About Professor Tim Somervaille

Human acute myeloid leukaemias (AMLs) are heterogeneous with respect to both genetics and the function of the cells that make up the disease. A minority of the cells are leukaemia stem cells (LSCs) which have the ability to self-renew for an extended if not indefinite period, thus maintaining and expanding the disease. In order to cure a patient these cells must be eliminated completely, because if they are not they have the ability to regenerate the disease and induce relapse.

Recent years have seen significant progress in the development of better therapies for people with blood cancer, with concomitant improvements in response. However, there remains a substantial unmet need for more effective and less toxic treatments. For example, outcomes in acute myeloid leukaemia are particularly poor in older adults and those with relapsed or refractory disease and malignancies, such as multiple myeloma, are incurable for the great majority. The overarching goal of the Leukaemia Biology group is to deliver a bench-to-bedside programme of blood cancer research.  

Much of our effort is focused on understanding how transcription factors and their associated chromatin cofactors sustain myeloid blood cancers such as AML. In keeping with this, we recently reported our discovery of how a small molecule bromodomain inhibitor of the acetyltransferases EP300 and CBP induces cell cycle arrest and cellular differentiation in blood cancer, as well as our preliminary data from the early phase clinical trial evaluation of CCS1477, where we see promising signs of clinical activity across a range of haematological malignancies.