ICAM1 and cancer: In turn, over-expression of this integrin enhanced the adhesion of CT26 to ICAM-1-expressing angiogenic hepatic myofibroblasts and endothelial cells; and endowed CT26 cells with the capability to further increase VEGF secretion, via COX-2, in response to soluble ICAM-1 (Figure 3B), a factor increasing both in the hepatic blood after cancer cell infiltration, and in the peripheral blood of patients affected by numerous cancer types [18,19].