Abstract
Chronic myelogenous leukemia (CML) is driven by constitutively activated BCR-ABL tyrosine kinase that reportedly activates downstream PI3-kinase (PI3K) and extracellular signal-regulated kinase (ERK) signaling. The inhibitory role of p210BCR-ABL on stromal adhesion is speculated to cause abnormal circulation and proliferation of CML progenitors. Recently, it has been reported that p210BCR-ABL expression downregulates membrane expression of the CXC chemokine receptor 4 (CXCR4) which may be associated with migration defects in CML, and that tyrosine kinase inhibitor Imatinib restores CXCR4 expression in CML blast crisis cells (
Cancer Res
2005
;65
:2676
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2005, The American Society of Hematology
2005
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