The molecular pathways of ultraviolet-induced carcinogenesis
Abstract
Cancer development requires the accumulation of numerous genetic changes which are usually believed to occur through the presence of unrepaired DNA lesions. Exogenous or endogenous DNA-damaging agents can lead to mutations in the absence of efficient error-free repair, via replication of DNA damage. Several DNA repair pathways are present in living cells and well-conserved from bacteria to human cells. The nucleotide excision repair (NER), the most versatile of these DNA repair systems, recognizes and eliminates a wide variety of DNA lesions and particularly those induced by ultraviolet (UV) light. The phenotypic consequences of a NER defect in humans are apparent in rare but dramatic diseases characterized by hypersensitivity to UV and a striking clinical and genetic heterogeneity. The xeroderma pigmentosum (XP) syndrome is a human disorder inherited as an autosomal recessive trait. Persistence of unrepaired DNA damage produced by exposure to UV light is associated, in the XP syndrome, with an extremely high level of skin tumors in sun-exposed sites. Several key genes are mutagenized by UV-light and are responsible for skin cancer development. Mutations are found on ras oncogenes, p53 and PTCH tumour suppressor genes in skin cancers from DNA repair proficient as well as XP patients. The typical signature of UV-induced mutations found on these genes allows one to conclude that the uvB part of sunlight is responsible for the initiation of the carcinogenesis process.
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Exposure to UV irradiation in sunlight causes NMSC by inducing DNA damage that, if replicated, leads to mutations in genes such as KRAS or TP53.
“Exposure to UV irradiation in sunlight causes NMSC by inducing DNA damage that if replicated, leads to mutations in genes such as KRAS or TP537”
From Modulation of UVB-induced Carcinogenesis by Activation of Alternative DNA Repair Pathways (2018) · cites this paper as [7]
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- Authors
- Sarasin, A.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- Corresponding author
- Sarasin, Alain
- ORCID
- Sarasin, Alain
- Venue
- Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis
- Publisher
- Elsevier BV
- Published
- 1999-07
- Volume
- 428
- Issue
- 1-2
- Pages
- 5-10
- ISSN
- 0027-5107 (ISSN-L)
- 1386-1964
- OpenAlex
- W2042064223
- Cited by
- 215
- References
- 20
- Citations by year
- 2025: 3 · 2024: 3 · 2023: 2 · 2022: 3 · 2021: 3 · 2020: 3 · 2019: 6 · 2018: 6 · 2017: 5 · 2016: 10 · 2015: 9 · 2014: 11 · 2013: 11 · 2012: 9
- FWCI
- 3.79
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Mutation research. Fundamental and molecular mechanisms of mutagenesis (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
- Keywords
- DNA repair, nucleotide excision repair, xeroderma pigmentosum, UV-induced mutations, skin cancer, oncogenic Ras, p53, UV-B radiation, DNA damage, UV hypersensitivity
- MeSH terms
- Patched Receptors, Patched-1 Receptor, DNA Damage, DNA Repair, Humans, Membrane Proteins, Mutation, Neoplasms, Genes, ras, Receptors, Cell Surface, Skin Neoplasms, Ultraviolet Rays, Xeroderma Pigmentosum, Genes, p53
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