Different types of DNA damage play different roles in the etiology of sunlight‐induced melanoma

Mitchell, David L.; Fernandez, André A.

doi:10.1111/j.1755-148x.2010.00789.x

Cited by 26 publications

(21 citation statements)

References 56 publications

(65 reference statements)

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“…Importantly, the mutagenicity of a site-specific CPD containing the 5'-TC sequence also is very low with >95% accurate lesion bypass [63], and the bypass of a CPD-containing 5-methylcytosine is even more than 99% accurate [64]. The exact contribution of (6-4)PPs to UV mutagenesis is essentially unknown [6, 7, 65] and may strongly depend on wavelength [50]. Although (6-4)PPs are mutagenic when studied as single site-specific lesions in vitro or in transfection experiments, their direct contribution to solar UV mutagenesis in mammalian cells is probably minor.…”

Section: Uv Mutagenesismentioning

confidence: 99%

“…Although (6-4)PPs are mutagenic when studied as single site-specific lesions in vitro or in transfection experiments, their direct contribution to solar UV mutagenesis in mammalian cells is probably minor. This is because they are repaired much more rapidly than the CPD photoproducts [53, 65, 66] and because they are induced only at very low levels by wavelengths in terrestrial sunlight [50]. Importantly, using a set of mutation reporter cell lines expressing exogenous photolyase genes [either CPD-specific photolyase or (6-4)-specific photolyase] we have shown that the CPDs are responsible for >80% of the UVB-induced mutations in DNA repair-proficient mammalian cells [43].…”

Section: Uv Mutagenesismentioning

confidence: 99%

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UV wavelength-dependent DNA damage and human non-melanoma and melanoma skin cancer

Pfeifer

Besaratinia

2012

Photochem Photobiol Sci

381

299

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Ultraviolet (UV) irradiation from the sun has been epidemiologically and mechanistically linked to skin cancer, a spectrum of diseases of rising incidence in many human populations. Both non-melanoma and melanoma skin cancers are associated with sunlight exposure. In this review, we discuss the UV wavelength-dependent formation of the major UV-induced DNA damage products, their repair and mutagenicity and their potential involvement in sunlight-associated skin cancers. We emphasize the major role played by the cyclobutane pyrimidine dimers (CPDs) in skin cancer mutations relative to that of (6-4) photoproducts and oxidative DNA damage. Collectively, the data implicate the CPD as the DNA lesion most strongly involved in human cancers induced by sunlight.

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Section: Uv Mutagenesismentioning

confidence: 99%

Section: Uv Mutagenesismentioning

confidence: 99%

UV wavelength-dependent DNA damage and human non-melanoma and melanoma skin cancer

Pfeifer

Besaratinia

2012

Photochem Photobiol Sci

381

299

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“…Of biological relevance for human exposure are the UVA (320–400 nm) and the UVB (280–320 nm) components of sunlight that reach the earth’s surface. While UVA is weakly mutagenic and produces both oxidative DNA damage products, mostly at guanines, and low levels of cis-syn cyclobutane pyrimidine dimers (CPDs) (1–5), UVB is considered a more powerful mutagen due to its ability to effectively produce CPDs and to a lesser extent (6–4)PPs (3, 6). The earth’s atmospheric layer removes most of the radiation with wavelengths less than 300 nm making UVB-induced photoproducts the type of DNA damage with the highest biological relevance.…”

Section: Introductionmentioning

confidence: 99%

Formation of cyclobutane pyrimidine dimers at dipyrimidines containing 5-hydroxymethylcytosine

Kim

Jin

Pfeifer

2013

Photochem Photobiol Sci

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Much of the cancer-causing effects of ultraviolet radiation from the sun have been linked to the formation of dimerized DNA bases. These dimeric DNA photoproducts include the cyclobutane pyrimidine dimers (CPDs) and the pyrimidine(6–4)pyrimidone photoproducts [(6–4)PPs). CPDs are highly mutagenic and are produced in substantial quantities by UVB radiation. These dimers can form between any two adjacent pyrimidines and can involve thymine, cytosine, or 5-methylcytosine. Very recently, a sixth DNA base, 5-hydroxymethylcytosine (5hmC) has been identified and characterized as a normal component of mammalian DNA. Here, we investigated the formation of CPDs at different DNA sequences containing 5hmC following irradiation with UVA, UVB, or UVC light sources. We show that the formation of CPDs at dipyrimidines containing 5hmC occurs at different DNA sequences but is not enhanced relative to cytosine or 5-methylcytosines at the same sequence positions. In fact, in some sequence contexts, CPDs containing 5hmC are formed at very low levels. Nonetheless, CPD formation at 5hmC pyrimidines is expected to be biologically relevant since three types of human skin-derived cells, fibroblasts, keratinocytes and melanocytes, all contain detectable levels of this modified base.

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“…the latter can further undergo a UVB -dependent conversion to Dewar pyrimidinones, their valence isomers (40). it is believed that cPDs play a major role in UV-induced mutagenesis (25,30). Mutations known to be caused by UV (UV-signatures) have been found in the P53 gene of about 80% of precancerous skin lesions and in about 90% of squamous skin cancers (32).…”

Section: Uv Damage Basicsmentioning

confidence: 99%

Repair, Abort, Ignore? Strategies for Dealing With UV Damage

Tummala¹,

Khalil²,

Zhelev³

2011

Biotechnology & Biotechnological Equipment

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Different types of DNA damage play different roles in the etiology of sunlight‐induced melanoma

Cited by 26 publications

References 56 publications

UV wavelength-dependent DNA damage and human non-melanoma and melanoma skin cancer

UV wavelength-dependent DNA damage and human non-melanoma and melanoma skin cancer

Formation of cyclobutane pyrimidine dimers at dipyrimidines containing 5-hydroxymethylcytosine

Repair, Abort, Ignore? Strategies for Dealing With UV Damage

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