A dynamic platelet—tumor cell axis

Adam Corken, Jerry Ware


A dynamic reciprocating crosstalk between cancer cells and platelets presents both opportunities and challenges for an increased understanding of tumorigenesis and improved patient therapies (1). The importance of understanding this relationship finds merit in the widespread use of cardiovascular therapies that target normal platelet function but impact diseases seemingly unrelated to hemostasis or thrombosis (2). In the case of cancer, there exists expanding databases to support anti-cancer effects for common medications, such as aspirin (3). However, major questions remain for “how, where, and when” aspirin exerts its effect on the progression of cancer. A systematic approach for understanding the “how, when and where” question can be based on defining the platelet’s relevance within each component of the “hallmarks of cancer” (4-6).