Drug resistance by evasion of antiangiogenic targeting VEGF signaling in late-stage pancreatic islet tumors (Cancer Cell, 2005, 8:299-309)

報告日期: 2006/04/21
報告時間: 15:10/16:00
報告學生: 蔡宗霖
講評老師: 吳梨華


Drug resistance by evasion of antiangiogenic targeting of VEGF signaling in late-stage pancreatic islet tumors


OCTOBER 2005 · VOL. 8 Cancer Cell


Speaker:蔡宗霖                  Commentator:吳梨華 老師


Time2006/4/21 (15:00~15:50)       place:Classroom 602



     Vascular endothelial growth factor (VEGF or VEGF-A) and its receptors play a crucial role in the neovascularization and progression of cancer. VEGF binds to two types of cell-membrane receptors, VEGF receptor (VEGFR)-1 and VEGFR-2, located in the endothelium, and stimulates endothelial migration, proliferation, permeability, function and survival. In this paper, by using VEGF receptors R1 and R2 monoclonal antibodies for function-blocking, author find that   

Inhibition of VEGFR2 but not VEGFR1 markedly disrupted angiogenic process, and also demonstrate that VEGFR2 blockade is an effective antiangiogenic and antitumor agent. But, In late-stage, phenotypic resistance emerges to anti-VEGFR2 therapy, and this resistance is associated with hypoxia-mediated induction of FGF family. Counteracting such mechanisms of resistance by multitargeting of VEGFR2 and FGF family may improve efficacy of antiangiogenic therapies.



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