Abstract

it is a form of superficial squamous cell carcinoma (SCC) [7-9]. Sunlight kerato-sis results from abnormal proliferation of keratinocytes of sun-exposed skin. Common sites of occurrence are neck, hands, arms and head including the vermilion border of the lips, most frequently the lower lip [10, 11]. Sunlight keratotic lesions are dry, skin-coloured or brownish, rough macules or papules [1, 4]. The term sunlight keratosis refers only to the appearance of the lesion and to its aetiology, but not to its pathobiological behaviour or histopathological features. If left untreated the risk of progression of sunlight keratosis to invasive SCC can be as high as 20% per year [4, 9]. Keratinocytes of sunlight keratosis that are destined to remain stable and those that are destined to progress to SCC are morphologically indistinguishable. They both arise from keratinocytes that have undergone initial sunlight-induced transformation [7, 8, 12]. Sunli-ght keratosis may represent the first change in the con-tinuum of sunlight-induced carcinogenesis [13, 14] and the potential for progression to SCC can only be judged retrospectively on the basis of DNA molecular profile and their behaviour. Sunlight keratosis should be treated promptly as soon as it is diagnosed [9, 11].The aetiology of sunlight keratosis is long-term cumu-lative exposure to the ultraviolet-B (UVB) component of sunlight. Those at risk of sunlight keratosis include people with fair complexions, those in outdoor occupa-tions, those who are immunocompromized, and those with certain hereditary conditions, importantly oculocu-taneous albinism and xeroderma pigmentosum [4, 11]. Protective measures against sunlight keratosis should be related to the aetiological and risk factor [15].

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