FIGURE 7.

Schematic summary. Proposed model of breast tumor‐mediated EC activation. Breast cancer cells promote EC activation, which is further enhanced by the presence of platelets. Tumor‐secreted VEGF‐A, as well as other potential mediators including TGF‐β1, play an important role in modulating breast cancer‐induced VWF secretion, which is negatively regulated by LMWH. Elevated VEGF‐A from breast tumor cells also contributes to a pro‐angiogenic effect on EC. VWF multimers released from activated EC in response to increased VEGF‐A levels can tether circulating breast tumor cells, which is inhibited by LMWH. Increased vascular permeability and tumor transendothelial migration is attenuated by LMWH.