Cited by 960Cancer-related Molecular PathwaysCancer, Hypoxia, and MetabolismMetabolism, Diabetes, and Cancer

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p53 and metabolism

Vousden, Karen H., Ryan, Kevin M.·2009·Nature Reviews Cancer

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Abstract

Although metabolic alterations have been observed in cancer for almost a century, only recently have the mechanisms underlying these changes been identified and the importance of metabolic transformation realized. p53 has been shown to respond to metabolic changes and to influence metabolic pathways through several mechanisms. The contributions of these activities to tumour suppression are complex and potentially rather surprising: some reflect the function of basal p53 levels that do not require overt activation and others might even promote, rather than inhibit, tumour progression.

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Authors: Vousden, K. H., & Ryan, K. M.
Affiliations: Cancer Research UK Scotland Institute (GB)
ORCID: Vousden, Karen H.
Ryan, Kevin M.
Venue: Nature Reviews Cancer
Publisher: Springer Science and Business Media LLC
Published: 2009-09-17
Volume: 9
Issue: 10
Pages: 691-700
ISSN: 1474-175X (ISSN-L)
1474-1768
DOI: 10.1038/nrc2715
OpenAlex: W1991510903
Cited by: 959
References: 134
Citations by year: 2026: 23 · 2025: 39 · 2024: 37 · 2023: 36 · 2022: 49 · 2021: 46 · 2020: 44 · 2019: 39 · 2018: 49 · 2017: 52 · 2016: 60 · 2015: 78 · 2014: 84 · 2013: 97 · 2012: 82
FWCI: 6.60
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Nature reviews. Cancer (publishedVersion)
PubMed (publishedVersion)
ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (submittedVersion)
Funders: Cancer Research UK
Topics: Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Keywords: p53, cancer metabolism, tumor suppression, tumor progression, metabolic pathways, cancer cells
MeSH terms: Autophagy, Cell Transformation, Neoplastic, Glycolysis, Humans, Neoplasms, Tumor Suppressor Protein p53, Oxidative Stress, Cell Proliferation

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