Angiogenic profile of childhood primitive neuroectodermal brain tumours/medulloblastomas

被引:57
作者
Huber, H
Eggert, A
Janss, AJ
Wiewrodt, R
Zhao, H
Sutton, LN
Rorke, LB
Phillips, PC
Grotzer, MA [1 ]
机构
[1] Childrens Hosp Philadelphia, Div Oncol, Philadelphia, PA 19104 USA
[2] Univ Penn, Med Ctr, Div Pulm & Crit Care Med, Philadelphia, PA 19104 USA
[3] Childrens Hosp Philadelphia, Div Biostat, Philadelphia, PA 19104 USA
[4] Childrens Hosp Philadelphia, Dept Neurosurg, Philadelphia, PA 19104 USA
[5] Childrens Hosp Philadelphia, Dept Pathol, Philadelphia, PA 19104 USA
[6] Univ Zurich, Childrens Hosp, CH-8032 Zurich, Switzerland
关键词
angiogenesis; brain tumour; medulloblastoma; vascular endothelial growth factor; basic fibroblast growth factor; angiopoetin; transforming growth factor-alpha; platelet-derived endothelial growth factor;
D O I
10.1016/S0959-8049(01)00225-8
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Primitive neuroectodermal brain tumours (PNET) including medulloblastomas (PNET/MB) are the most common malignant brain tumours of childhood. Similar to many other brain tumours, PNET/MB often show marked neovascularisation. To determine which angiogenic factors contribute to PNET/MB angiogenesis, we examined the expression of eight angiogenic factors (vascular endothelial growth factors ( VEGF, VEGF-B. VEGF-C), basic fibroblast growth factor (bFGF), angiopoetins (Ang-1, Ang-2), transforming growth factor (TGF-alpha). and platelet-derived endothelial growth factor (PDGF-A)) by semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR) in six PNET cell lines and 28 primary PNET/MB. Expression levels of angiogenic factors were compared with microvessel density. TrkC mRNA expression. clinical variables and survival outcomes. Our results indicate that all PNET/MB tested produce a wide range of angiogenic factors that are, individually or together, likely to play a direct role in PNET/MB tumour growth. This suggests that anti-angiogenesis approaches targeting VEGF alone may be insufficient in PNET/MB. (C) 2001 Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:2064 / 2072
页数:9
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