Putting p53 in context
Open accessAbstract
TP53 is the most frequently mutated gene in human cancer. Functionally, p53 is activated by a host of stress stimuli and, in turn, governs an exquisitely complex anti-proliferative transcriptional program that touches upon a bewildering array of biological responses. Despite the many unveiled facets of the p53 network, a clear appreciation of how and in what contexts p53 exerts its diverse effects remains unclear. How can we interpret p53's disparate activities and the consequences of its dysfunction to understand how cell type, mutation profile, and epigenetic cell state dictate outcomes, and how might we restore its tumor-suppressive activities in cancer?
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TP53 is the most commonly mutated gene in human cancer.
“Because TP53 is the most commonly mutated gene in human cancer3,52”
From Single-cell multi-omics identifies chronic inflammation as a driver of TP53-mutant leukemic evolution (2023) · cites this paper as [3]
p53 plays a key role in manifestation of cellular senescence via several different mechanisms.
“p53, famously known as the ‘Guardian of the genome’ plays a key role in manifestation of cellular senescence via several different mechanisms (Lane, 1992; Kastenhuber and Lowe, 2017).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Kastenhuber and Lowe, 2017
Activated p53 regulates expression of a set of anti-proliferative genes.
“Activated p53 regulates expression of a set of anti-proliferative genes (Olivier et al., 2010; Kastenhuber and Lowe, 2017).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Kastenhuber and Lowe, 2017
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- Authors
- Kastenhuber, E. R., & Lowe, S. W.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Corresponding author
- Lowe, Scott W.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2017-09
- Volume
- 170
- Issue
- 6
- Pages
- 1062-1078
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC5743327
- OpenAlex
- W2752942423
- Cited by
- 1,906
- References
- 194
- Citations by year
- 2026: 155 · 2025: 221 · 2024: 214 · 2023: 268 · 2022: 250 · 2021: 244 · 2020: 247 · 2019: 172 · 2018: 119 · 2017: 14 · 2016: 1
- FWCI
- 15.86
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NCI/National Institutes of Health (F31CA192835)
- Howard Hughes Medical Institute
- Geoffrey Beene Chair for Cancer Biology
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- TP53, p53, tumor suppressor, cancer, p53 activation, stress response, transcriptional programs, antiproliferative activity, cell types, mutational landscape, p53 restoration, p53 dysfunction
- MeSH terms
- Animals, Humans, Mutation, Neoplasms, Genes, p53, Tumor Suppressor Protein p53, Epigenesis, Genetic
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