Normal cells have defenses against the thread of cancer. One of these defense mechanisms is a permanent stop of its ability to reproduce, remaining however viable. This arrested stage is known as cellular senescence. Benign tumours are basically composed of senescent cells that cannot further progress to malignant tumours. Understanding the molecular basis of senescence is important because it may help to design novel anticancer strategies that, among other things, could convert a malignant tumour into a benign tumour which could be easily removed by surgery. In our studies of molecular profiling of senescent cells, we identified a protein called CHES1 which is able to regulate senescence. We will try to determine how this protein can achieve this task. To validate these findings, we will also generate a mouse model where this protein is inactivated, as has been seen in multiple human tumours. We expect these mice will develop tumours, providing a model to study the normal functions of CHES1 and to also develop drugs that could compensate for its absence.