Current Concepts in Ultraviolet Carcinogenesis

Granstein, Richard D.; Sober, Arthur J.

doi:10.3181/00379727-170-41406

Cited by 29 publications

(14 citation statements)

References 33 publications

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“…Our results could be interpreted as supporting the theory that it is the effect of intermittent episodes of acute exposure rather than that of cumulative exposure that is related to the development of melanoma other than LMM (Granstein & Sober, 1982;MacKie & Aitchison, 1982). However, they are also consistent with a dose-related theory of solar UV exposure and melanoma aetiology, where a high UV dose has been accumulated from multiple intense sunburning exposures.…”

Section: Discussionsupporting

confidence: 79%

“…There are no established criteria for measuring harmful sun exposure at the target-cell (melanocyte) level on which to base comparisons between populations or individuals. Ideally such criteria would allow quantitation of actual ultraviolet (UV) dose, as the specific carcinogenic wavelengths in sunlight are thought to lie in the UV range (Setlow, 1974), and especially in the UV-B band (280-320 nm) (Granstein & Sober, 1982 In a case-control study in Queensland, Australia, we have examined the relation of UV exposure to cutaneous melanoma by comparing the sunburn experiences accumulated over a lifetime in incident cases, with those of the general population. …”

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confidence: 99%

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Sunburn and malignant melanoma

Green¹,

Siskind²,

Bain³

et al. 1985

Br J Cancer

137

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Summary We investigated the relationship between cutaneous malignant melanoma and multiple sunburns in the Queensland population. Interview data were gathered from 236 case-control pairs concerning their lifetime experience of severe sunburns, their occupational and recreational sun exposure, and their skin type. Excluding the lentigo maligna melanoma subtype, an association between multiple sunburns and melanoma was evident. After controlling for other major risk factors there was a significant dose-response relationship (P < 0.05): the estimated relative risk associated with 2-5 sunburns in life was 1.5, and with 6 or more was 2.4. This observation extends the hitherto circumstantial evidence of a causal relationship between exposure to solar ultraviolet radiation and melanoma, and suggests that precautionary measures could prevent the development of this disease in a proportion of cases in fair-skinned populations.In spite of the widely held view that exposure to sunlight is related to melanoma, there is a lack of direct supporting evidence (Editorial, Lancet 1981). This may be related in part to problems in quantifying the harmful solar radiation that penetrates the epidermis during sun exposure. There are no established criteria for measuring harmful sun exposure at the target-cell (melanocyte) level on which to base comparisons between populations or individuals. Ideally such criteria would allow quantitation of actual ultraviolet (UV) dose, as the specific carcinogenic wavelengths in sunlight are thought to lie in the UV range (Setlow, 1974), and especially in the UV-B band (280-320 nm) (Granstein & Sober, 1982 In a case-control study in Queensland, Australia, we have examined the relation of UV exposure to cutaneous melanoma by comparing the sunburn experiences accumulated over a lifetime in incident cases, with those of the general population. Materials and methods SubjectsCases were residents of Queensland, who were reported as having a first primary cutaneous melanoma between 1 July, 1979 and 30 June, 1980. The histological diagnoses were provided by pathology laboratories throughout the state. From the year's total of 871 cases, 243 eligible cases were selected at random, 236 (97%) of whom were successfully contacted and interviewed. Controls were randomly selected from the total population by means of electoral rolls (enrolment is compulsory). They were matched to individual cases by age within 5 years, sex and place of residence. The 236 controls represented 92% of the eligible persons contacted (a further 13 were not at the address listed and could not be contacted). ProtocolAll subjects were interviewed by one of us (A.G.) using a standard questionnaire. Respondents were asked to recall all episodes of severe sunburn where pain had persisted longer than 48 h, with or without blistering. The number of sunburn experiences (to a maximum of 9) was recorded for the age groups 0-9, 10-19, 20-29 years, and 30 years and over. Virtually all burns reported occurred before age 40 (there were only 8 sunburns...

