Nicholas Camarda

The advent of modern targeted cancer therapeutics has led to a tremendous improvement in patient survival. However, many of these therapies cause significant cardiovascular toxicity, and the molecular mechanisms by which these therapeutics induce vascular toxicity remain unknown. Specifically, I am investigating two types of drug-induced vascular toxicity: 1) hypertension caused by VEGF receptor inhibitors and 2) increased risk of arterial occlusive events (heart attack, stroke and peripheral vascular occlusion) by various tyrosine kinase inhibitors used to treat CML. Using a combination of cell culture, mouse models, and proteomic data-driven computational approaches, our goal is to identify mechanisms and co-treatments that will prevent vascular toxicity induced by novel cancer therapeutics.