In vivo intracellular signaling as a marker of antiangiogenic activity.
作者： Gary E. Gallick , David J. McConkey , Corazon D. Bucana , Lee M. Ellis , Young D. Jung
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摘要: Alterations in endothelial cell (EC) signaling could serve as a marker of effective antiangiogenic therapy. We determined the effect an tyrosine kinase inhibitor, SU6668, on tumor EC liver metastases mice. In vitro immunofluorescence verified that pretreatment ECs with SU6668 before exposure to VEGF decreased phosphorylation Erk and Akt. Using double-fluorescence immunohistochemistry, phosphorylated Akt were constitutively expressed untreated mice, but blocked activation these intermediates. Determining status pathways may surrogate for effectiveness regimens.
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