Myc is a key oncogene in various cancers occurring across a diverse range of tissues. In order to better understand and treat these cancers, it is vital that we understand how the opposing functions of Myc, proliferation and apoptosis, are balanced and regulated in healthy tissue, and how this goes wrong in cancer. In collaboration with the Evan lab (Department of Biochemistry, University of Cambridge) we aim to build comprehensive executable models of the Myc transcriptional program in a range of cancers, including melanoma and breast cancer. Analysis of this executable network model could help identify unknown interactions between genes in the network. Furthermore, it will help find key regulators of Myc function, which could act as potential drug targets. We aim to combine such network models with physical modelling of cell to cell interactions to investigate tumour heterogeneity. These hybrid models allow us to see the effects of the properties of the network on overall tumour structure, but also how this structure, through its effect on the micro-environment, feeds back into the behaviour of individual cells. As such we can investigate the competition and cooperation between clones in heterogeneous tumours at multiple scales.