Quantification of murine endothelial cell adhesion molecules in solid tumors

Coordinated adhesive interactions between lymphocyte receptors and endothel ial cell adhesion molecules (CAMs)are a prerequisite for effector cell entr y into tumor stroma. Whereas the diminished leukocyte-endothelial cell inte ractions observed in tumor microvessels have been attributed to a reduced e xpression of endothelial CAMs, there is no quantitative data bearing on thi s issue. The dual-radiolabeled monoclonal antibody technique was used to qu antify constitutive and tumor necrosis factor (TNF)-alpha-induced expressio n of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion mol ecule 1 (VCAM-1), ICAM-2, P-selectin, E-selectin, and platelet-endothelial cell adhesion molecule 1 (PECAM-1) in different vascular beds of normal (C5 7B1/6) and RM-1 tumor-hearing mice. When corrected for endothelial surface area, the constitutive expression of selectins in tumor vessels was higher than that observed in other vascular beds. Both constitutive and induced ex pression of endothelial CAMs in peripheral vascular beds did not differ bet ween normal and tumor-bearing mice. Within the tumor, the magnitude of the upregulation of P-selectin, ICAM-1, and VCAM-1 after TNF-alpha was similar to that within other vascular beds. E-selectin expression in tumors was ref ractory to TNF-alpha, whereas PECAM-1 and ICAM-2 expression were significan tly reduced. Our findings suggest that the presence of a solid tumor does n ot influence endothelial CALM expression in other vascular beds and that th e higher density of selectins in nonstimulated tumor vessels may promote th e recruitment of rolling leukocytes in this tissue.