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BCR — VEGFA
Text-mined interactions from Literome
Mayerhofer et al., Blood 2002
:
BCR/ABL induces expression of
vascular endothelial growth factor and its transcriptional activator, hypoxia inducible factor-1alpha, through a pathway involving phosphoinositide 3-kinase and the mammalian target of rapamycin ... We show here that the CML associated oncogene
BCR/ABL induces
VEGF gene expression in growth factor dependent Ba/F3 cells ...
BCR/ABL also
induced VEGF promoter activity and increased VEGF protein levels in Ba/F3 cells ...
BCR/ABL induced
VEGF gene expression was counteracted by the phosphoinositide 3-kinase ( PI3-kinase ) inhibitor LY294002 and rapamycin, an antagonist of mammalian target of rapamycin (mTOR), but not by inhibition of the mitogen activated protein kinase pathway ... Together, our data show that
BCR/ABL induces
VEGF- and HIF-1alpha gene expression through a pathway involving PI3-kinase and mTOR ...
BCR/ABL induced
VEGF expression may contribute to the pathogenesis and increased angiogenesis in CML
Ebos et al., Mol Cancer Res 2002
(Leukemia, Myelogenous, Chronic, BCR-ABL Positive...) :
Imatinib mesylate ( STI-571 ) reduces
Bcr-Abl mediated
vascular endothelial growth factor secretion in chronic myelogenous leukemia ... Transfection of
BCR-ABL into murine myeloid 32D and human megakaryocyte MO7e hematopoietic cells
resulted in enhanced
VEGF expression, which could be further elevated by the exposure to cytokines such as interleukin 3 and granulocyte macrophage colony stimulating factor
Li et al., J Int Med Res 2009
(Leukemia, Myelogenous, Chronic, BCR-ABL Positive) :
Studies have shown that
vascular endothelial growth factor ( VEGF ), a major and potent inducer of angiogenesis, is directly
triggered by the disease related oncogene
Bcr-Abl in Bcr-Abl positive cells