We hypothesized that a synthetic matrix rich in integrin-binding peptides derived from collagen and fibronectin/vitronectin, mimicking aspects of the remodeled epithelium that is observed natively during tumor progression, would activate breast cancer cells relative to a matrix rich in integrin-binding peptides derived from laminin, mimicking aspects of a healthy mammary epithelium, with the potential for synergies with matrix stiffness. The gene discussed is VTN; the disease is neoplasm.