Evidence for DNA Damage as a Biological Link Between Diabetes and Cancer
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OBJECTIVE: This review examines the evidence that: Diabetes is a state of DNA damage; pathophysiological factors in diabetes can cause DNA damage; DNA damage can cause mutations; and DNA mutation is linked to carcinogenesis. DATA SOURCES: We retrieved information from the PubMed database up to January, 2014, using various search terms and their combinations including DNA damage, diabetes, cancer, high glucose, hyperglycemia, free fatty acids, palmitic acid, advanced glycation end products, mutation and carcinogenesis. STUDY SELECTION: We included data from peer-reviewed journals and a textbook printed in English on relationships between DNA damage and diabetes as well as pathophysiological factors in diabetes. Publications on relationships among DNA damage, mutagenesis, and carcinogenesis, were also reviewed. We organized this information into a conceptual framework to explain the possible causal relationship between DNA damage and carcinogenesis in diabetes. RESULTS: There are a large amount of data supporting the view that DNA mutation is a typical feature in carcinogenesis. Patients with type 2 diabetes have increased production of reactive oxygen species, reduced levels of antioxidant capacity, and increased levels of DNA damage. The pathophysiological factors and metabolic milieu in diabetes can cause DNA damage such as DNA strand break and base modification (i.e., oxidation). Emerging experimental data suggest that signal pathways (i.e., Akt/tuberin) link diabetes to DNA damage. This collective evidence indicates that diabetes is a pathophysiological state of oxidative stress and DNA damage which can lead to various types of mutation to cause aberration in cells and thereby increased cancer risk. CONCLUSIONS: This review highlights the interrelationships amongst diabetes, DNA damage, DNA mutation and carcinogenesis, which suggests that DNA damage can be a biological link between diabetes and cancer.
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Reduced expression of DNA repair genes due to increased levels of oxidative stress has been implicated in several other human diseases, including diabetes, obesity, and glaucoma.
“In fact, reduced expression of DNA repair genes due to increased levels of oxidative stress has been implicated with several other human diseases, including diabetes [84], obesity [137], and glaucoma [109].”
From DNA repair deficiency and senescence in concussed professional athletes involved in contact sports (2019) · cites this paper as [84]
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- Authors
- Lee, S. C., & Chan, J. C.
- Affiliations
- Shanxi University (CN)
- Corresponding author
- Lee, Shao Chin
- Venue
- Chinese Medical Journal
- Published
- 2015-06-05
- Volume
- 128
- Issue
- 11
- Pages
- 1543-1548
- ISSN
- 0366-6999 (ISSN-L)
- PMC
- PMC4733759
- OpenAlex
- W1500301819
- Cited by
- 106
- References
- 61
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 13 · 2023: 12 · 2022: 12 · 2021: 14 · 2020: 7 · 2019: 13 · 2018: 9 · 2017: 7 · 2016: 8 · 2015: 1 · 2014: 1
- FWCI
- 0.81
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by-nc-nd
- Locations
- Chinese Medical Journal (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
- Keywords
- DNA damage, diabetes mellitus, cancer, type 2 diabetes, carcinogenesis, oxidative stress, reactive oxygen species, antioxidant capacity, DNA strand breaks, DNA base modification, hyperglycemia, advanced glycation end products, free fatty acids, palmitic acid, mutagenesis, cancer risk
- MeSH terms
- Animals, Diabetes Mellitus, Type 2, DNA Damage, Humans, Neoplasms, Reactive Oxygen Species, Oxidative Stress
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