Metastatic tumour spread is a pathologic process which can be described as altered cell growth associated with a series of adhesion/de-adhesion events which are coupled with regulated tissue degradation. Adhesion to, and migration through, the extracellular matrix (ECM) is necessary for the tumour invasion which is an important part of the metastatic process. Efficient proteolytic digestion of the molecules of the ECM appears to be facilitated by the localization of proteases at the cell surface-tissue interface (see also review by Stetler-Stevenson). Indeed, there is evidence from in-vitro studies to suggest that restriction of these enzymes to focal contact sites (areas of cell-substratum contact) may occur and that this sub-cellular juxtaposition of receptors and enzymes co-ordinates regulation of adhesion and proteolysis by the neoplastic cells. How such co-ordinated regulation is achieved and how this dynamic interplay is controlled during tumour development and progression are important areas of investigation.