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Official Journal of the Italian Society of Dermatology and Sexually Transmitted Diseases
Indexed/Abstracted in: EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,014
Online ISSN 1827-1820
Nino M., Santoianni P.
Unit of Dermatology Department of Systemic Pathology Federico II University, Naples, Italy
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.