An investigation into the potential use of Beta-Galactoside binding protein as a novel anti-leukaemic agent

Abstract

Chronic myelogenous leukaemia (CML) is characterised at the molecular level by a (9;22) translocation which places the abl proto-oncogene under the control of the breakpoint cluster region (bcr) gene promoter generating a fusion protein (p210) with enhanced tyrosine kinase activity. CML cells are inherently resistant to apoptosis induced by conventional chemotherapeutic agents.