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Glucose transport regulation by p210 Bcr-Abl in a chronic myeloid leukaemia model
J Bentley1, I Walker, E McIntosh
1School of Biochemistry and Molecular Biology, University of Leeds, Leeds, UK. Johanne.Bentley@ncl.ac.uk
Abstract:
The regulation of nutrient transport by both cytokines and oncogenes has been linked to haemopoietic cell survival. In this study, we found that activation of Bcr--Abl protein tyrosine kinase was associated with the stimulation of glucose transport in the multipotent haemopoietic cell line FDCP-mix, a cell model for chronic-phase chronic myeloid leukaemia (CML). Bcr--Abl upregulation of glucose transport was mediated by phosphatidylinositol-3-kinase. The observation that Bcr--Abl can regulate glucose transport in a CML cell model raises the possibility that glucose transport regulation may have a role to play in the aberrant survival of stem cells in the chronic phase of CML.