Advertisement

UVR-Induced Skin Cancer

  • Jyoti Singh
Chapter

Abstract

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.

Keywords

Epidemiological Photocarcinogenesis DNA damage Mutation 

References

  1. Benjamin, C. L., & Ananthaswamy, H. N. (2007). p53 and the pathogenesis of skin cancer. Toxicology and Applied Pharmacology, 224(3), 241–248.CrossRefGoogle Scholar
  2. Birch-Machin, M. A., Russell, E. V., & Latimer, J. A. (2013). Mitochondrial DNA damage as a biomarker for ultraviolet radiation exposure and oxidative stress. British Journal of Dermatology, 169, 9–14.CrossRefGoogle Scholar
  3. 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
  4. De Gruijl, F. R. (2008). UV-induced immunosuppression in the balance. Photochemistry and Photobiology, 84(1), 2–9.PubMedGoogle Scholar
  5. de Laat, W. L., Jaspers, N. G., & Hoeijmakers, J. H. (1999). Molecular mechanism of nucleotide excision repair. Genes & Development, 13(7), 768–785.CrossRefGoogle Scholar
  6. Hanneman, K. K., Cooper, K. D., & Baron, E. D. (2006). Ultraviolet immunosuppression: mechanisms and consequences. Dermatologic Clinics, 24(1), 19–25.CrossRefGoogle Scholar
  7. Kripke, M. L., Cox, P. A., Alas, L. G., & Yarosh, D. B. (1992). Pyrimidine dimers in DNA initiate systemic immunosuppression in UV-irradiated mice. Proceedings of the National Academy of Sciences, 89(16), 7516–7520.CrossRefGoogle Scholar
  8. 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
  9. Levine, A. J. (1997). p53, the cellular gatekeeper for growth and division. Cell, 88(3), 323–331.CrossRefGoogle Scholar
  10. 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
  11. 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
  12. 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
  13. Schuch, A. P., Moreno, N. C., Schuch, N. J., Menck, C. F. M., & Garcia, C. C. M. (2017). Sunlight damage to cellular DNA: Focus on oxidatively generated lesions. Free Radical Biology and Medicine, 107, 110–124.CrossRefGoogle Scholar
  14. Schwarz, A., Ständer, S., Berneburg, M., Böhm, M., Kulms, D., van Steeg, H., Grosse-Heitmeyer, K., Krutmann, J., & Schwarz, T. (2002). Interleukin-12 suppresses ultraviolet radiation-induced apoptosis by inducing DNA repair. Nature Cell Biology, 4(1), 26.CrossRefGoogle Scholar
  15. Schwarz, A., Noordegraaf, M., Maeda, A., Torii, K., Clausen, B. E., & Schwarz, T. (2010). Langerhans cells are required for UVR-induced immunosuppression. Journal of Investigative Dermatology, 130(5), 1419–1427.CrossRefGoogle Scholar
  16. Setlow, R. B. (1982). DNA repair, aging, and cancer. National Cancer Institute Monograph, 60, 249–255.PubMedGoogle Scholar
  17. 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
  18. Toews, G. B., Bergstresser, P. R., & Streilein, J. W. (1980). Epidermal Langerhans cell density determines whether contact hypersensitivity or unresponsiveness follows skin painting with DNFB. The Journal of Immunology, 124(1), 445–453.PubMedGoogle Scholar

Copyright information

© Springer Nature Singapore Pte Ltd. 2019

Authors and Affiliations

  • Jyoti Singh
    • 1
    • 2
  1. 1.Photobiology laboratory, Systems Toxicology and Health Risk Assessment GroupCSIR-Indian Institute of Toxicology ResearchLucknowIndia
  2. 2.Academy of Scientific and Innovative ResearchNew DelhiIndia

Personalised recommendations