The lab has made several key contributions to understanding transcriptional and epigenetic mechanisms linked to the curability and resistance of testicular cancer. The goal of the lab is to leverage this information toward success in treating refractory testicular cancer and other solid tumors. The 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 Ib clinical trial of hypomethylating agent (HMA) plus cisplatin for cisplatin resistant testicular cancer which yielded promising results. Recently we conducted genome-wide epigenomic studies to establish a role for DNA hypermethylation and repression of the polycomb pathway in testicular cancer promotion, resistance, and response to therapy and the role of PFAS in promoting epigenetic mechanisms of testicular cancer progression. This work included preclinical validation of the polycomb demethylase, GSK-J4, for treating cisplatin refractory TGCTs. Our lab is one of the few labs in the world performing highly mechanistic basic and translational science in the area of cisplatin resistance and epigenetics of TGCTs. Our work has attracted worldwide attention, and we frequently interact with the Children’s Oncology Group (COG) and MaGIC, an international consortium dedicated to germ cell tumors, and are involved in planning the new HMA MaGIC/COG nationwide  trial. We also have a funded and active project involving breast cancer.