"Anchorage-dependence" (AD) defines the requirement for adhesion to substrate for progression through the cell cycle and the onset of DNA replication in response to growth factors. AD is thought to be largely dependent on active signaling by surface integrins, a highly conserved family of adhesion receptors involved in cell-extracellular matrix, as well as cell-cell adhesion. Numerous studies have unveiled the existence of a close relationship between loss of AD and tumorigenicity, by showing that the requirement for integrin-generated signals becomes less pronounced with increasing degrees of cell transformation. As integrins are devoid of catalytic function, we hypothesise that they transduce signals by dynamic association with intracellular adaptors and effector molecules. Comprehensive goal of our research is therefore the identification and functional characterisation of genes and mechanisms causally related to the integration of mitogenic signals by adhesion receptors. We hypothesise that altered expression or function of genes involved in such processes may be amongst the early changes occurring in cell transformation.