The DOI matches its Crossref record; 188 of the 195 references it cites were found in a registry or an index.
p53, cancer and the immune response
Open accessAbstract
The importance of cancer-cell-autonomous functions of the tumour suppressor p53 (encoded by TP53) has been established in many studies, but it is now clear that the p53 status of the cancer cell also has a profound impact on the immune response. Loss or mutation of p53 in cancers can affect the recruitment and activity of myeloid and T cells, allowing immune evasion and promoting cancer progression. p53 can also function in immune cells, resulting in various outcomes that can impede or support tumour development. Understanding the role of p53 in tumour and immune cells will help in the development of therapeutic approaches that can harness the differential p53 status of cancers compared with most normal tissue.
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In the citing paper
“These mutations can affect the tumor immune microenvironment (TIME) by altering cytokine expression and regulating the tumor’s sensitivity to immune checkpoint inhibitors.”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [610]
In the citing paper
“It is widely accepted that gene mutations, including those affecting undruggable proteins, have a significant impact on the efficacy of cancer immunotherapy.”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [610]
In the citing paper
“For examples, cancer cells with functional wild-type genes tend to have a desirable cancer-restrictive TIME, while an imbalance in their expression can create a cancer-supportive TIME.610,611”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [610]
In the citing paper
“In brief, the status of genes can influence tumor cells not only through the impact of wild-type gene loss but also through their effects on the TIME.”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [610]
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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
Immunity, Inflammation, and Cancer
Grivennikov, S. I., Greten, F. R., & Karin, M. (2010) · Cell · doi:10.1016/j.cell.2010.01.025 · Cited by 10,755
Vogelstein, B., Lane, D., & Levine, A. J. (2000) · Nature · doi:10.1038/35042675 · Cited by 6,607
Freeman, G. J., Long, A. J., Iwai, Y., Bourque, K., Chernova, T., Nishimura, H., Fitz, L. J., Malenkovich, N., Okazaki, T., Byrne, M. C., et al. (2000) · The Journal of Experimental Medicine · doi:10.1084/jem.192.7.1027 · Cited by 5,294
Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
Donehower, L. A., Harvey, M., Slagle, B. L., McArthur, M. J., Montgomery, C. A., Butel, J. S., & Bradley, A. (1992) · Nature · doi:10.1038/356215a0 · Cited by 4,649
Helicobacter pylori Infection and the Development of Gastric Cancer
Uemura, N., Okamoto, S., Yamamoto, S., Matsumura, N., Yamaguchi, S., Yamakido, M., Taniyama, K., Sasaki, N., & Schlemper, R. J. (2001) · New England Journal of Medicine · doi:10.1056/nejmoa001999 · Cited by 4,492
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
Self-citationIFNγ and lymphocytes prevent primary tumour development and shape tumour immunogenicity
Shankaran, V., Ikeda, H., Bruce, A. T., White, J. M., Swanson, P. E., Old, L. J., & Schreiber, R. D. (2001) · Nature · doi:10.1038/35074122 · Cited by 2,896
Recommendations for myeloid-derived suppressor cell nomenclature and characterization standards
Bronte, V., Brandau, S., Chen, S.-H., Colombo, M. P., Frey, A. B., Greten, T. F., Mandruzzato, S., Murray, P. J., Ochoa, A., Ostrand-Rosenberg, S., et al. (2016) · Nature Communications · doi:10.1038/ncomms12150 · Cited by 2,751
Mutations in the p53 gene occur in diverse human tumour types
Nigro, J. M., Baker, S. J., Preisinger, A. C., Jessup, J. M., Hosteller, R., Cleary, K. R., Signer, S. H., Davidson, N. E., Baylin, S., Devilee, P., et al. (1989) · Nature · doi:10.1038/342705a0 · Cited by 2,730
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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
Drugging p53 in cancer: one protein, many targets
Hassin, O., & Oren, M. (2022) · Nature Reviews Drug Discovery · doi:10.1038/s41573-022-00571-8 · Cited by 771
Understanding the complexity of p53 in a new era of tumor suppression
Liu, Y., Su, Z., Tavana, O., & Gu, W. J. (2024) · Cancer Cell · doi:10.1016/j.ccell.2024.04.009 · Cited by 538
Mutant p53 in cancer: from molecular mechanism to therapeutic modulation
Chen, X., Zhang, T., Su, W., Dou, Z., Zhao, D., Jin, X., Lei, H., Wang, J., Xie, X., Cheng, B., et al. (2022) · Cell Death & Disease · doi:10.1038/s41419-022-05408-1 · Cited by 494
Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials
Xie, X., Yu, T., Li, X., Zhang, N., Foster, L. J., Peng, C., Huang, W., & He, G. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01589-z · Cited by 396
Metadata
- Authors
- Blagih, J., Buck, M. D., & Vousden, K. H.
- Affiliations
- The Francis Crick Institute (GB)
- Venue
- Journal of Cell Science
- Publisher
- The Company of Biologists
- Published
- 2020-03-01
- Volume
- 133
- Issue
- 5
- ISSN
- 0021-9533 (ISSN-L)
- 1477-9137
- OpenAlex
- W3009145316
- Cited by
- 333
- References
- 195
- Citations by year
- 2026: 27 · 2025: 48 · 2024: 63 · 2023: 63 · 2022: 63 · 2021: 51 · 2020: 18
- FWCI
- 5.34
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Cell Science (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Figshare (submittedVersion, cc-by)
- HighWire Press Open Archive (submittedVersion)
- The Francis Crick Institute (cc-by)
- Funders
- Cancer Research UK (C596/A26855, FC001557)
- Francis Crick Institute
- Medical Research Council (FC001557)
- Wellcome Trust (FC001557)
- Canadian Institutes of Health Research
- European Molecular Biology Organization (ALTF 1096-2018)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Keywords
- p53, antitumor immunity, immune evasion, TP53 mutation, myeloid cells, T cells, tumor progression, cancer immunotherapy, cancer cells
- MeSH terms
- Humans, Immunity, Mutation, Neoplasms, Tumor Suppressor Protein p53
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