Title: A Computational Model for Genetic and Epigenetic Signals in Colon Cancer
Supervisor: Prof. Heather Ruskin
Cancer, a class of diseases, characterized by abnormal cell growth, has one of the highest overall death rates world-wide. Its development has been linked to aberrant genetic and epigenetic events, affecting the regulation of key genes that control cellular mechanisms. However, a major issue in cancer research is the lack of precise information on tumour pathways, so that delineation of these and the processes underlying disease proliferation is an important area of investigation. A computational approach to modelling malignant system events can help to improve understanding of likely triggers, i.e. initiating abnormal micro-molecular signals that occur during cancer development. Here, we introduce a network-based model for genetic and epigenetic events observed at different stages of colon cancer, with a focus on the gene relationships and tumour pathways. These changes are studied in relation to ageing, also considered to be one of the major risk factors in neoplastic disease development. Gender is also specifically accounted for in the genetic/epigenetic framework. Additionally, further directions, including a detailed plan of development, are presented. The current work aims to provide improved insight on the way in which aberrant modifications characterize cancer initiation and progression. The framework dynamics are described in terms of interdependencies of three main layers: genetic and epigenetic events, gene relationships andcancer stage levels.