Our laboratory is primarily interested in studying how triggering "biomechanical ECM switches" within the stromal microenvironment governs angiogenesis, inflammation and tumor progression. We study the cellular and molecular mechanisms by which integrin receptors and proteolytic enzymes trigger unique biomechanical ECM switches that result in the exposure of cryptic ECM epitopes that modulate stromal and tumor cell behavior. We are especially interested in understanding how integrin receptor binding to these control sites regulates signaling pathways that contribute to these processes. Surprisingly, inhibition of cellular interactions with one of these cryptic ECM control elements significantly alters expression of insulin-like growth factor binding protein-4 (IGFBP-4) as well as the endogenous angiogenesis inhibitor TSP-1. Establishing a more in depth molecular understanding of the diverse functions of biomechanical ECM switches in vivo may contribute to the development of unique clinical strategies for imaging and control of tumor progression.