Cited by 1,906Cancer-related Molecular PathwaysPI3K/AKT/mTOR signaling in cancerCell death mechanisms and regulation

Putting p53 in context

Open access
Kastenhuber, Edward R., Lowe, Scott W.·2017·Cell

Abstract

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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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)
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
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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