Our laboratory is focused on tumor metabolism and mechanisms of drug resistance, as well as the development of new tumor models for clinical use.  We found that cisplatin resistant (CR) cells activate kynurenine pathway (L-tryptophan catabolism) when they encounter excessive oxidative stress in order to maintain a finite level of reactive oxygen species (ROS) for their growth and proliferation. Consequently, this pathway becomes an essential pathway for their survival.  Importantly, kynurenine (L-KYN), which is oxidized through indoleamine 2,3-dioxygenase (IDO), plays a key role in reprogramming naïve T-cells to immune suppressive regulatory T-cell (T-reg) phenotype in CR tumor microenvironments.