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血管内皮生长因子是人类胶质瘤在体内一种潜在的肿瘤血管生成因子。

Vascular endothelial growth factor is a potential tumour angiogenesis factor in human gliomas in vivo.

作者信息

Plate K H, Breier G, Weich H A, Risau W

机构信息

Max-Planck-Institut für Psychiatrie, Martinsried, Germany.

出版信息

Nature. 1992 Oct 29;359(6398):845-8. doi: 10.1038/359845a0.

Abstract

Clinical and experimental studies suggest that angiogenesis is a prerequisite for solid tumour growth. Several growth factors with mitogenic or chemotactic activity for endothelial cells in vitro have been described, but it is not known whether these mediate tumour vascularization in vivo. Glioblastoma, the most common and most malignant brain tumour in humans, is distinguished from astrocytoma by the presence of necroses and vascular proliferations. Here we show that expression of an endothelial cell-specific mitogen, vascular endothelial growth factor (VEGF), is induced in astrocytoma cells but is dramatically upregulated in two apparently different subsets of glioblastoma cells. The high-affinity tyrosine kinase receptor for VEGF, flt, although not expressed in normal brain endothelium, is upregulated in tumour endothelial cells in vivo. These observations strongly support the concept that tumour angiogenesis is regulated by paracrine mechanisms and identify VEGF as a potential tumour angiogenesis factor in vivo.

摘要

临床和实验研究表明,血管生成是实体肿瘤生长的一个先决条件。已经描述了几种在体外对内皮细胞具有促有丝分裂或趋化活性的生长因子,但尚不清楚这些因子是否介导体内肿瘤血管形成。胶质母细胞瘤是人类最常见且最恶性的脑肿瘤,其与星形细胞瘤的区别在于存在坏死和血管增殖。我们在此表明,内皮细胞特异性促有丝分裂原血管内皮生长因子(VEGF)在星形细胞瘤细胞中被诱导表达,但在胶质母细胞瘤细胞的两个明显不同的亚群中显著上调。VEGF的高亲和力酪氨酸激酶受体flt虽然在正常脑内皮中不表达,但在体内肿瘤内皮细胞中上调。这些观察结果有力地支持了肿瘤血管生成受旁分泌机制调节的概念,并确定VEGF为体内潜在的肿瘤血管生成因子。

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