Angiogenesis modulates the tumour immune response

Outgrowth of solid tumors and metastases is dependent on the process of ang iogenesis. Tumors escape from the formation of an effective infiltrate by d ownregulation of endothelial adhesion molecules. This downregulation of adh esion receptors is governed by the exposure to angiogenic factors. In recen t years proof for this has been provided by demonstrating that freshly isol ated tumor endothelial cells exhibit a decreased expression of ICAM-1 and - 2 as compared to endothelial cells in normal tissue. In addition, adhesion molecules are downregulated on normal tissue endothelial cells when culture d with angiogenesis stimulators such as basic fibroblast growth factor and vascular endothelial cell growth factor, while under these conditions endot helial cells become less responsive to cytokines such as tumor necrosis fac tor-a with respect to the upregulation of endothelial adhesion molecules. V ery recently it has been demonstrated that this harmful endothelial cell an ergy can be counteracted by inhibitors of angiogenesis.