RET is a receptor protein that resides on the cell surface and relays messages for cell growth and motility. Inappropriate activation of RET causes thyroid cancer and is linked to aggressiveness in some other tumours.  When RET is activated in cancer, it leads to tumours that have early and widely distributed metastasis. Current therapies primarily focus on the original tumour but are less successful for treatment of small or distant metastases.  We have shown that RET interacts with another molecule, beta-catenin, which has roles in regulating the interactions between cells that can prevent tumour cells from detaching and moving away. Beta-catenin molecules are part of a large protein complex that links cells together, giving structural integrity to tissues. Our hypothesis is that the interactions between RET and these protein complexes in tumours favour loss of cell-to-cell interactions and contribute to tumour formation and spread. In this study, we will further investigate the contribution of RET to cell-to-cell interactions, and how RET may affect these interactions and contribute to tumorigenesis.