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Formation of UV-induced DNA damage contributing to skin cancer development
Open accessAbstract
UV-induced DNA damage plays a key role in the initiation phase of skin cancer. When left unrepaired or when damaged cells are not eliminated by apoptosis, DNA lesions express their mutagneic properties, leading to the activation of proto-oncogene or the inactivation of tumor suppression genes. The chemical nature and the amount of DNA damage strongly depend on the wavelength of the incident photons. The most energetic part of the solar spectrum at the Earth's surface (UVB, 280-320 nm) leads to the formation of cyclobutane pyrimidine dimers (CPDs) and pyrimidine (6-4) pyrimidone photoproducts (64PPs). Less energetic but 20-times more intense UVA (320-400 nm) also induces the formation of CPDs together with a wide variety of oxidatively generated lesions such as single strand breaks and oxidized bases. Among those, 8-oxo-7,8-dihydroguanine (8-oxoGua) is the most frequent since it can be produced by several mechanisms. Data available on the respective yield of DNA photoproducts in cells and skin show that exposure to sunlight mostly induces pyrimidine dimers, which explains the mutational signature found in skin tumors, with lower amounts of 8-oxoGua and strand breaks. The present review aims at describing the basic photochemistry of DNA and discussing the quantitative formation of the different UV-induced DNA lesions reported in the literature. Additional information on mutagenesis, repair and photoprotection is briefly provided.
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Metadata
- Authors
- Cadet, J., & Douki, T.
- Affiliations
- Université de Sherbrooke (CA)
- Centre National de la Recherche Scientifique (FR)
- Corresponding author
- Cadet, Jean
- Douki, Thierry
- Venue
- Photochemical & Photobiological Sciences
- Published
- 2018-12
- Volume
- 17
- Issue
- 12
- Pages
- 1816-1841
- ISSN
- 1474-905X (ISSN-L)
- 1474-9092
- OpenAlex
- W2784555568
- Cited by
- 435
- References
- 346
- Citations by year
- 2026: 47 · 2025: 41 · 2024: 41 · 2023: 62 · 2022: 83 · 2021: 65 · 2020: 49 · 2019: 38 · 2018: 9
- FWCI
- 6.53
- Type
- journal article
- Language
- en
- Open access
- green
- hal.science
- Licence
- Locations
- Photochemical & Photobiological Sciences (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- 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
- UV-induced DNA damage, skin cancer, cyclobutane pyrimidine dimers, 6-4 pyrimidone photoproducts, 8-oxo-7,8-dihydroguanine, UVA, UV-B radiation, DNA photoproducts, mutational signatures, DNA repair, photoprotection, apoptosis, proto-oncogenes, tumor suppressor, DNA strand breaks
- MeSH terms
- Proto-Oncogene Mas, Animals, DNA Damage, DNA Repair, Guanine, Humans, Melanins, Pyrimidine Dimers, Skin Neoplasms, Ultraviolet Rays, DNA Adducts
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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