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胶质母细胞瘤:靶向血管生成和酪氨酸激酶途径

Glioblastoma: Targeting Angiogenesis and Tyrosine Kinase Pathways.

作者信息

Arbab Ali S, Ali Meser M

机构信息

Tumor Angiogenesis Laboratory, Georgia Cancer Center, Augusta University, USA.

Cellular and Molecular Imaging Lab, Department of Neurosurgery, Henry Ford Hospital, USA.

出版信息

Nov Approaches Cancer Study. 2020;4(5):398-401. Epub 2020 May 29.

PMID:32924014
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7486014/
Abstract

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.

摘要

血管生成是胶质母细胞瘤(GBM)的一个标志,并且在其治疗中仍然是一个重要的治疗靶点,尤其是对于复发性GBM。GBM的特征是释放血管内皮生长因子(VEGF),它是血管生成的重要调节因子和促进因子。因此,针对VEGF或VEGF受体(VEGFRs)的抗血管生成疗法(AATs)被设计出来,并被认为是控制GBM生长的有效工具。然而,最近使用抗VEGF人源化单克隆抗体(贝伐单抗)以及单独或与其他治疗药物联合靶向不同VEGFRs的酪氨酸激酶抑制剂(TKIs)的不同临床试验结果显示出喜忧参半的结果,大多数报告表明GBM对抗血管生成治疗产生了耐药性。

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