The DOI matches its Crossref record; 56 of the 57 references it cites were found in a registry or an index.
Short- and Long-Wave UV Light (UVB and UVA) Induce Similar Mutations in Human Skin Cells
Open accessAbstract
While the mutagenic and carcinogenic properties of longwave UV light (UVA) are well established, mechanisms of UVA mutagenesis remain a matter of debate. To elucidate the mechanisms of mutation formation with UVA in human skin, we determined the spectra of UVA- and UVB-induced mutations in primary human fibroblasts. As with UVB, we found the majority of mutations to be C-to-T transitions also with UVA. For both UVA and UVB, these transitions were found within runs of pyrimidines, at identical hotspots, and with the same predilection for the nontranscribed strand. They also included CC-to-TT tandem mutations. Therefore, these mutations point to a major role of pyrimidine dimers not only in UVB but also in UVA mutagenesis. While some differences were noted, the similarity between the spectra of UVA- and UVB-induced mutations further supports similar mechanisms of mutation formation. A non-dimer type of DNA damage does not appear to play a major role in either UVA or UVB mutagenesis. Therefore, the previously reported increasing mutagenicity per dimer with increasing wavelengths cannot be due to non-dimer DNA damage. Differences in the cellular response to UVA and UVB, such as the less prominent activation of p53 by UVA, might determine a different mutagenic outcome of UVA- and UVB-induced dimers.
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“It was found that most mutations were C fi T transitions at bipyrimidine sites (11,90,91), in fact the mutational hallmark of UV-induced CPDs.”
From Photoinduced Damage to Cellular DNA: Direct and Photosensitized Reactions† (2012) · cites this paper as [90]
Citations
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Fairbanks, B. D., Schwartz, M. P., Bowman, C. N., & Anseth, K. S. (2009) · Biomaterials · doi:10.1016/j.biomaterials.2009.08.055 · Cited by 1,206
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Metadata
- Authors
- Kappes, U. P., Luo, D., Potter, M., Schulmeister, K., & Rünger, T. M.
- Affiliations
- Boston University (US)
- AIT Austrian Institute of Technology GmbH (AT)
- Corresponding author
- Rünger, Thomas M.
- Venue
- Journal of Investigative Dermatology
- Publisher
- Elsevier BV
- Published
- 2006-03
- Volume
- 126
- Issue
- 3
- Pages
- 667-675
- ISSN
- 0022-202X (ISSN-L)
- OpenAlex
- W1983180437
- Cited by
- 200
- References
- 57
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 10 · 2023: 6 · 2022: 8 · 2021: 10 · 2020: 11 · 2019: 11 · 2018: 14 · 2017: 5 · 2016: 13 · 2015: 11 · 2014: 7 · 2013: 10 · 2012: 8
- FWCI
- 13.62
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of Investigative Dermatology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Cancer Society
- Deutsche Forschungsgemeinschaft
- Topics
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
- Keywords
- pyrimidine dimers, C-to-T transitions, mutational hotspots, primary human fibroblasts, skin cancer, p53 activation, DNA damage
- MeSH terms
- Base Sequence, Cell Line, DNA Damage, Humans, Molecular Sequence Data, Mutation, Pyrimidine Dimers, Skin, Ultraviolet Rays, Genes, p53
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