I have studied skin carcinogenesis and the biology of keratinocytes in response to DNA damaging agents like ultraviolet (UV) light for more than 12 years. I have made several key contributions to understanding the process of skin carcinogenesis by studying how the p53 family of tumor suppressors is involved in transcriptional regulation and coordinating keratinocyte responses to DNA damaging agents. By delivering a nuclear-targeted DNA repair protein through the epidermis to increase the rate of...[Read full text]I have studied skin carcinogenesis and the biology of keratinocytes in response to DNA damaging agents like ultraviolet (UV) light for more than 12 years. I have made several key contributions to understanding the process of skin carcinogenesis by studying how the p53 family of tumor suppressors is involved in transcriptional regulation and coordinating keratinocyte responses to DNA damaging agents. By delivering a nuclear-targeted DNA repair protein through the epidermis to increase the rate of repair of UV-induced DNA damage in basal keratinocytes, I demonstrated the feasibility of a potential clinical strategy for prevention of SCC, which may one day be of use for patients such as organ transplant recipients who are at up to 100 fold increased risk of developing SCC compared to the general population. My current research aims to understand how and why UV-damaged keratinocytes remain within the skin structure to later become cancerous rather than undergoing apoptosis or exiting the skin through differentiation. I am studying the roles of cell-cell adhesion desmosomal proteins in coordinating global keratinocyte responses to UV exposure within the 3D skin structure, including cell cycle arrest, proliferation, apoptosis, and differentiation. My research offers novel and unique perspectives about epidermal recovery in response to environmental injury, a topic on which very little is currently known.[Shorten text]
