Our findings thus suggested at least two mechanisms whereby lymphatic HS might be specifically required for CCL21-mediated colonization of lymph nodes by tumor cells: Namely, through the ability of lymphatic endothelial HS to as serve as either a co-receptor for chemokine-mediated tumor migration signaling or as an essential scaffold for peri-lymphatic chemokine gradients (or both). Here, CCL21 is linked to neoplasm.