Angiogenesis: A Target in Solid Tumors, Also in Leukemia?

被引:62
|
作者
Schmidt, Thomas [1 ]
Carmeliet, Peter [2 ,3 ]
机构
[1] Heidelberg Univ, Dept Gen Visceral & Transplantat Surg, D-69115 Heidelberg, Germany
[2] VIB, VRC, Lab Angiogenesis & Neurovasc Link, Louvain, Belgium
[3] Katholieke Univ Leuven VIB, Vesalius Res Ctr, Lab Angiogenesis & Neurovasc Link, B-3000 Louvain, Belgium
关键词
ENDOTHELIAL GROWTH-FACTOR; LENALIDOMIDE PLUS DEXAMETHASONE; BONE-MARROW ANGIOGENESIS; ACUTE MYELOID-LEUKEMIA; MULTIPLE-MYELOMA; ANTIANGIOGENIC THERAPY; BEVACIZUMAB; INHIBITION; EXPRESSION; CELLS;
D O I
10.1182/asheducation-2011.1.1
中图分类号
G40 [教育学];
学科分类号
040101 ; 120403 ;
摘要
Targeting angiogenesis has become an established therapeutic approach to fighting solid tumor growth in cancer patients. Even though increased angiogenesis has long been recognized in various types of hematologic malignancies, the molecular basis underlying this angiogenic switch in leukemias remains poorly understood. The BM stroma is gaining increasing attention for its role in promoting leukemia growth and resistance against current treatments with tyrosine kinase inhibitors. This article provides a brief overview of the role of angiogenesis in leukemias, discusses recent insights into the role of placenta growth factor (PlGF), a VEGF family member, as a novel disease candidate in chronic myeloid leukemia (CML), and highlights the therapeutic potential of PlGF blockade for imatinib-resistant CML.
引用
收藏
页码:1 / 8
页数:8
相关论文
共 50 条