Temporal changes in the incidence of malignant melanoma: Explanation from action spectra

Setlow, R. B.; Woodhead, Avril D.

doi:10.1016/0027-5107(94)90310-7

Cited by 87 publications

(55 citation statements)

References 24 publications

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“…Setlow's findings (17,18) were in agreement with the hypothesis that UVA was the predominant cause of melanoma (12,16,34,40).…”

Section: Introductionsupporting

confidence: 82%

“…The fish model is Xiphophorus, a swordtail-platyfish hybrid (17). The action spectrum for a melanocytic tumor resembling or possibly the same as melanoma in fish includes three peaks in the UVA, with a prominent peak at 365 nm (17,18,35). If the fish model is applicable to humans, convolution of the solar spectrum with the action spectrum for the fish model suggests that 90% of human melanoma is due to UVA (17).…”

Section: Discussionmentioning

confidence: 99%

“…Historically, it has been thought that the most important action spectrum for human melanoma is solely UVB (14,15), although a role for ultraviolet A (UVA) has been suspected (12,13,(16)(17)(18)(19)(20). The reported associations of sunscreen usage with melanoma and other skin cancers could not be explained by predisposing factors such as skin type.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Epidemiologic Evidence for Different Roles of Ultraviolet A and B Radiation in Melanoma Mortality Rates

Garland

Gorham

2003

Annals of Epidemiology

126

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“…Setlow's findings (17,18) were in agreement with the hypothesis that UVA was the predominant cause of melanoma (12,16,34,40).…”

Section: Introductionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Epidemiologic Evidence for Different Roles of Ultraviolet A and B Radiation in Melanoma Mortality Rates

Garland

Gorham

2003

Annals of Epidemiology

126

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“…An action spectrum for melanoma induction was proposed with maxima in the UVB (302/313 nm) and UVA (365 nm) ranges. Because UVA fluence is quantitatively much greater than UVB in sunlight incident to the earth's surface (∼10-fold), Setlow suggested that, on the basis of this action spectrum, UVA was more effective than UVB in causing melanomas in the human population (2,4). This report had significant public health consequences; it suggested that the use of commercially available sunscreens that effectively blocked UVB but not UVA encouraged more lengthy recreational sunlight exposure and thereby increased the exposure to UVA and its associated risks.…”

mentioning

confidence: 99%

Ultraviolet A does not induce melanomas in a Xiphophorus hybrid fish model

Mitchell

Fernandez

Nairn

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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We examined the wavelength dependence of ultraviolet (UV) radiation (UVR)-induced melanoma in a Xiphophorus backcross hybrid model previously reported to be susceptible to melanoma induction by ultraviolet A (UVA) and visible light. Whereas ultraviolet B (UVB) irradiation of neonates yielded high frequencies of melanomas in pigmented fish, UVA irradiation resulted in melanoma frequencies that were not significantly different from unirradiated fish. Spontaneous and UV-induced melanoma frequencies correlated with the degree of pigmentation as expected from previous studies, and the histopathology phenotypes of the melanomas were not found in significantly different proportions in UV-treated and -untreated tumor-bearing fish. Our results support the conclusion that a brief early-life exposure to UVB radiation causes melanoma formation in this animal model. These data are consistent with an essential role for direct DNA damage, including cyclobutane dimers and (6-4) photoproducts, in the etiology of melanoma.ultraviolet B | DNA damage | cyclobutane dimer | reactive oxygen species | melanin I n the late 1980s Setlow and coworkers used genetic hybrids from interspecific crosses involving several species of the fish genus Xiphophorus to investigate the effects of UVR on the induction of cutaneous malignant melanoma (CMM) (1). These pioneering studies demonstrated that ultraviolet B (UVB) irradiation of backcross hybrids generated from a specific genetic crossing scheme induced melanomas at significant frequencies above spontaneous levels. These results were later confirmed, and the genetic basis of UVB-induced melanoma susceptibility in this cross was recognized to be the same as in the well-studied spontaneous Xiphophorus hybrid melanoma model (2). In 1993, Setlow used a different Xiphophorus interspecies cross (designated as Sp-couchianus; Fig. 1) to study the wavelength dependence of melanoma induction and reported that wavelengths in the ultraviolet A (UVA) and visible ranges were effective in inducing melanomas in first-generation backcross (BC 1 ) hybrids generated from this particular cross (3). An action spectrum for melanoma induction was proposed with maxima in the UVB (302/313 nm) and UVA (365 nm) ranges. Because UVA fluence is quantitatively much greater than UVB in sunlight incident to the earth's surface (∼10-fold), Setlow suggested that, on the basis of this action spectrum, UVA was more effective than UVB in causing melanomas in the human population (2, 4). This report had significant public health consequences; it suggested that the use of commercially available sunscreens that effectively blocked UVB but not UVA encouraged more lengthy recreational sunlight exposure and thereby increased the exposure to UVA and its associated risks. Over the past 20 years, these data have become central to the debate on the role of UVA in melanoma and the risks associated with recreational and artificial exposures to UVA wavelengths.Debate over the action spectrum for melanoma has only intensified because subsequent r...

