胶质母细胞瘤:靶向血管生成和酪氨酸激酶途径。

A. Arbab, Meser M. Ali
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引用次数: 5

摘要

血管生成是胶质母细胞瘤(GBM)的标志,也是其治疗的重要靶点,尤其是复发性GBM。GBMs的特征是释放血管内皮生长因子(VEGF),这是血管生成的重要调节因子和启动子。因此,针对VEGF或VEGF受体(VEGFR)的抗血管生成疗法(AAT)被设计并被认为是控制GBM生长的有效工具。然而,使用抗VEGF的人源化单克隆抗体(贝伐单抗)以及单独或与其他治疗剂联合靶向不同VEGFR的酪氨酸激酶抑制剂(TKIs)的不同临床试验的最新结果表明,结果喜忧参半,大多数报告表明GBM对抗血管生成治疗产生了耐药性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Glioblastoma: Targeting Angiogenesis and Tyrosine Kinase Pathways.
Angiogenesis is a hallmark of glioblastoma (GBM) and remains an important therapeutic target in its treatment, especially for recurrent GBM. GBMs are characterized by the release of vascular endothelial growth factor (VEGF), an important regulator and promoter of angiogenesis. Therefore, antiangiogenic therapies (AATs) targeting VEGF or VEGF receptors (VEGFRs) were designed and thought to be an effective tool for controlling the growth of GBM. However, recent results of different clinical trials using humanized monoclonal antibodies against VEGF (bevacizumab), as well as tyrosine kinase inhibitors (TKIs) that target different VEGFRs alone or in combination with other therapeutic agents demonstrated mixed results, with the majority of reports indicating that GBM developed resistance against antiangiogenic treatments.
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