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基于尿基质金属蛋白酶活性检测贝伐单抗治疗恶性脑胶质瘤的失败。

Detection of failure of bevacizumab treatment for malignant glioma based on urinary matrix metalloproteinase activity.

机构信息

Department of Neurosurgery, Institute of Clinical Medicine, Tennodai, Tsukuba, Ibaraki, 305-8575, Japan.

出版信息

Brain Tumor Pathol. 2010 Oct;27(2):89-94. doi: 10.1007/s10014-010-0271-y. Epub 2010 Nov 3.

DOI:10.1007/s10014-010-0271-y
PMID:21046310
Abstract

Although antiangiogenic treatment for malignant glioma using bevacizumab in combination with irinotecan chemotherapy has a promising effect on survival, the high incidence of increasing infiltrative tumors can be a problem in resistance to antiangiogenic therapy. In this study, we detected failure of bevacizumab treatment for malignant glioma through upregulation of metalloproteinase activity in the urine, as well as infiltrative tumors on MRI. In addition, MMP9 has been proved as a molecule that facilitates its infiltrative behavior in vivo in the brain animal model.

摘要

尽管贝伐单抗联合伊立替康化疗治疗恶性脑胶质瘤的抗血管生成治疗在生存方面有很好的效果,但浸润性肿瘤发生率的增高可能是抗血管生成治疗耐药的一个问题。在这项研究中,我们通过检测尿液中金属蛋白酶活性的上调以及 MRI 上浸润性肿瘤的方式,来发现贝伐单抗治疗恶性脑胶质瘤的失败。此外,MMP9 已被证明是一种在脑动物模型中促进其浸润行为的分子。

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Brain Tumor Pathol. 2010 Oct;27(2):89-94. doi: 10.1007/s10014-010-0271-y. Epub 2010 Nov 3.
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