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Various wavelengths of UV light are absorbed by the DNA and other molecules in the skin to cause DNA damage and induce oxidative stress. The exposure to excessive ultraviolet (UV) radiation and\/or accumulation of damage over time can lead to photocarcinogenesis and photoaging. The nucleotide excision repair (NER) system is the sole mechanism for removing UV photoproduct damage from DNA, and genetic disruption of this repair pathway leads to the photosensitive disorder xeroderma pigmentosum (XP). Interestingly, recent work has shown that NER is controlled by the circadian clock, the body's natural time\u2010keeping mechanism, through regulation of the rate\u2010limiting repair factor xeroderma pigmentosum group A (XPA). Studies have shown reduced UV\u2010induced skin cancer after UV exposure in the evening compared to the morning, which corresponds with times of high and low repair capacities, respectively. However, most studies of the circadian clock\u2013NER connection have utilized murine models, and it is therefore important to translate these findings to humans to improve skin cancer prevention and chronotherapy.<\/jats:p>","DOI":"10.1111\/php.12662","type":"journal-article","created":{"date-parts":[[2016,11,16]],"date-time":"2016-11-16T13:59:45Z","timestamp":1479304785000},"page":"296-303","source":"Crossref","is-referenced-by-count":54,"title":["Impact of the Circadian Clock on UV\u2010Induced DNA Damage Response and Photocarcinogenesis"],"prefix":"10.1111","volume":"93","author":[{"given":"Panshak","family":"Dakup","sequence":"first","affiliation":[{"name":"Experimental and Systems Pharmacology College of Pharmacy Washington State University Spokane WA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shobhan","family":"Gaddameedhi","sequence":"additional","affiliation":[{"name":"Experimental and Systems Pharmacology College of Pharmacy Washington State University Spokane WA"},{"name":"Sleep and Performance Research Center Washington State University Spokane WA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2016,12,18]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2011.02.013"},{"key":"e_1_2_8_3_1","unstructured":"2016 National Cancer Institute Bethesda National Cancer Institute N. 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