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Prepublished online as a Blood First Edition Paper on January 9, 2003; DOI 10.1182/blood-2002-11-3376.
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Blood, 15 May 2003, Vol. 101, No. 10, pp. 4088-4097
NEOPLASIA
Cell context-specific effects of the BCR-ABL oncogene
monitored in hematopoietic progenitors
Stephane Wong,
Jami McLaughlin,
Donghui Cheng, and
Owen N. Witte
From the Molecular Biology Interdepartmental PhD
Program, the Department of Microbiology, Immunology and Molecular
Genetics, University of California, Los Angeles; and the Howard Hughes
Medical Institute, Los Angeles, CA.
Acute BCR-ABL expression during in vitro hematopoietic
development of embryonic stem (ES) cells causes expansion of
multipotent and myeloid progenitors with a concomitant reduction in
differentiation toward erythroblasts. Progenitor cell expansion is due
to a rapid, cell autonomous, suppression of programmed cell death with
an increase in expression of the antiapoptotic molecule
BCL-XL. Other antiapoptotic effectors, including AKT,
STAT5, and BCL-2 are not up-regulated by BCR-ABL in this system. In
addition, the proapoptotic p38 mitogen-activated protein
kinase (MAPK) pathway is suppressed by BCR-ABL expression in ES-derived
hematopoietic progenitors. Inhibition of p38 MAPK by the small molecule
inhibitor SB203580 expanded ES-derived hematopoietic progenitors by an
antiapoptotic mechanism and is sufficient to expand ES-derived
hematopoietic progenitors to levels approaching 80% of that seen
following BCR-ABL expression. In the cellular context of ES-derived
hematopoietic progenitors, BCR-ABL expression expands cells by
suppressing programmed cell death with a set of antiapoptotic pathways
distinct from those previously reported in continuous cell line studies.
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