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Ultraviolet radiation and skin cancer: molecular mechanisms
Author(s) -
Hussein Mahmoud R.
Publication year - 2005
Publication title -
journal of cutaneous pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.597
H-Index - 75
eISSN - 1600-0560
pISSN - 0303-6987
DOI - 10.1111/j.0303-6987.2005.00281.x
Subject(s) - carcinogenesis , cancer research , skin cancer , cancer , biology , dna damage , cell cycle , suppressor , melanoma , basal cell carcinoma , cell , hedgehog signaling pathway , dna repair , tumor suppressor gene , gene , dna , genetics , basal cell , pathology , medicine
Every living organism on the surface of the earth is exposed to the ultraviolet (UV) fraction of the sunlight. This electromagnetic energy has both life‐giving and life‐endangering effects. UV radiation can damage DNA and thus mutagenize several genes involved in the development of the skin cancer. The presence of typical signature of UV‐induced mutations on these genes indicates that the ultraviolet‐B part of sunlight is responsible for the evolution of cutaneous carcinogenesis. During this process, variable alterations of the oncogenic, tumor‐suppressive, and cell‐cycle control signaling pathways occur. These pathways include (a) mutated PTCH (in the mitogenic Sonic Hedgehog pathway) and mutated p53 tumor‐suppressor gene in basal cell carcinomas, (b) an activated mitogenic ras pathway and mutated p53 in squamous cell carcinomas, and (c) an activated ras pathway, inactive p16 , and p53 tumor suppressors in melanomas. This review presents background information about the skin optics, UV radiation, and molecular events involved in photocarcinogenesis.