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在用芬戈莫德治疗复发缓解型多发性硬化症后发生的胶质母细胞瘤。

Glioblastoma following treatment with fingolimod for relapsing-remitting multiple sclerosis.

作者信息

Sharim Justin, Tashjian Randy, Golzy Nima, Pouratian Nader

机构信息

Department of Neurosurgery, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.

Department of Pathology and Laboratory Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.

出版信息

J Clin Neurosci. 2016 Aug;30:166-168. doi: 10.1016/j.jocn.2016.02.003. Epub 2016 Mar 9.

DOI:10.1016/j.jocn.2016.02.003
PMID:26970935
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4925177/
Abstract

Glioblastoma is an uncommon and aggressive primary brain tumor with incidence of 3 per 100,000 annually. We report a 50-year-old woman diagnosed with glioblastoma within threeyears of induction of fingolimod therapy for relapsing-remitting multiple sclerosis. Fingolimod, an immunomodulating agent used in the treatment of relapsing-remitting multiple sclerosis, has also been suggested to impart a cardioprotective role in heart failure and arrhythmia via activation of P21-activated kinase-1 (Pak1). In the brain, Pak1 activation has been shown to correlate with decreased survival time amongst patients with glioblastoma. A molecular mechanism underlying a link between fingolimod use and glioblastoma development may involve activation of Pak1. To our knowledge, this is the first report of a potential association between fingolimod use and glioblastoma development.

摘要

胶质母细胞瘤是一种罕见且侵袭性强的原发性脑肿瘤,年发病率为十万分之三。我们报告了一名50岁女性,在接受芬戈莫德治疗复发缓解型多发性硬化症三年内被诊断出患有胶质母细胞瘤。芬戈莫德是一种用于治疗复发缓解型多发性硬化症的免疫调节剂,也有人认为它通过激活p21激活激酶-1(Pak1)在心力衰竭和心律失常中发挥心脏保护作用。在大脑中,已表明Pak1激活与胶质母细胞瘤患者的生存时间缩短相关。芬戈莫德使用与胶质母细胞瘤发生之间联系的分子机制可能涉及Pak1的激活。据我们所知,这是关于芬戈莫德使用与胶质母细胞瘤发生之间潜在关联的首次报告。

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本文引用的文献

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Activation of Pak1/Akt/eNOS signaling following sphingosine-1-phosphate release as part of a mechanism protecting cardiomyocytes against ischemic cell injury.S1P 释放后通过 Pak1/Akt/eNOS 信号通路的激活作为保护心肌细胞免受缺血性细胞损伤的机制的一部分。
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