|109, Cockcroft Building, Salford, M5 4WT.|
|0161 295 5067|
My interest is to dissect the epigenetic mechanism that block the differentiation in acute myeloid leukaemia using proteomic approaches using in vivo and in vitro profiling of purified genomic loci. A novel drug should target only malignant cells and leave non-malignant cells intact. Current chemotherapeutic approaches used in acute myeloid leukaemia also target normal haematopoietic differentiation. By isolating right epigenetic complex – and targeting it by small molecule inhibitors – we can not only target specifically malignant clone but also leave non-malignant cells intact.
Genetic changes that occur within malignant cells, such as activation of oncogenes or loss of tumour suppressors, are responsible for many aspects of cancer development; however, they are not sufficient. Tumour progression is dependent on ancillary processes provided by cells of the tumour environment but that are not necessarily derived from malignant clone of cells. Inflammation has long been associated with the development and progression of cancer. My interest is to evaluate the role of malignant and non- malignant clone derived macrophages in tumour microenvironment. The model system I am using is chronic haematopoietic malignancies and the bone marrow microenvironment in those malignancies.