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Glucose transport regulation by p210 Bcr-Abl in a chronic myeloid leukaemia model.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

Published
  • J. Bentley
  • I. Walker
  • E. McIntosh
  • Anthony D. Whetton
  • P. Jane Owen-Lynch
  • S. A. Baldwin
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<mark>Journal publication date</mark>01/2001
<mark>Journal</mark>British Journal of Haematology
Issue number1
Volume112
Number of pages4
Pages (from-to)212-215
Publication StatusPublished
<mark>Original language</mark>English

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.