Hyperactivation of the Wnt pathway has been linked to a wide range of cancers. Notably, the majority of colorectal cancers are due to inactivating mutations of the APC tumour suppressor, or to activating mutations in beta-catenin, a key effector of the canonical Wnt pathway. In normal development, this pathway controls cell proliferation and differentiation in many tissues, including the intestinal stem cell compartment. Our aim is to understand the molecular events underlying Wnt signal transduction. We focus on positively-acting components of this pathway that are potential drug targets, and on their molecular interactions. These include the recently discovered Pygopus-BCL9 complex that facilitates the transcriptional activity of beta-catenin in colorectal cancer cell lines. We also study Dishevelled and its role as a dynamic polymeric adaptor between the Wnt transmembrane receptors and the Axin-APC complex, which itself promotes the inactivation and degradation of beta-catenin.