We aim to stop cancer before it starts. Most current cancer research is based on the idea that cancer is fundamentally a genetic disease – that is not to say inherited from parents, as much as to say that the hallmark of cancer is that the DNA has been corrupted, and that this corruption leads to all of the later effects on the cell and the body. Consequently, hundreds of different cancers have been identified, depending on which genes have been mutated, and in which tissues, leading to hundreds of different therapies at enormous cost in R&D. We believe that this paradigm may be wrong: rather than a mutation of DNA being the trigger of cancer, there is some evidence that the cellular behaviour change is the initiating factor, and this leads to a cascade of events among which DNA mutations are common (but not necessarily the root cause).

Our lab looks at the epigenetics, which is to say the control system by which genes get turned on or off at different times in the life of a cell. We have evidence that under certain conditions, that likely occur naturally in the body, cells undergo changes in epigenetics that are remarkably close to both the status of the early stages of life (conception and embryo formation), and also to the vast majority of cancers. We are one of the only labs in the world focusing on the similarities between embryonic stem cells and cancers in this way. The striking similarity between these two very different types of cell is interesting, as the embryo must evade the host’s (mother’s) immune system in much the same way that is observed in cancer. The proposed PhD project involves testing crucial elements of this hypothesis, which if proven correct may pave the way for future prophylactic cancer prevention medication – stopping cancer before it starts, and tackling the root-cause of relapse following chemotherapy.