From the epidemiological point of view, it is suggested that regular contacts to UVR irradiation since our childhood are the primary cause of skin tumors. UVR-induced ROS production caused DNA damage, immune suppression, and deactivation of tumor suppression genes or overactivation of proto-oncogene. These processes are interconnected with each other. Cyclobutane pyrimidine dimers (CPDs) and (6–4) photoproducts are main key products of DNA damage. Our body system has DNA repair mechanism which mainly involves nuclear excision repair and base excision repair pathways. Defect in repair pathways and continuous accumulation of mutation lead to photocarcinogenesis. DNA lesions are an important molecular mediator in initiation of immunosuppression which has a important role in the induction of UVR-mediated skin cancer. DNA damage induced by UVR involves inhabitation of cell cycle progress or apoptosis. P53 plays an important role in cell cycle; it arrests the G1 phage and removes DNA lesion. Mutations in P53 gene come into light as an early event in the progress of UV-induced skin cancers.
KeywordsEpidemiological Photocarcinogenesis DNA damage Mutation
- Chaisiriwong, L., Wanitphakdeedecha, R., Sitthinamsuwan, P., Sampattavanich, S., Chatsiricharoenkul, S., Manuskiatti, W., & Panich, U. (2016). A case-control study of involvement of oxidative DNA damage and alteration of antioxidant defense system in patients with basal cell carcinoma: Modulation by tumor removal. Oxidative Medicine and Cellular Longevity, 2016, 5934024.CrossRefGoogle Scholar
- Kulms, D., Pöppelmann, B., Yarosh, D., Luger, T. A., Krutmann, J., & Schwarz, T. (1999). Nuclear and cell membrane effects contribute independently to the induction of apoptosis in human cells exposed to UVB radiation. Proceedings of the National Academy of Sciences, 96(14), 7974–7979.CrossRefGoogle Scholar
- Mueller, G., Saloga, J., Germann, T., Schuler, G., Knop, J., & Enk, A. H. (1995). IL-12 as mediator and adjuvant for the induction of contact sensitivity in vivo. The Journal of Immunology, 155(10), 4661–4668.Google Scholar
- Nakazawa, H., English, D., Randell, P. L., Nakazawa, K., Martel, N., Armstrong, B. K., & Yamasaki, H. (1994). UV and skin cancer: Specific p53 gene mutation in normal skin as a biologically relevant exposure measurement. Proceedings of the National Academy of Sciences, 91(1), 360–364.CrossRefGoogle Scholar
- Rochette, P. J., Therrien, J. P., Drouin, R., Perdiz, D., Bastien, N., Drobetsky, E. A., & Sage, E. (2003). UVA-induced cyclobutane pyrimidine dimers form predominantly at thymine–thymine dipyrimidines and correlate with the mutation spectrum in rodent cells. Nucleic Acids Research, 31(11), 2786–2794.CrossRefGoogle Scholar
- Sharma, P., Jha, A. B., Dubey, R. S., & Pessarakli, M. (2012). Reactive oxygen species, oxidative damage, and antioxidative defense mechanism in plants under stressful conditions. Journal of Botany, 2012.Google Scholar