Both xenogeneic and syngeneic activated natural killer (A-NK) cells adhere to tumor vasculature when injected into the tumor's blood supply. However, the molecular and biophysical mechanisms of this localization in tumor vasculature have not been defined. Previous studies have suggested that localization of these cells in tumor vessels is due primarily to their adhesive characteristics rather than mechanical or hemodynamic considerations. Studies of NK cell adhesion in vitro have documented the involvement of both .beta.1 and .beta.2 integrins in the absence of shear stress or rate-limited binding conditions. Lymphocyte adhesion to activated endothelium under a range of shear stress conditions has been shown to involve multiple cellular adhesion molecules (CAMs): in particular, intracellular and vascular CAMS (ICAM-1 and VCAM-1) and E-selectin. In addition, several studies have documented increased expression of these CAMs in the tumor vasculature and significant infiltration of lymphocytes, especially in the periphery of growing tumors. These observations suggest that the tumor microenviroment may modulate the expression of CAMs on the endothelial cells of tumor vessels and may facilitate adhesion of certain lymphocytes.