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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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“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]
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“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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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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