Epidemiological evidence suggests that skin cancers, non-melanocytic skin cancers (NMSCs) and melanoma are caused in the main by exposure to UV radiation (UVR) and repeated episodes of sunburn (erythema) in childhood and adulthood. Genetic susceptibility or phenotype, including the number of naevi on the skin, may have a role in the development of skin cancers for some populations and individuals. Exposure to UVR and susceptibility (phenotype) are risk factors associated with the incidence of sunburn, solar keratoses and precancerous lesions. The type of exposure - intermittent (i.e. lying for long periods in the sun on annual foreign holidays) or continuous (i.e. daily exposure over long periods, as in those working outdoors) - may differ between the three main types of cancer.7 It is thought that risk increases with increasing intermittency of exposure. Evidence supports this increased risk for melanoma, probably for BCC, but not for SCC. The risk for SCC appears to depend only on the accumulated amount of exposure to the sun.
The incidence of melanoma rises rapidly in Caucasians after 20 years of age. Fair-skinned individuals exposed to the sun are at higher risk. The best risk-reduction strategy is protection from UVR. Individuals with certain types of pigmented lesions (dysplastic or atypical naevi), several large non-dysplastic naevi, many small naevi, or with moderate freckling have a two- to three-fold risk of developing melanoma. Individuals with familial dysplastic naevus syndrome or with several dysplastic or atypical naevi are at high risk (greater than fivefold) risk of developing melanoma.8 Evidence for the relationship between total exposure to the sun and melanoma remains to be proved. Further evidence that UVR causes skin cancer has been provided from the observation that people with the rare genetic condition xeroderma pigmentation have a very high risk for skin cancer. Some studies show that individuals who have occupational sun exposure have a lower risk for melanoma than those with less exposure.9-11
Mutation of the p53 gene appears to be an important step in the development of skin cancers. Exposure to sunlight causes a number of chemical changes in DNA. If these changes are not repaired then mutation begins. DNA damage can produce signature mutations in DNA and these are hypothesised as being linked definitively to carcinogenesis. Signature mutations have been found on the tumour suppresser p53 gene in normal skin cells and their presence has been correlated with extent of exposure. Signature mutations in the p53 gene have also been found in BCC and SCC of the skin whereas they are rare in this gene in other types of cancer. In the general population there is conflicting evidence about excision repair of DNA and the risk for BCC.12-14
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