“…Inhibition of the BCR-ABL oncoprotein with imatinib in BCR-ABL-positive leukaemia cells resulted in decreased glucose uptake, lactate production and improved cellular energetics (Gottschalk et al, 2004), which were not recorded in their imatinib-resistant counterpart (Kominsky et al, 2009). These effects were coupled with translocation of the glucose transporter GLUT-1 from the plasma membrane to the cytoplasm in sensitive but not resistant lines, indicating an inhibition of glucose uptake following treatment with imatinib (Kominsky et al, 2009). As aberrant BCR promotes the expression of the proglycolytic protein C-MYC (Mahon et al, 2003), decreased glycolysis in response to imatinib treatment could be mediated through C-MYC suppression.…”