All multicellular organisms must be able to respond to changes in environmental oxygen in order to survive. These changes in oxygen tension can be sensed at a cellular level by a family of proteins that include the prolyl hydroxylase (PHD) enzymes encoded by the EGLN genes. The Tennant research group investigates the ways in which the PHD enzymes tranduce alterations in oxygen tension into changes in cell physiology, specifically changes in cell metabolism. In solid tumours, dysfunctional and inadequate vasculature means that there are significant areas of low oxygen (hypoxia), which inactivate the PHD enzymes. The PhD project available will study the role of the oxygen sensor, PHD1, in cell metabolism and tumour malignancy. Using both the in vitro and in vivo models available, the project will elucidate the aspects of cell phenotype controlled by PHD1, and how the functional inactivation of PHD1 in tumours alters tumour phenotype.