期刊
CENTRAL EUROPEAN NEUROSURGERY
卷 71, 期 3, 页码 139-142出版社
GEORG THIEME VERLAG KG
DOI: 10.1055/s-0029-1242756
关键词
auranofin; cathepsin B; extracellular matrix; glioblastoma; urokinase
Cathepsin B activity is absent in normal brain tissue but overexpressed in glioblastomas. Immunohistochemistry localizes cathepsin B to areas of invasion and neovascularization. Several research teams have confirmed the relationship between higher cathepsin B expression, more aggressive glioblastoma course and a shorter overall survival. An old anti-rheumatoid arthritis drug, auranofin, has a documented micromolar range for the inhibition of cathepsin B. Such levels are clinically achievable with the adequately tolerated doses that are used to treat rheumatoid arthritis. The side-effect profile of auranofin, although not entirely problem-free, is benign enough to warrant further trials in good fidelity rodent glioblastoma models followed by a translation to clinical trials if these confirm a potential for benefit. A newly discovered amplification loop between cathepsin B and urokinase-type plasminogen activator outlined in this paper is active in glioblastoma and makes auranofin inhibition particularly attractive for its potential to inhibit the matrix degrading feedback cycle.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据