The major focus of my work is to determine the molecular mode of action of the abl oncogene.This oncogene is the causative agent in Chronic Myeloid Leukaemia and functions as a disregulated protein tyrosine kinase leading to abherrent survival of blood cell progenitors in the bone marrow. Activation of the Abl oncogene in cell line models of CML results in suppression of apoptosis, drug resistance, decreased adhesion to stromal cell layers, elevated levels of glucose transport and enhanced proliferative potential. Projects ongoing in this area include:
The overall objective is to use the information gained from studies as described above to identify possible novel approaches for the treatment of leukaemia. In collaboration with the haematology department at Manchester and Lancaster hospitals studies will be continued using samples from patients with CML.
Another ongoing area of research concerns an investigation of the mechanisms of cortical development, i.e. how layering of neurones and glial cells is achieved, focusing on the role of specific cell types and signalling molecules linked to this process. The aim here is to discover how this process of normal development is disrupted in Hydrocephalus.