B7h triggering inhibits adhesion of humbilical vascular endothelial cells to colon carcinoma cell lines and polymorphonuclear cells Minelli R and Dianzani C Colon cancer represents one of the most important cause of death in developed countries. At the moment the best therapeutic option for treating this tumour is surgical resection, but chemoprevention is very important in preventing metastasis and tumour spread. The process of metastatization is due to cell migration through blood vessels or lymphatic vessels and involves several adhesion molecules. The key role played by adhesion molecules has been suggested by the observation that colon carcinomas cells, derived from patients, express an increased level of the adhesion molecules ICAM-1, VCAM-1 (1, 2); moreover, several data have also demonstrated that the ability of metastatization of colon cancer cells is directly linked to the ability of the cells to bind the CD62E (3). On the base of these observations we propose that drugs that inhibit the adhesive activity of cancer cells may be helpful tools in preventing metastasis formation. Our experiments have been performed on human umbilical vascular endothelial cells (HUVEC), providing a simplified model to mimic the tissue microvascular circulation which is involved in the interactions with tumours cells (1). Our recent experiments have shown that the fusion molecule human ICOS-mouse Ig, a stimulator of B7h receptor (membrane receptor belonging to the B7 family and expressed by activated T cell) is able to reduce the adhesion of human polymorphonuclear cells (PMNs) to HUVEC
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