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Primary Prevention of Melanoma - UpToDate

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  Authors:  Alan C Geller, RN, MPH, Susan Swetter, MD Section Editors: Michael B Atkins, MD, Hensin Tsao, MD, PhD Deputy Editor: Rosamaria Corona, MD, DScContributor Disclosures All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through:  May 2019. | This topic last updated:  Jan 16, 2019. INTRODUCTION Melanoma has become a worldwide public health concern [1-3]. At least two-thirds of melanoma in light-skinned populations worldwide may be attributed to ultraviolet (UV)radiation exposure from both natural and artificial sources [4]. Based upon this andother data implicating UV light as a risk factor for melanoma, reducing exposure toUV radiation has been advocated as a method to reduce the incidence of thismalignancy [4,5].The observed decline in the incidence of invasive melanoma in the state of Queensland, Australia, among men and women under the age of 40 years from theperiod of 1995 to 2014 may be the result of sun awareness campaigns implementedin Australia on a national scale [6]. A similar reduction in melanoma incidence inyounger men and women (age ≤45) has been observed in the United States from theperiod of 2005 to 2014 [7]. Whether this reduction is related to increased sunprotection behaviors, decreased intentional tanning, or reduced use of tanning bedsamong adolescents and young adults remains unclear [7,8]. Interventions that may be relevant to the primary prevention of melanoma will be reviewed here. Screening and risk factors for melanoma are discussed separately. (See Screening and early detection of melanoma in adults and adolescents  and Risk factors for the development of melanoma .) ULTRAVIOLET RADIATION  Ultraviolet (UV) radiation is a known carcinogen [9]. Although a direct causalrelationship between UV radiation and melanoma has not been demonstrated inhumans, there is strong evidence in support of this relationship:Epidemiologic studies have found that the risk of melanoma is higher among fair-skinned people who have increased sensitivity to sunlight [5]. In the UnitedStates, the incidence of melanoma is at least 20 times greater in whites thanblacks, and the highest incidence of melanoma worldwide occurs in Queensland, Australia, a subtropical region with a predominantly Celtic population [10]. (See Risk factors for the development of melanoma , section on 'Geographic andethnic variation'.) ●  A study aimed at quantifying the global population attributable fraction (PAF) of melanomas due to UV radiation estimated that 168,000 new melanoma cases in2012 were attributed to excess exposure to UV radiation, representingapproximately 76 percent of all melanoma cases worldwide [11]. The globalburden was higher in men than in women (95,000 attributable cases; 81.3percent of all melanomas and 73,000; 69.4 percent, respectively). ●  Among families predisposed to melanoma because of genetic mutations, theincidence of melanoma is 21-fold higher for individuals born after 1959 comparedwith those born before 1900, presumably due to an interaction betweenincreased sun exposure and the predisposing gene mutation [12]. (See Inherited susceptibility to melanoma .) ● In the laboratory, melanocytic lesions, including melanoma, can be induced inhuman skin grafted onto mice after exposure to ultraviolet B (UVB) radiation, withor without an initiating carcinogen [13]. ● Other data implicate ultraviolet A (UVA) radiation as well as UVB as contributorsto melanoma development. Psoriasis patients treated over long periods with acombination of UVA and oral psoralen (PUVA) had a significant increase inmelanoma incidence [14,15]. (See Risk factors for the development of  melanoma , section on 'PUVA therapy'.) ● Several systematic reviews and meta-analyses of case-control studies found anapproximately 20 percent increase of melanoma risk among ever users of indoor tanning devices compared with nonusers [16-18]. The risk was higher for  ●  The exact pathways through which UV radiation can cause melanoma areincompletely understood. Two different, divergent epigenetic pathways that canresult in cutaneous melanoma are suggested by epidemiologic population-based data[20]. Individuals with an inherently low propensity for melanocyte proliferation mayrequire chronic sun exposure to drive clonal expansion. In contrast, those with a highpropensity for melanocyte proliferation (characterized by high nevus count) mayrequire less solar exposure to stimulate carcinogenesis [20]. (See Risk factors for the development of melanoma , section on 'Typical nevi'.)Unlike keratinocytes, which undergo apoptosis (programmed cell death) whenseverely damaged by UV radiation, damaged melanocytes tend to be preserved [21].This may be related to an effort by the body to continue to produce melanin, whichhas a photoprotective function in the skin [5]. The result, however, is that severelydamaged melanocytes that are at risk for incomplete DNA repair and subsequentmutation are preserved. UVB radiation (290 to 320 nm) causes the majority of DNAdamage in the epidermis. However, UVA may also be important in the pathogenesisof melanoma [22]. (See Risk factors for the development of melanoma , section on 'Ultraviolet radiation'.)The pattern and timing of exposure to sunlight appear to be important for melanomadevelopment. In contrast to nonmelanoma skin cancers (particularly squamous cellcarcinoma), which are associated with cumulative sun exposure and occur mostfrequently in areas maximally exposed to the sun (ie, the face, back of hands, andforearms), most melanomas are associated with intense, intermittent sun exposureindividuals reporting first use of sunbeds at a young age (before age 35) and for those with high exposure (≥10 sessions in lifetime). (See 'Tanning bed use' belowand Risk factors for the development of melanoma , section on 'Indoor tanning'.)One population-based cohort study using data from the Norwegian Women andCancer Study and including more than 140,000 women followed up for a mean of 14 years found that the risk of melanoma was increased by 25 percent amongwomen reporting ever use of indoor tanning versus never use and was higher for those who initiated indoor tanning use before the age of 30 years [19]. The riskincreased with increasing duration of use (≥10 years) and cumulative number of indoor tanning sessions (relative risk 1.61, 95% CI 1.27-2.05 for the highestquartile of cumulative number of sessions). ●  and tend to occur in areas exposed to the sun sporadically (eg, the back in men andwomen and lower legs in women) [23,24].Exposure in childhood seems particularly important; a history of five or more severesunburns in adolescence more than doubles the risk of developing melanoma [25].Furthermore, the incidence of melanoma is increased among people who migratedfrom northern to more equatorial latitudes but only among immigrants who werechildren at the time of migration [26,27]. (See Risk factors for the development of  melanoma , section on 'Ultraviolet radiation'.) SUN PROTECTION The classification of ultraviolet (UV) radiation as carcinogenic to humans and a riskfactor for melanoma and other skin cancers is used to support recommendations for sun protection [9]. Sun protection behaviors include the use of broad-spectrumsunscreen with a sun protection factor (SPF) of 15 for everyday use and at least SPF30 for intense sun exposure; wearing hats, sunglasses, and sun-protective clothing;reducing sun exposure; seeking shade during midday hours (10 AM to 4 PM); andavoiding indoor tanning bed use [28]. (See Risk factors for the development of  melanoma .) SunscreenEfficacy  — A systematic review for the US Preventive Services Task Force(USPSTF) in 2018 noted that although interventions focused on increasing sunprotection behavior (eg, reduced sun exposure, sunscreen use, use of protectiveclothing, avoidance of indoor tanning) were associated with a moderate increase of sun protection behaviors in both adults and children, there was no consistentassociation between these interventions and reduced sunburn frequency, nevuscount, or skin cancer incidence over one to three years of follow-up [29]. However,data from a follow-up study of a community-based, randomized trial in Queensland, Australia, a Norwegian population-based cohort study, and an Australian case-controlstudy support the use of sunscreen products [30].In the Australian trial, 1621 participants were randomly assigned to anintervention group (unlimited supply of SPF 16 sunscreen provided andparticipants instructed to engage in daily sunscreen use) or a discretionary ●
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