It has become apparent that nitric oxide (NO) and other small redox-reactive molecules promote the disease progression of human cancers. Our research goals are focused on the identification of redox-related mechanisms and biomarkers that are expressed during chronic inflammation as it relates to the disease progression and poor clinical outcome of triple negative breast cancer (TNBC). Our collaborative work has demonstrated that elevated tumor expression of the inducible NO synthase isoform (iNOS or NOS2) and more recently, elevations in both NOS2 and cyclooxygenase-2 (COX2) strongly predict poor survival (HR 6 and HR 21, respectively) in TNBC patients. Mechanistically, these proteins promote drug resistance, metastasis and immunosuppression within the tumor microenvironment. We focus on using redox-specific mechanistic information to develop agents that target these pro-tumor pathways for improved clinical outcome.
