The pathophysiologic role of VEGF in hematologic malignancies: therapeutic implications

被引：263

作者：

Podar, K ^{[1
]}

Anderson, KC ^{[1
]}

机构：

[1] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol,Jerome Lipper Multiple Myeloma Ctr, Boston, MA 02115 USA

来源：

BLOOD | 2005年 / 105卷 / 04期

关键词：

D O I：

10.1182/blood-2004-07-2909

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Besides its role as an essential regulator of physiologic and pathologic anglogenesis, vascular endothelial growth factor (VEGF) triggers growth, survival, and migration of leukemia and multiple myeloma cells; plays a pivotal role in hematopolesis; inhibits maturation of dendritic cells; and increases osteoclastic bone-resorbing activity as well as osteoclast chemotaxis. Dysregulation of VEGF expression and signaling pathways therefore plays an important role in the pathogenesis and clinical features of hematologic malignancies, in particular multiple myeloma. Direct and indirect targeting of VEGF and its receptors therefore may provide a Potent novel therapeutic approach to overcome resistance to therapies and thereby improve patient outcome. (C) 2005 by The American Society of Hematology.

引用

页码：1383 / 1395

页数：13

共 293 条

[1] Vascular endothelial growth factor stimulates tyrosine phosphorylation and recruitment to new focal adhesions of focal adhesion kinase and paxillin in endothelial cells [J].