Non-melanoma skin cancers (NMSCs) occur more frequently in the human population than any other type of malignancy. The exposure of skin to solar ultraviolet B (UVB) radiation causes DNA damage, most notably mutations in the p53 tumor suppressor gene. It is becoming increasingly clear that cell cycle regulators are potential targets for UVB-induced damage.  Particularly, the deregulation of cyclin D1 stability is a critical target in UVB-induced skin carcinogenesis, and its regulation is likely to be a key event in short- and long-term responses to UVB radiation. UVB-induced genotoxic/cellular stress leading to alteration in cell cycle regulation is closely linked to other signaling pathways, such as the hedgehog pathway for BCC development and p53-dependent DNA damage checkpoint signaling for SCC development. Dr. Kim's research interests focus on understanding the factors that influence cell cycle proliferation and other signaling pathways in UVB-induced cutaneous photodamage, leading to non-melanoma skin cancers.  Dr. Kim's research also focuses on the implementation of senescence, a state of terminal and irreversible growth arrest, as a potent anti-carcinogenic program.  Most conventional chemo/radiation modalities of cancer treatment, which induce cells to undergo apoptosis, are known to induce senescence in cancer cells.  However, the mechanisms of senescence in the tumor cell environment remain to be determined.  Identifying both the synthetic and natural compounds that can induce the senescence program in cancer cells, and determining the mechanisms involved in senescent induction in tumor cells, will be important for broadening the range of cancer prevention and treatment options.