We have a broad interest in molecular mechanisms of cancer therapeutics and mechanism of chemoresistance.  Our lab has made several key contributions to understanding transcriptional mechanisms linked to the retinoic acid induced differentiation of testicular cancer and to the curability and resistance of testicular cancer through global gene expression and genome-wide analysis.  This includes our finding that testicular cancer cells display a hyperactive p53 response to chemotherapy that is tightly linked to their curability.  The goal of the lab is to leverage this information toward success in treating refractory testicular cancer and other solid tumors.  For example, we have identified key molecular targets important for progression of glioblastoma and breast cancer.  Recently our lab made the discovery that testicular cancers, even those resistant to cisplatin, highly overexpress DNA methyltransferase 3B and have increased sensitivity to very low doses of DNA demethylating agents compared to somatic cancer cells. This work provided the rationale for a phase I clinical trial.  We seek to elucidate mechanisms that will inform epigenetic-based therapies for refractory testicular cancers and other solid tumors.  Understanding these mechanisms will inform epigenetic-based therapies for refractory testicular cancers and other solid tumors. Through collaborative research we have also generated and characterized several genetically engineered mouse models of cancer including developing cyclin E overexpressing mice as a model of lung cancer, the USP18 knockout mouse as a model of leiomyosarcoma and the G0S2 knockout mouse.