My laboratory has a long-standing interest in understanding the molecular mechanisms by which inflammatory cytokines and cellular stresses activate the NF-κB and JNK pathways. NF-κB is constitutive activated in many types of cancer, and is known to promote cancer progression by inducing the expression of cytokines, chemokines, angiogenic-factors and anti-apoptotic proteins. However, targeting the core elements of the NF-κB pathway (e.g. TAK1, IKK and p65) for cancer therapy has failed repeatedly, due to severe side effects associated with immune suppression and disruption of epithelial homeostasis. Our long-term goal is to identify cell type- and disease-specific effectors upstream of the TAK1-IKK-NF-κB axis that lead to constitutive NF-κB activation in cancer cells, and to provide a foundation for the development of pathway-specific anti-cancer drugs.