Genetic and epigenetic mechanisms contribute to the development of human tumors, yet the typical analysis of tumors is focused on only one or the other mechanism. This approach has led to a biased, primarily genetic view of human tumorigenesis. Epigenetic alterations such as aberrant DNA methylation are sufficient to induce tumor formation, and can modify the incidence and tumor type in genetic models of cancer. These initial studies raise important questions which our research addresses: understanding the degree to which genetic and epigenetic pathways cooperate in human tumorigenesis, the identity of the specific cooperating genes and how they interact functionally to determine the differing biological and clinical course of tumors.
To better understand the relative contribution of genetic and epigenetic mechanisms in human tumorigenesis, our lab utilizes global DNA methylation screening methods along with gene specific analysis, integrated comparative genomics and comparative epigenomics, and primary tumor xenografts. In collaborative research, we are focused on understanding the epigenetic regulation of cancer stem cells, particularly those in malignant brain tumors.