Antibodies against EphB4 were found to inhibit tumor growth and angiogenesis, some of which are being investigated for anticancer therapy in preclinical studies. Eph receptor antibodies that were conjugated to small molecule drugs caused internalization of drugs and inhibition of tumor growth in vivo. Soluble extracellular domain of EphB4 targeting ephrin-B2 has been used in inhibiting angiogenesis and tumor growth in vivo. We have found that mAb EC8 potently antagonized ephrin-B2 binding to EphB4, which would block forward and reverse signaling by EphB4 and ephrin-B2 interaction. Similar to the observation of EphB4 upregulation in some tumors, when human tissue array was probed with mAb EC8, ephrin-B2 was found to be also overexpressed in tumors in lung, breast, ovary, colon, and prostate over respective normal tissue. Consistent with the previous observation of ephrinB2 expression in tumor-associated vasculature, EC8 delineated ephrin-B2 expression in newly formed vessels within the tumor. Upregulation of ephrin-B2 was also found in colorectal cancer cell lines, COLO205 and HT108 both in cell culture and as a tumor xenograft in mice. Notably, due to the cross-reactive nature of antibody with murine ephrin-B2, mAb EC8 also identified tumorassociated vasculature, simultaneously detecting ephrin-B2 in human tumor as well as ephrin-B2 in murine host. Neovasculatures in adults sprouting from arterial vessels and capillaries, whether caused by VEGF-signaling, tissue injury, or tumor growth, were found to express ephrin-B2. It is unknown how ephrin-B2 upregulation in some of the tumors of epithelium origin would perturb the balance BAY 43-9006 between ephrin-B2 and Eph4 expressed in arterial and venous vessels, respectively, and contribute to the tumor growth and metastasis. Given the observation that overexpression of ephrin-B2 in some tumors is correlated with poor prognosis, it will be an interesting question if the role of ephrin-B2 together with EphB receptors in some tumor is associated with the promotion of the vasculature growth and the adenoma-carcinoma transition, facilitating tumor metastasis. We propose that high affinity and antagonist antibodies such as EC8 would provide a valuable tool for examining the role of ephrin-B2 expression on tumor angiogenesis and migration. Body weight is normally maintained within a narrow range by an appropriate balance between energy intake and energy expenditure. An increase of energy intake leads to excess energy storage in white adipose tissue and weight gain. Genetic background, excessive food consumption, sedentary lifestyle, and decreased physical activity are the main predisposing factors for alteration of energy balance. However a multitude of perinatal factors can alter the metabolic fate of offspring. We previously demonstrated, on a widely used animal model of nutritional programming, that low birth weight, as a consequence of an intrauterine growth restriction, leads to metabolic alterations and feeding behaviour abnormalities when followed by a rapid catch-up growth. In complement to that work we demonstrated that rapid catch-up growth of IUGR rats lead to a reduction of leptin sensitivity at postnatal day 5 and 12 in arcuate nucleus. Since leptin is a critical neurotrophic factor and seems essential for the normal axonal outgrowth of NPY/AgRP and POMC neurons from the ARC to the PVH that occur during that period, a reduced action will have consequence on the ontogeny of hypothalamic regulatory.