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“…Most studies have concentrated on the role of UV irradiation due to its high energy, photoreactivity, wide range of biological chromophores, specific cellular responses, and association with pathologies such as skin melanoma and cataract (1)(2)(3)(4). However, the role of visible light has been less extensively investigated, even though studies have demonstrated that visible light can induce cellular dysfunction and cell death both in vitro and in vivo (1)(2)(3)(5)(6)(7). The blue region (400 -500 nm) of the visible spectrum is likely to be particularly important because it has a relatively high energy, can penetrate tissue(s), and is associated with the occurrence of malignant melanoma in animal models (6,7).…”

mentioning

confidence: 99%

Blue Light Induces Mitochondrial DNA Damage and Free Radical Production in Epithelial Cells

Godley

Shamsi

Liang

et al. 2005

Journal of Biological Chemistry

379

294

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Exposure of biological chromophores to ultraviolet radiation can lead to photochemical damage. However, the role of visible light, particularly in the blue region of the spectrum, has been largely ignored. To test the hypothesis that blue light is toxic to non-pigmented epithelial cells, confluent cultures of human primary retinal epithelial cells were exposed to visible light (390 -550 nm at 2.8 milliwatts/cm 2 ) for up to 6 h. A small loss of mitochondrial respiratory activity was observed at 6 h compared with dark-maintained cells, and this loss became greater with increasing time. To investigate the mechanism of cell loss, the damage to mitochondrial and nuclear genes was assessed using the quantitative PCR. Light exposure significantly damaged mitochondrial DNA at 3 h (0.7 lesion/10 kb DNA) compared with darkmaintained controls. However, by 6 h of light exposure, the number of lesions was decreased in the surviving cells, indicating DNA repair. Isolated mitochondria exposed to light generated singlet oxygen, superoxide anion, and the hydroxyl radical. Antioxidants confirmed the superoxide anion to be the primary species responsible for the mitochondrial DNA lesions. The effect of lipofuscin, a photoinducible intracellular generator of reactive oxygen intermediates, was investigated for comparison. Exposure of lipofuscin-containing cells to visible light caused an increase in both mitochondrial and nuclear DNA lesions compared with non-pigmented cells. We conclude that visible light can cause cell dysfunction through the action of reactive oxygen species on DNA and that this may contribute to cellular aging, age-related pathologies, and tumorigenesis.

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Temporal changes in the incidence of malignant melanoma: Explanation from action spectra

Cited by 87 publications

References 24 publications

Epidemiologic Evidence for Different Roles of Ultraviolet A and B Radiation in Melanoma Mortality Rates

Epidemiologic Evidence for Different Roles of Ultraviolet A and B Radiation in Melanoma Mortality Rates

Ultraviolet A does not induce melanomas in a Xiphophorus hybrid fish model

Blue Light Induces Mitochondrial DNA Damage and Free Radical Production in Epithelial Cells

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