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GIORNALE ITALIANO DI DERMATOLOGIA E VENEREOLOGIA

A Journal on Dermatology and Sexually Transmitted Diseases


Official Journal of the Italian Society of Dermatology and Sexually Transmitted Diseases
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Giornale Italiano di Dermatologia e Venereologia 2006 October;141(5):471-4

language: English

Pathogenesis of actinic keratoses

Nino M., Santoianni P.

Unit of Dermatology Department of Systemic Pathology Federico II University, Naples, Italy


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Experimental, epidemiologic and clinical studies in the last years underline the importance of longer ultraviolet (UV) in actinic keratoses. Most UV-induced lesions are repaired but mutations and immunological modifications can appear and modify the surveillance against UV-induced cancerogenetic elements. Oncosuppressor genes (p53 and others) have a protective role and UV modifies the expression of some molecules (ligand CD05, TRIAL e TRIAL receptors) that preserve cell integrity and transformation. Numerous important photoprotection endogenous systems activated by radiation, become not sufficient after intense and prolonged UV-irradiation. Actinic keratoses can evolve into epitheliomas. Transformation is induced by cumulative solar radiation effects. Progression of actinic keratoses versus carcinoma is correlated with region 9 p21 deletion codifying for tumor suppressor p 16 (INK4a). An initial step of actinic keratoses progression from dysplastic status versus carcinoma is the expression of metalloproteinase (MMP-1). UV-induced DNA damage activates repairing systems and MSH2 system. Recent studies demonstrate that feomelanin/eumelanin can represent a parameter as risk index for skin damage.

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