network, Weinstein, J. N., Collisson, E. A., Mills, G. B., Shaw, K. R. M., Ozenberger, B. A., Ellrott, K., Shmulevich, I., Sander, C., & Stuart, J. M. (2013) · Nature Genetics · doi:10.1038/ng.2764 · Cited by 9,092
Self-citationp53 Mutations in Human Cancers
Hollstein, M., Sidransky, D., Vogelstein, B., & Harris, C. C. (1991) · Science · doi:10.1126/science.1905840 · Cited by 8,018
Lane, D. P. (1992) · Nature · doi:10.1038/358015a0 · Cited by 5,138
Genetic instabilities in human cancers
Lengauer, C., Kinzler, K. W., & Vogelstein, B. (1998) · Nature · doi:10.1038/25292 · Cited by 4,168 · cited 1×
“Moreover, amplifications have been shown experimentally to be enhanced by mutant TP53 due in part to defective double-strand break repair and absence of p53-mediated apoptosis in response to proliferation of cells with double-strand DNA breaks (Hanel and Moll, 2012; Lengauer et al., 1998; Livingstone et al., 1992).”
BackgroundBlinded 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
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
Cited by
Targeting p53 pathways: mechanisms, structures, and advances in therapy
Wang, H., Guo, M., Wei, H., & Chen, Y. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01347-1 · Cited by 1,016
New Horizons in the Treatment of Osteosarcoma
Meltzer, P. S., & Helman, L. J. (2021) · New England Journal of Medicine · doi:10.1056/nejmra2103423 · Cited by 672
Bernard, E., Nannya, Y., Hasserjian, R. P., Devlin, S. M., Tuechler, H., Medina-Martinez, J. S., Yoshizato, T., Shiozawa, Y., Saiki, R., Malcovati, L., et al. (2020) · Nature Medicine · doi:10.1038/s41591-020-1008-z · Cited by 648
Ordered and deterministic cancer genome evolution after p53 loss
Baslan, T., Morris, J. P., Zhao, Z., Reyes, J., Ho, Y.-J., Tsanov, K. M., Bermeo, J., Tian, S., Zhang, S., Askan, G., et al. (2022) · Nature · doi:10.1038/s41586-022-05082-5 · Cited by 221
Kopetz, S., Murphy, D. A., Pu, J., Ciardiello, F., Desai, J., Van Cutsem, E., Wasan, H. S., Yoshino, T., Saffari, H., Zhang, X., et al. (2024) · Nature Medicine · doi:10.1038/s41591-024-03235-9 · Cited by 82
Metadata
- Authors
- Donehower, L. A., Soussi, T., Korkut, A., Liu, Y., Schultz, A., Cardenas, M., Li, X., Babur, O., Hsu, T.-K., Lichtarge, O., Weinstein, J. N., Akbani, R., & Wheeler, D. A.
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2019-07
- Volume
- 28
- Issue
- 5
- Pages
- 1370-1384.e5
- ISSN
- 2211-1247 (ISSN-L)
- OpenAlex
- W2964649258
- Cited by
- 710
- References
- 18
- FWCI
- 30.11
- Type
- journal article
- Language
- en
- Open access
- gold
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- Donehower, L. A., Soussi, T., Korkut, A., Liu, Y., Schultz, A., Cardenas, M., Li, X., Babur, O., Hsu, T.-K., Lichtarge, O., Weinstein, J. N., Akbani, R., & Wheeler, D. A. (2019). Integrated Analysis of TP53 Gene and Pathway Alterations in The Cancer Genome Atlas. Cell Reports. https://doi.org/10.1016/j.celrep.2019.07.001
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