Sunscreen use and intentional exposure to ultraviolet A and B radiation: a double blind randomized trial using personal dosimeters

Autier, Philippe; Jf, Doré; Ac, Reis; Grivegnee, André-Robert; Ollivaud, L.; Truchetet, F.; Chamoun, E; Rotmensz, Nicole; Severi, Gianluca; Jp, Césarini

doi:10.1054/bjoc.2000.1429

Cited by 123 publications

(72 citation statements)

References 24 publications

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“…In contrast to NCTC 2544 and empty vector control cells (NCTC-EV), the basal mRNA expression of AHR in NCTC-shAHR KC was decreased by approximately 80% (Figure 1a). Irradiation with 200 J/m 2 UVB, equivalent to the minimal erythema dose of fair-skinned individuals, 17 led to a significantly lower induction of the AHR target genes CYP1A1, COX-2, and plasminogen activator inhibitor-2 (PAI-2; involved in regulation of extracellular matrix degradation 18 ) in NCTC-shAHR cells compared with NCTC 2544 and NCTC-EV cells (Figure 1b), providing evidence that AHR signaling is significantly suppressed in these KC.…”

Section: Resultsmentioning

confidence: 99%

“…Based on our previous findings that UVB exposure of KC increases the expression of CYP1A1 and COX-2 in an AHR-dependent manner, it was postulated that AHR signaling contributes to the development of UVB-induced NMSC, 4,14 an idea that is further strengthened by the results of our present study. As the UVB doses used in this study, with 200 J/m 2 being equivalent to the minimal erythema dose of fair-skinned human individuals, 17 can be easily reached during recreational sunbathing, we propose that a transient antagonism of this signaling pathway, especially in times of extensive UV exposure, will be beneficial for the prevention of NMSC. It will be interesting to see, if this newly described anti-apoptotic…”

Section: Discussionmentioning

confidence: 98%

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Evidence for a novel anti-apoptotic pathway in human keratinocytes involving the aryl hydrocarbon receptor, E2F1, and checkpoint kinase 1

et al. 2013

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Exposure of keratinocytes (KC) to ultraviolet (UV) radiation results in the initiation of apoptosis, a protective mechanism that eliminates cells harboring irreparable DNA damage. Hence, a manipulation of UV-induced apoptosis may significantly influence photocarcinogenesis. We have discovered that the aryl hydrocarbon receptor (AHR), a key regulator of drug metabolism and an UVB-sensitive transcription factor, serves an anti-apoptotic function in UVB-irradiated human KC. Chemical and shRNA-mediated inhibition of AHR signaling sensitized KC to UVB-induced apoptosis by decreasing the expression of E2F1 and its target gene checkpoint kinase 1 (CHK1). The decreased expression of these cell-cycle regulators was due to an enhanced expression of p27 KIP1 and an associated decrease in phosphorylation of both cyclin-dependent kinase 2 and its substrate molecule retinoblastoma protein. The subsequent inhibition of E2F1 autoregulation and downstream CHK1 expression resulted in an enhanced susceptibility of damaged cells to undergo apoptosis. Accordingly, ectopic overexpression of either E2F1 or CHK1 in AHR-knockdown KC attenuated the observed sensitization to UVB-induced apoptosis. Using an AHR-knockout SKH-1 hairless mouse model, we next demonstrated the physiological relevance of the anti-apoptotic function of AHR. In contrast to their AHR-proficient littermates, the constitutive expression of E2F1 and CHK1 was significantly reduced in the skin of AHR-knockout mice. Accordingly, a single exposure of the animals to UVB resulted in an enhanced cleavage of caspase-3 in the skin of AHR-knockout mice. These results identify for the first time the AHR-E2F1-CHK1 axis as a novel anti-apoptotic pathway in KC, which may represent a suitable target for chemoprevention of non-melanoma skin cancer. With an annual incidence of two to three million new cases worldwide, non-melanoma skin cancer (NMSC) is one of the most frequent forms of cancer in humans (World Health Organization; http://www.who.int/uv/faq/skincancer/en/index1 .html). Typically, NMSCs, such as basal cell and squamous cell carcinomas, occur on sun-exposed areas of the skin, indicating that solar ultraviolet (UV) radiation, especially its UVB part (290-320 nm), is the most important etiological factor. 1,2 In fact, it is well established that UVB radiation gives rise to skin cancer without additional initiators or promoters and thus is a complete carcinogen. 1 Because of the thinning of the ozone layer, the increase in recreational sunbathing and the enhanced usage of UV tanning beds, the incidence of NMSC is expected to increase in future years, 1,2 underscoring the urgent need for novel preventives against UV-induced skin malignancies.When skin is exposed to solar radiation, high-energy UVB photons penetrate into the epidermis and initiate the so-called UVB response. 3 The main trigger of this stress response is the absorbance of UVB rays by DNA, which leads to the generation of highly mutagenic DNA photoproducts. 3,4 In addition, UVB exposure results in the formation...

