Joshua Lewis completed his undergraduate training at the State University of New York College of Environmental Science and Forestry in conjunction with Syracuse University receiving a bachelor's degree in biotechnology. He then completed his Ph.D. in Molecular Genetics and Genomics at the Center of Human Genomics and Personalized Medicine at Wake Forest University School of Medicine. Dr. Lewis completed his postdoctoral fellowship at the University of Maryland School of Medicine in the Division of Endocrinology, Diabetes, and Nutrition and in the Program in Personalized and Genomic Medicine. He was recruited to the Department of Medicine at the University of Maryland in 2012.
Cardiovascular disease is currently the leading causes of death in the United States. The goal of Dr. Lewis' research is to identify and functionally characterize genes contributing to cardiovascular disease in order to ultimately translate genetic discoveries into individualized patient care through pharmacogenomics and/or other clinical approaches.
Aspirin and clopidogrel therapy significantly improves cardiovascular outcomes in patients with various coronary syndromes by inhibiting platelet function. However, variable inter-individual responses to anti-platelet therapies exist resulting in increased risk of recurrent cardiovascular events in some patients. Dr. Lewis' objective is to identify genetic variants through candidate gene studies, genome-wide association analyses, and other "omics" approaches that contribute to differences in platelet response and to functionally elucidate the molecular mechanisms responsible for this variability. Studies by Dr. Lewis have shown that genetic variants in the Platelet Endothelial Aggregation Receptor 1 (PEAR1) gene are associated with platelet reactivity and cardiovascular outcomes in patients on aspirin therapy. He is currently exploring further the functional consequences of these polymorphisms in cellular models as well as in human populations. In addition, potential pharmacogenetic effects of paraoxonase 1 (PON1), carboxyesterase 1 (CES1), and ATP-binding cassette sub-family C member 4 (ABCC4) on clopidogrel efficacy are currently being investigated.