Stem cells drive the regeneration and repair of damaged tissues and are, thus, essential for survival. The proliferative capacity of stem cells is, however, a double-edged sword. With every cell division there is a chance of an error occurring during DNA replication and/or repair, which makes stem cells prone to undergo malignant transformation into cancer cells. Fortunately, the body has protection barriers, known as tumour suppressor systems, that prevent uncontrolled growth of damaged cells. The most important of such systems is the p53 pathway. The p53 protein acts as a subcellular sensor that is triggered by potentially cancer-inducing stimuli, such as exposure to DNA damaging agents. In response to such stress conditions, p53 enhances DNA repair, inhibits cell proliferation, or induces programmed cell death. Due to these activities, p53 is regarded as highly attractive target for cancer therapy. Although the nearly 40,000 research articles published on p53 have revealed some of its secrets, they have also uncovered new layers of complexity, resulting in even more unanswered questions. Given the intrinsic complexity and implicit quantitative nature of some these questions, we aim to exploit theoretical thinking and mathematical modelling to gain deeper insight into the regulatory mechanisms of the p53 pathway. It is anticipated that the proposed research will complement and reinforce the biological knowledge acquired by empirical methods.