研究目的
Investigating the genetic and molecular mechanisms of human skin response to ultraviolet radiation, including pigmentation, tanning, DNA damage and repair, and the role of MC1R gene expression and p53 mutation.
研究成果
Ultraviolet radiation induces DNA strand breaks either directly or through oxidative pathways that may eventually lead to tumorigenesis. UV-induced melanomagenesis can be mediated via various pathways. UV radiation can enhance vitamin D3 synthesis in skin, thereby increasing the chances of survival of melanoma patients. For protection from UV-induced lesions, repair systems of the cells work efficiently. Nucleotide excision repair (NER) clears DNA damages such as CPDs and 6-4 PP. p53 gene mutation is most common mutation that consequently can lead to cancer transformation associated with chronic sun exposure.