nervous systems.144'145

The migratory aspects of intravasation entail specific cellular capabilities. The cell must exhibit the mechanical ability for translocation; the development and advancement of pseudopodia permit such locomotion.146 A variety of motil-ity factors promote pseudopodia-mediated translocation; these include autocrine molecules, for example, insulin-like growth factor II147 and autotaxin,148 paracrine molecules such as insulin-like growth factor I,149 and the extracellular matrix molecules laminin, fibronectin,150 and collagen.151

For the metastatic cell to transit successfully beyond its microenvironment, it must traverse the extracellular matrix. Abetting this penetration, metalloproteinases degrade the extracellular matrix,152,153 with expression levels of metallo-proteinase expression correlating with the proclivity of cells to metastasize.154,155

Tumor-associated blood vessel formation furthers the intravasation process. Extracellular matrix degradation takes place via the degradative effects of endothelial cell-released collagenases and urokinases.156 As well, VEGF expression accompanies the expansion of the tumor vascular network. VEGF, which is also known as vascular permeability factor,157 causes the formation of leaky permeable vessels. Such leaki-ness, important for the expansion of the tumor vasculature,158 also contributes to the successful intravasation of metasta-sizing tumor cells.

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