Mutations induced by ultraviolet light

Pfeifer, Gerd P.; You, Young-Hyun; Besaratinia, Ahmad

doi:10.1016/j.mrfmmm.2004.06.057

Cited by 684 publications

(662 citation statements)

References 105 publications

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“…UVC irradiation (<280 nm) caused direct DNA photodamage by inducing cyclobutane pyrimidine dimmers that were associated with mutagenesis and tumorigenesis (Pfeifer et al, 2005). DNA damage following UVC exposure induced G1/S cell cycle arrest (Gentile et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

In Vitro Biological Characterization of DCUN1D5 in DNA Damage Response

Wei

Li²,

Xu³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Background: Novel prognostic biomarkers or therapeutic molecular targets for laryngeal squamous cell carcinoma (LSCC) are an urgent priority. We here sought to identify multiple novel LSCC-associated genes. Methods: Using high-density microarray expression profiling, we identified multiple genes that were significantly altered between human LSCCs and paired normal tissues. Potential oncogenic functions of one such gene, DCUN1D5, were further characterized in vitro. Results: Our results demonstrated that DCUN1D5 was highly expressed in LSCCs. Overexpression of DCUN1D5 in vitro resulted in 2.7-fold increased cellular migration, 67.5% increased invasive capacity, and 2.6-fold increased proliferation. Endogenous DCUN1D5 expression was decreased in a time-dependent manner after genotoxic stress, and silencing of DCUN1D5 by siRNA decreased the number of cells in the S phase by 10.2% and increased apoptosis by 11.7%. Conclusion: Our data suggest that DCUN1D5 in vitro might have vital roles in DNA damage response, but further studies are warranted to assess its significance in vivo.

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Section: Discussionmentioning

confidence: 99%

In Vitro Biological Characterization of DCUN1D5 in DNA Damage Response

Wei

Li²,

Xu³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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“…11,12 These bulky DNA lesions can be repaired by the nucleotide excision repair (NER) system. 3,6 If not properly corrected, they are premutagenic by three conceivable models 6,11,[13][14][15][16] : (1) incorporation of T opposite the altered bases by DNA polymerases that treat them as if they were an adenine (A); (2) direct lesion bypass by an error-prone DNA polymerase that incorporates an A opposite a C within the pyrimidine dimer; and (3) deamination of C within the dimer, giving rise to T or the related uracil, followed by "correct" bypass during DNA replication. These errors may precede or occur during DNA replication, and cause C→T transitions (about 70%) or CC→TT tandem mutations (about 10%) that are termed "signature mutations" for UV(B) mutagenesis, namely they are specific to this mutagen.…”

Section: Direct Dna Damagementioning

confidence: 99%

“…18,19 Its genotoxic and cytotoxic actions are the result of photodynamic effects that are strongly oxygen-dependent (Figure 2). 6,[12][13][14]18 Once UVR is absorbed, mutagenic oxidative reactions between the excited chromophores and cellular DNA may be triggered via two main mechanisms 6,[12][13][14]18 : In type I photosensitized reactions the energy is directly transferred to DNA, whereas in type II photosensitized reactions the energy is transferred to molecular oxygen, with DNA damage occurring via ensuing reactive oxygen species (ROS).…”

Section: Direct Dna Damagementioning

confidence: 99%

The dark side of the light: mechanisms of photocarcinogenesis

Coelho

Matos

Apetato

2016

Clinics in Dermatology

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Ultraviolet radiation (UVR) can have a beneficial biologic impact on skin, but it is also the most significant environmental risk factor for skin cancer development. Photocarcinogenesis comprises a complex interplay between the carcinogenic UVR, skin, and the immune system. UVB is absorbed by the superficial skin layers and is mainly responsible for direct DNA damage, which, if unrepaired, can lead to mutations in key cancer genes. UVA is less carcinogenic, penetrates deeper in the dermis, and mainly causes indirect oxidative damage to cellular DNA, proteins, and lipids, via photosensitized reactions. UVR not only induces mutagenesis, altering proliferation and differentiation of skin cells, but also has several immunosuppressive effects that compromise tumor immunosurveillance by impairing antigen presentation, inducing suppressive cells, and modulating the cytokine environment. This review focuses upon molecular and cellular effects of UVR, regarding its role in skin cancer development.

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“…It is thought that UVA induced mutagenesis is mainly mediated by photosensitising reactions that generate reactive oxygen species. In one system it was suggested that T to G transversions are typical of UVA induced damage (Drobetsky et al, 1995) but in another G to T transversions were seen as well as small tandem base deletions (Pfeifer et al, 2005). There is no consensus on UVA signature somatic mutations in tumours.…”

Section: Wavelength Nm Relative Effectivenessmentioning

confidence: 99%