Normal somatic cells undergo a finite number of divisions and then cease dividing whereas cancer cells are able to proliferate indefinitely. This irreversible program of cell cycle arrest is triggered in response to a variety of intrinsic and extrinsic stimuli including alteration in telomere length and structure, DNA damage, physiological stresses and activation of certain oncogenes. It can lead to removal of defective and potentially cancerous cells from the proliferating pool thereby preventing neoplastic transformation and tumour development. It can also compromise tissue repair and regeneration and contribute to organismal ageing. The acquisition of an infinite proliferative potential is one of the six key events that are required for neoplastic transformation and one of the least understood since the underlying mechanism that controls cellular senescence and the signal transduction pathways involved are poorly understood. My research is aimed at identifying the underlying molecular basis for the finite proliferative life span and then if and how the key components are abrogated in cancer cells. We also aim to determine if these key components are conserved across species and in different cell types. Such components should represent novel, important and direct targets for both cancer and anti-ageing therapies.