光発癌

抄録

The exposure of mammalian cells to ultraviolet radiation (UV) leads to DNA damage, resulting in mutation and possible cancer. UV irradiation has been shown to act both as a tumor initiator and as a tumor promoter. The initiation step by UV involves genetic changes in oncogenes and tumor suppressor genes such as ras, p53, and patched. p53 mutations can be detected in normal skin from sun-exposed sites, indicating the early event of multi-step carcinogenesis. Furthermore, the activation of telomerase may precede the p53 mutation. The molecular mechanisms of UV-induced tumor promotion, principally the epigenetic phenomenon, remain elusive. Molecules acting as tumor promoters in photocarcinogenes include PKC, free radicals, tumor necrosis factor-α, and cyclooxygenase-2. In addition, UV-induced apoptosis is deeply involved in tumor promotion, because resistance to apoptosis is closely associated with the acceleration of tumor formation. The roles of p 53, Fas/FasL, tumor necrosis factor-α, nerve growth factor, and DNA damage in UV-induced apoptosis are discussed.