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Section: Discussionsupporting

confidence: 79%

mentioning

confidence: 99%

Sunburn and malignant melanoma

Green¹,

Siskind²,

Bain³

et al. 1985

Br J Cancer

137

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“…6) ERCC1 polymorphisms may contribute to the risk of squamous cell carcinoma of the head and neck. 11) There have been considerable efforts to search for naturally occurring substances that intervene in photodamage and photoaging.…”

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confidence: 99%

“…[4][5][6] The major types of DNA damage induced by UVB in the skin are DNA photoproducts, of which about 75% are cyclobutane pyrimidine dimers (CPDs) and the remaining 25% are (6-4) photoproducts (6-4 PPs) and Dewar isomers of 6-4 PPs.7) Most UVB-induced DNA lesions are removed by nucleotide excision repair (NER). 8) There are more than 20 proteins involved in NER.…”

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Ginsenoside Rb1 Suppresses Ultraviolet Radiation-Induced Apoptosis by Inducing DNA Repair

Cai

Jin

Luo

et al. 2009

Biological & Pharmaceutical Bulletin

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UV radiation, in particular the middle wavelength (UVB, range 290-320 nm), can be harmful to human health because it induces cancer, premature skin aging, immunosuppression, and cell death.1-3) UV-induced DNA damage is the crucial molecular trigger for many UV-induced effects, such as apoptosis, immunosuppression, and carcinogenesis. [4][5][6] The major types of DNA damage induced by UVB in the skin are DNA photoproducts, of which about 75% are cyclobutane pyrimidine dimers (CPDs) and the remaining 25% are (6-4) photoproducts (6-4 PPs) and Dewar isomers of 6-4 PPs.7) Most UVB-induced DNA lesions are removed by nucleotide excision repair (NER). 8) There are more than 20 proteins involved in NER. 9) Among them, Xeroderma pigmentosum (XP)-C is considered to be one of the first proteins to recognize DNA damage during global genomic repair (GGR), a subpathway of NER. XPC is one of the most common complementation groups of XP. XPC patients have sun sensitivity and a 1000-fold increase in the incidence of skin cancers.10) The excision repair cross-complementing 1 (ERCC1)/XPF heterodimer is a DNA structure-specific endonuclease that participates in NER through cutting DNA at junctions where a single strand moves 5Ј to 3Ј away from a branch point with duplex DNA. 6) ERCC1 polymorphisms may contribute to the risk of squamous cell carcinoma of the head and neck. 11)There have been considerable efforts to search for naturally occurring substances that intervene in photodamage and photoaging. Ginseng has long been used as an herbal drug in traditional Oriental medicine. It has been suggested to have pharmacologic activities in the cardiovascular, endocrine, immune, and central nervous systems.12-16) The major pharmacologically active components of ginseng are ginsenosides, which are steroidal saponins comprising 3-6% of ginseng.17) Among 26 identified ginsenosides, ginsenosideRb1, -Ro, -Rg1, -Rc, and -Re are abundant. In particular, ginsenoside-Rb1 makes up 0.37-0.5% of ginseng extracts (http://www.netnam.vn/icasia/english/products/redkogin/ redkogind/redkogind.htm). These ginsenosides have been reported to show various biological functions including antiinflammatory activity and anti-tumor effects.18,19) However, their protective effects against UV-induced DNA damage have not been thoroughly studied. Therefore, in the present work, we investigated cell apoptosis, the production and clearance of CPDs induced by UVB, and XPC and ERCC1 protein levels and evaluated the protective effects of ginsenoside Rb1 on cultured skin keratinocytes. MATERIALS AND METHODS Cell Cultures and UV Irradiation XpcϪ knockout keratinocytes were isolated and cultured from the dorsal skin of Xpc Ϫ knockout mice. These keratinocytes were grown in MCDB 153 medium (Sigma, U.S.A.) supplemented with CaCl 2 30 mM, bovine pituitary extract, epidermal growth factor, insulin, hydrocortisone, ethanolamine, phosphoethanolamine, high amino acids, penicillin, and streptomycin. The keratinocyte cell line HaCaT was cultured in RPMI 1640 culture (Gibco, U.S.A.) medi...

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