Our data suggest the upregulation of E-selectin on tumor associated vasculature (in contrast to P-selectin) may be less about metastatic cell homing and more as a factor directly contributing to the survival and regeneration of malignant cells such as by the creation of a protective niche and induction of pro-survival (AKT/NF-kB/mTOR pathway) signaling thereby promoting therapy resistance. Here, SELE is linked to neoplasm.