The onset and development of breast cancer is known to be a complex process involving reciprocal interactions between multiple cell types within the body. Epithelial, endothelial, mesenchymal and hematopoietic cells act together to alter and shape the microenvironment of the tumor to modulate the initiation, progression and dissemination of cancer. Their actions result in a dramatically altered extracellular matrix (ECM) from both a biochemical, but also biomechanical context. As such, over the past decade, solid tumors have become increasingly recognized as discrete organs, showing a complexity that approaches and perhaps even exceeds that of healthy tissue. These significant changes are the result of normal homeostatic mechanisms gone awry and as such make targeting them incredibly difficult.
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