Metastatic tumour spread is a pathologic process which can be describe
d as altered cell growth associated with a series of adhesion/de-adhes
ion events which are coupled with regulated tissue degradation. Adhesi
on to, and migration through, the extracellular matrix (ECM) is necess
ary for the tumour invasion which is an important part of the metastat
ic process. Efficient proteolytic digestion of the molecules of the EC
M appears to be facilitated by the localization of proteases at the ce
ll surface-tissue interface (see also review by Stetler-Stevenson). In
deed, there is evidence from in-vitro studies to suggest that restrict
ion of these enzymes to focal contact sites (areas of cell-substratum
contact) may occur and that this sub-cellular juxtaposition of recepto
rs and enzymes co-ordinates regulation of adhesion and proteolysis by
the neoplastic cells. How such coordinated regulation is achieved and
how this dynamic interplay is controlled during tumour development and
progression are important areas of investigation.