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糖原合酶激酶-3β(GSK-3β)及其在多形性胶质母细胞瘤中的失调。

Glycogen synthase kinase-3β (GSK-3β) and its dysregulation in glioblastoma multiforme.

机构信息

Department of Surgery, The University of Melbourne, The Royal Melbourne Hospital, Grattan Street, Parkville, VIC 3050, Australia.

出版信息

J Clin Neurosci. 2013 Sep;20(9):1185-92. doi: 10.1016/j.jocn.2013.02.003. Epub 2013 Jun 12.

DOI:10.1016/j.jocn.2013.02.003
PMID:23768967
Abstract

Glioblastoma multiforme (GBM) is the most frequently occurring and devastating human brain malignancy, retaining almost universal mortality and a median survival of only 14 months, even with recent advances in multimodal treatments. Gliomas are characterised as being both highly resistant to chemo- and radiotherapy and highly invasive, rendering conventional interventions palliative. The continual dismal prognosis for GBM patients identifies an urgent need for the evolutionary development of new treatment modalities. This includes molecular targeted therapies as many signaling molecules and associated pathways have been implicated in the development and survival of malignant gliomas including the protein kinase, glycogen synthase kinase 3 beta (GSK-3β). Here we review the activity and function of GSK-3β in a number of signaling pathways and its role in gliomagenesis.

摘要

多形性胶质母细胞瘤(GBM)是最常见和最具破坏性的人类脑恶性肿瘤,即使采用了最近的多模式治疗方法,其死亡率仍然几乎普遍存在,中位生存期仅为 14 个月。神经胶质瘤的特点是对化疗和放疗具有高度耐药性和高度侵袭性,使常规干预措施成为姑息性的。GBM 患者持续的预后不良表明迫切需要开发新的治疗模式。这包括分子靶向治疗,因为许多信号分子和相关途径已被牵连到恶性神经胶质瘤的发展和存活中,包括蛋白激酶、糖原合酶激酶 3β(GSK-3β)。在这里,我们回顾了 GSK-3β 在许多信号通路中的活性和功能及其在神经胶质瘤发生中的作用。

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