VEGF Receptor Phosphorylation Status and Apoptosis is Modulated by a Green Tea Component, Epigallocatechin-3-gallate (EGCG) in B cell Chronic Lymphocytic Leukemia. Lee YK, Bone ND, Strege AK, Jelinek DF, Kay NE. Abstract: We recently reported that chronic lymphocytic leukemia (CLL) cells synthesize and release VEGF under normoxic and hypoxic conditions. CLL B cells also express VEGF membrane receptors (VEGF-R1 and VEGF-R2), suggesting that they use VEGF as a survival factor. To assess the mechanism of apoptosis resistance related to VEGF, we determined the impact of VEGF on CLL B cells, and we studied the impact of epigallocatechin (EGCG), a known receptor tyrosine kinase (RTK) inhibitor, on VEGF receptor status and viability of CLL B cells. VEGF165 significantly increased apoptotic resistance of CLL B cells and immunoblotting revealed that VEGF-R1 and VEGF-R2 are spontaneously phosphorylated on CLL B cells. EGCG significantly increased apoptosis/cell death in 8 of 10 CLL samples measured by annexin V/propidium iodide (PI) staining. The increase in annexin V/PI staining was accompanied by caspase 3 activation and PARP cleavage at low concentrations of EGCG (3 micro g/ml). Moreover, EGCG suppressed the proteins Bcl-2, XIAP and Mcl-1 in CLL B cells. Finally, EGCG (3-25 micro g/ml) suppressed VEGF-R1 and VEGF-R2 phosphorylation, albeit incompletely. Thus, these results suggest that VEGF signaling regulates survival signals in CLL cells and that interruption of this autocrine pathway results in caspase activation and subsequent leukemic cell death. Blood. 2004 Mar 2 [Epub ahead of print] Remember we are NOT Doctors and have NO medical training. This site is like an Encylopedia - there are many pages, many links on many topics. Support our work with any size DONATION - see left side of any page - for how to donate. You can help raise awareness of CAM.