Double‐strand breaks in DNA caused by repair of damage due to ultraviolet light

Bradley, Matthews O.

doi:10.1002/jsscb.1981.380160404

Cited by 14 publications

(13 citation statements)

References 18 publications

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“…They detected the formation of micronuclei, which are cytogenetic indicators of chromosomal damage in normal fibroblasts exposed to controlled doses of UVA or UVB radiation. These round particles of genetic material are believed to result from DNA double-strand breaks, which are hypothesized to form as a result of DNA repair of UV-induced pyrimidine dimers and/or free-radical formation (Bradley, 1981). These observations support mechanisms for the initiation and promotion of cancer as well as the increased genomic instability and loss of heterozygosity (LOH) observed in NMSC and associated lesions Rehman et al, 1996;Waring et al, 1996;Happle, 1999).…”

Section: Solar Uvr and Chromosomal Aberrationsmentioning

confidence: 99%

Cytogenetic alterations in nonmelanoma skin cancer: A review

Ashton

Carless

Griffiths

2005

Genes Chromosomes & Cancer

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Since the advent of cytogenetic analysis, knowledge about fundamental aspects of cancer biology has increased, allowing the processes of cancer development and progression to be more fully understood and appreciated. Classical cytogenetic analysis of solid tumors had been considered difficult, but new advances in culturing techniques and the addition of new cytogenetic technologies have enabled a more comprehensive analysis of chromosomal aberrations associated with solid tumors. Our purpose in this review is to discuss the cytogenetic findings on a number of nonmelanoma skin cancers, including squamous- and basal cell carcinomas, keratoacanthoma, squamous cell carcinoma in situ (Bowen's disease), and solar keratosis. Through classical cytogenetic techniques, as well as fluorescence-based techniques such as fluorescence in situ hybridization and comparative genomic hybridization, numerous chromosomal alterations have been identified. These aberrations may aid in further defining the stages and classifications of nonmelanoma skin cancer and also may implicate chromosomal regions involved in progression and metastatic potential. This information, along with the development of newer technologies (including laser capture microdissection and comparative genomic hybridization arrays) that allow for more refined analysis, will continue to increase our knowledge about the role of chromosomal events at all stages of cancer development and progression and, more specifically, about how they are associated with nonmelanoma skin cancer.

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Section: Solar Uvr and Chromosomal Aberrationsmentioning

confidence: 99%

Cytogenetic alterations in nonmelanoma skin cancer: A review

Ashton

Carless

Griffiths

2005

Genes Chromosomes & Cancer

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“…Moreover, CPD, 6-4 PP, base damages or adducts in a single strand (not repaired before DNA replication) may stall replication fork and consequently may produce an SSB in the opposite strand [Bender et al, 1973;Natarajan et al, 1980]. Also, when there are 2 nearby (facing each other) SSB in both DNA strands these may behave as a DSB [Bradley, 1981].…”

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confidence: 99%

Asynchronously Replicating Eu/Heterochromatic Regions Shape Chromosome Damage

Tomaso

Martínez‐López²,

Palitti³

2010

Cytogenet Genome Res

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In order to shed more light on the influence of DNA replication on the formation and distribution of chromosome aberrations, breakpoints (BP) produced by UV-C and AluI were assigned either to the early replicating short euchromatic arm (Xp_e) or to the late replicating long heterochromatic arm (Xq_h) of the Chinese hamster (CHO9) X chromosome. Early (ES) or late (LS) S-phase cells were assessed by pulse incorporating the base analogue 5-bromo-2′-deoxyuridine (BrdU) immediately after UV-C irradiation (30 J/m²) or AluI (20 U) poration followed by BrdU immunodetection with FITC-tagged antibodies in metaphase spreads. Short (30 s) UV-C exposures (1 J/m²/s) induced BP preferentially in Xq_h in LS cells and a random distribution of BP along Xp_e and Xq_h in ES cells. However, BP induced by long (5 min) UV-C exposures (0.1 J/m²/s) clustered according to arm replication time (Xp_e during ES and Xq_h along LS). Giemsa-stained metaphases showed elevated frequencies of UV-C induced chromatid-type aberrations and gaps, especially in cells exposed to longer UV-C irradiation. BP induced by AluI clustered in Xp_e in ES but distributed randomly during LS. In contrast to UV-C, AluI did not produce an increase in the yield of gaps, neither in ES nor in LS cells. Putative mechanisms underlying the observed distributions of chromosome damage in replicating CHO9 cells exposed to UV-C and AluI are discussed.

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“…This was first suggested by experiments in a yeast (Kiefer 1987;FrankenbergSchwager et al 1987). It was previously assumed that the accumulation of excision repair related single-strand breaks may also lead to DSBs (Bradley 1981;Bradley and Taylor 1983), but it was later shown that UV-induced DSBs were also involved in excision-defective cells (Kiefer and Feige 1993). Experiments with transformed human fibroblasts defective in the ability to bypass pyrimidine dimers during DNA replication (XP variants) showed that DSBs originate at stalled replication forks (Limoli et al 2002).…”

Section: Primary Photoproducts In Dnamentioning

confidence: 98%

Effects of Ultraviolet Radiation on DNA

Kiefer¹

Chromosomal Alterations

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UV radiation is selectively absorbed by DNA, mainly in the UV-B and the UV-C regions. Excitation of DNA leads to typical photoproducts, the most important being pyrimidine dimers and the so-called 6-4-photoproduct. The yield of strand breaks is very low directly after exposure, but they may be formed indirectly upon further incubation. Although DNA absorbs only weakly in the UV-A region, it may be damaged indirectly via endogenous photosensitisers. Photoproducts are subject to repair processes which are genetically determined. Photoreactivation splits selectively pyrimidine dimers but it is limited to lower eukaryotes and does not occur in mammalian cells. Nucleotide excision repair acts on various types of damage. UVinduced damage manifests itself also at the level of chromosomes. Chromatid-type aberrations are more frequent with UV irradiation than chromosomal aberrations. The action spectrum for their formation demonstrates that an indirect mechanism plays an important role in the UV-A region. Also micronuclei are found after broadband UV exposure which are presumably due to indirectly formed double-strand breaks. UV radiation is a strong inducer of sister-chromatid exchanges, in contrast to ionising radiation, where the yields are low. This suggests that strand breaks play only a minor role.

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Double‐strand breaks in DNA caused by repair of damage due to ultraviolet light

Cited by 14 publications

References 18 publications

Cytogenetic alterations in nonmelanoma skin cancer: A review

Cytogenetic alterations in nonmelanoma skin cancer: A review

Asynchronously Replicating Eu/Heterochromatic Regions Shape Chromosome Damage

Effects of Ultraviolet Radiation on DNA

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