Slow Repair of Pyrimidine Dimers at p53 Mutation Hotspots in Skin Cancer
Abstract
Ultraviolet light has been linked with the development of human skin cancers. Such cancers often exhibit mutations in the p53 tumor suppressor gene. Ligation-mediated polymerase chain reaction was used to analyze at nucleotide resolution the repair of cyclobutane pyrimidine dimers along the p53 gene in ultraviolet-irradiated human fibroblasts. Repair rates at individual nucleotides were highly variable and sequence-dependent. Slow repair was seen at seven of eight positions frequently mutated in skin cancer, suggesting that repair efficiency may strongly contribute to the mutation spectrum in a cancer-associated gene.
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NER is the most versatile repair system.
“NER is the most versatile repair system and eliminates a wide repertoire of DNA lesions, among which are UV-induced CPD and 6-4PP, that represent the main determinants in solar mutagenesis and skin cancer [105,106].”
From Mind the gap: keeping UV lesions in check (2011) · cites this paper as [106]
CPD and 6-4PP are key drivers of sunlight-induced mutagenesis and skin cancer.
“NER is the most versatile repair system and eliminates a wide repertoire of DNA lesions, among which are UV-induced CPD and 6-4PP, that represent the main determinants in solar mutagenesis and skin cancer [105,106].”
From Mind the gap: keeping UV lesions in check (2011) · cites this paper as [106]
NER removes many DNA lesions, among them UV-induced CPD and 6-4PP.
“NER is the most versatile repair system and eliminates a wide repertoire of DNA lesions, among which are UV-induced CPD and 6-4PP, that represent the main determinants in solar mutagenesis and skin cancer [105,106].”
From Mind the gap: keeping UV lesions in check (2011) · cites this paper as [106]
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References 30 · Cited by 296
- Authors
- Tornaletti, S., & Pfeifer, G. P.
- Affiliations
- City Of Hope National Medical Center (US)
- ORCID
- Pfeifer, Gerd P.
- Venue
- Science
- Published
- 1994-03-11
- Volume
- 263
- Issue
- 5152
- Pages
- 1436-1438
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2005344674
- Cited by
- 296
- References
- 30
- Citations by year
- 2023: 1 · 2022: 2 · 2020: 4 · 2019: 1 · 2018: 1 · 2017: 3 · 2016: 2 · 2015: 5 · 2014: 5 · 2013: 7 · 2012: 7
- FWCI
- 12.66
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Environmental Health Sciences (ES-06070)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
- Keywords
- cyclobutane pyrimidine dimers, DNA repair, p53, skin cancer, UV irradiation, mutational hotspots, mutation spectrum, human fibroblasts, tumor suppressor
- MeSH terms
- Cells, Cultured, DNA Repair, Exons, HeLa Cells, Humans, Mutation, Phosphoglycerate Kinase, Pyrimidine Dimers, Skin, Skin Neoplasms, Ultraviolet Rays, Polymerase Chain Reaction, Genes, p53
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