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Glucose transport regulation by p210 Bcr-Abl in a chronic myeloid leukaemia model.
Bentley J, Walker I, McIntosh E, Whetton A, Owen-Lynch P, Baldwin S
Br J Haematol. 2001;112( 1):212-5.
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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.
Keyword(s)
Biological Transport; Cell Death; Cell Line; Humans; Research Support, Non-U.S. Gov't; metabolism: 1-Phosphatidylinositol 3-Kinase; metabolism: Deoxyglucose; metabolism: Fusion Proteins, bcr-abl; metabolism: Hematopoietic Stem Cells; metabolism: Leukemia, Myeloid, Chronic