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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