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 98%

Evidence for a novel anti-apoptotic pathway in human keratinocytes involving the aryl hydrocarbon receptor, E2F1, and checkpoint kinase 1

et al. 2013

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“…This same concern has been advanced in studies showing that population that used sunscreen had greater melanocytic nevi, an indicator of sun exposure [9,10,11,12,18,19,148], although a recent study from Canada found that sunscreen reduced nevi in a randomized prospective design [74]. The negative effects of sunscreen may be most evident when individuals choose to be outdoors in the sun rather than when their time in the sun is determined by factors out of their control such as work schedules.…”

Section: Does Sun Safety Increase Time In the Sun?mentioning

confidence: 93%

Melanoma Epidemiology and Prevention

Berwick

Buller

Cust

et al. 2015

Cancer Treatment and Research

122

121

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The epidemiology of melanoma is complex, and individual risk depends on sun exposure, host factors, and genetic factors, and in their interactions as well. Sun exposure can be classified as intermittent, chronic, or cumulative (overall) exposure, and each appears to have a different effect on type of melanoma. Other environmental factors, such as chemical exposures-either through occupation, atmosphere, or food-may increase risk for melanoma, and this area warrants further study. Host factors that are well known to be important are the numbers and types of nevi and the skin phenotype. Genetic factors are classified as

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“…16,17 These trials were representative of sun exposure behaviors of millions of light-skinned young subjects eager to acquire a tan during holidays or during leisure times. The 2 trials demonstrated that sun exposure, mainly sunbathing, was 19-25% longer duration with use of SPF 30 than with use of SPF 10 sunscreens.…”

Section: The European Randomized Trialsmentioning

confidence: 99%

Sunscreen use and increased duration of intentional sun exposure: Still a burning issue

Autier

Boniol

Doré

2007

Intl Journal of Cancer

195

144

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Sunscreen use is often proposed for sun protection because of their ability to block UV-induced sunburns (the sun protection factor -SPF). Among suntan seekers, however, risk of cutaneous melanoma may be increased because of extended sun exposure duration. We made a systematic review of the evidence linking sunscreen use to sun exposure duration. Five observational studies found that when sun exposure was associated with willingness to get a tan or to stay longer in the sun (i.e., intentional sun exposure), sunscreen use was associated with duration of sun exposure 13-39% longer. Paradoxically, sunburns tend to be more frequent among sunscreen users, probably because of greater natural sun sensitivity. When sun exposure was not intentional, sunscreen use did not increase time spent in the sun. Two European double-blind randomized trials conducted among young sun seekers found daily sun exposure duration, especially sunbathing, 19-25% longer with use of SPF 30 than with use of SPF 10 sunscreens. One randomized trial in a holiday resort in France found a 3-13% increase in sun exposure duration with use of SPF 12 versus SPF 40 sunscreen. But, the SPF 12 groups used 3.6-4.2 more sunscreen than the SPF 40 group, and thus the actual SPF in the SPF 12 group was higher than in the SPF 40 groups. In conclusion, sunscreen use leads to longer duration of sun exposure when sun exposure is intentional, but not when sun exposure is non intentional. ' 2007 Wiley-Liss, Inc.

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Sunscreen use and intentional exposure to ultraviolet A and B radiation: a double blind randomized trial using personal dosimeters

Cited by 123 publications

References 24 publications

Evidence for a novel anti-apoptotic pathway in human keratinocytes involving the aryl hydrocarbon receptor, E2F1, and checkpoint kinase 1

Evidence for a novel anti-apoptotic pathway in human keratinocytes involving the aryl hydrocarbon receptor, E2F1, and checkpoint kinase 1

Melanoma Epidemiology and Prevention

Sunscreen use and increased duration of intentional sun exposure: Still a burning issue

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