The research in the Smart Lab involves the identification and characterization of genes/signaling pathways that are determinants of susceptibility to cancer, particularly as it relates to gene-environment interactions. We utilize genetic/molecular/cellular-based systems and powerful genetically engineered mouse models to define mechanisms by which environmental stressors induce skin cancer. We are especially interested in how cells respond to DNA damage and tumor stress to make decisions to live or die. These decisions and the ability to influence these programmed cell death decisions have important implications for tumor development and tumor regression. We are actively studying the role of the basic leucine zipper transcription factors, CCAAT/enhancer binding proteins (C/EBPs) and long noncoding RNAs in this process. Our laboratory has identified novel and critical roles for C/EBPs in skin cancer and oncogenic Ras-induced tumorigenesis, the DNA damage response involving the regulation G1/S checkpoint, regulation of p53-mediated apoptosis and keratinocyte and sebocyte differentiation and the Type 1 IFN response.