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J Clin Pathol. 2007 Feb;60(2):218-21. doi: 10.1136/jcp.2006.036806.
2
Nuclear overexpression of mitotic regulatory proteins in biliary tract cancer: correlation with clinicopathologic features and patient survival.有丝分裂调节蛋白在胆管癌中的核过表达:与临床病理特征及患者生存的相关性
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3
Comparative immunohistochemical analysis of aurora-A and aurora-B expression in human glioblastomas. Associations with proliferative activity and clinicopathological features.人胶质母细胞瘤中极光激酶A和极光激酶B表达的比较免疫组织化学分析。与增殖活性及临床病理特征的相关性。
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Overexpression of an Aurora-C kinase-deficient mutant disrupts the Aurora-B/INCENP complex and induces polyploidy.极光激酶C缺陷型突变体的过表达会破坏极光激酶B/着丝粒蛋白复合体,并诱导多倍体形成。
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本文引用的文献

1
Aurora kinases, aneuploidy and cancer, a coincidence or a real link?极光激酶、非整倍体与癌症,是巧合还是存在实质联系?
Trends Cell Biol. 2005 May;15(5):241-50. doi: 10.1016/j.tcb.2005.03.004.
2
The molecular requirements for cytokinesis.胞质分裂的分子要求。
Science. 2005 Mar 18;307(5716):1735-9. doi: 10.1126/science.1096896.
3
Aurora-B dysfunction of multinucleated giant cells in glioma detected by site-specific phosphorylated antibodies.通过位点特异性磷酸化抗体检测胶质瘤中多核巨细胞的极光激酶B功能障碍。
J Neurosurg. 2004 Dec;101(6):1012-7. doi: 10.3171/jns.2004.101.6.1012.
4
Aurora-kinase inhibitors as anticancer agents.极光激酶抑制剂作为抗癌药物。
Nat Rev Cancer. 2004 Dec;4(12):927-36. doi: 10.1038/nrc1502.
5
Aurora B overexpression associates with the thyroid carcinoma undifferentiated phenotype and is required for thyroid carcinoma cell proliferation.极光激酶B的过表达与甲状腺癌的未分化表型相关,并且是甲状腺癌细胞增殖所必需的。
J Clin Endocrinol Metab. 2005 Feb;90(2):928-35. doi: 10.1210/jc.2004-1518. Epub 2004 Nov 23.
6
Aneuploidy and cancer.非整倍体与癌症。
Nature. 2004 Nov 18;432(7015):338-41. doi: 10.1038/nature03099.
7
Overexpression and amplification of STK15 in human gliomas.人胶质瘤中STK15的过表达与扩增
Int J Oncol. 2004 Dec;25(6):1789-94.
8
Triggering p53 after cytokinesis failure.胞质分裂失败后触发p53。
J Cell Biol. 2004 Jun 7;165(5):607-8. doi: 10.1083/jcb.200405089.
9
Aurora B expression in normal testis and seminomas.极光激酶B在正常睾丸和精原细胞瘤中的表达。
J Endocrinol. 2004 May;181(2):263-70. doi: 10.1677/joe.0.1810263.
10
Aurora kinases link chromosome segregation and cell division to cancer susceptibility.极光激酶将染色体分离和细胞分裂与癌症易感性联系起来。
Curr Opin Genet Dev. 2004 Feb;14(1):29-36. doi: 10.1016/j.gde.2003.11.006.

极光激酶B的表达与多形性胶质母细胞瘤的侵袭性行为相关。

Aurora B expression correlates with aggressive behaviour in glioblastoma multiforme.

作者信息

Zeng Weifen F, Navaratne Kapila, Prayson Richard A, Weil Robert J

机构信息

The Brain Tumor Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.

出版信息

J Clin Pathol. 2007 Feb;60(2):218-21. doi: 10.1136/jcp.2006.036806.

DOI:10.1136/jcp.2006.036806
PMID:17264249
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1860618/
Abstract

Chromosomal abnormalities and genomic instability are common features of, and possible driving forces in, tumorigenesis. Recently, several mitotic proteins that are critical to proper chromosome segregation have been identified. Members of the Aurora kinase family have been identified as having important roles in mitosis; overexpression induces multicellularity and fosters polyploidy. As aneuploidy is a common feature of malignant gliomas, particularly glioblastomas (GBMs), we examined 25 prospectively collected GBMs to assess the role that overexpression of one member of this family, Aurora B, might have in the clinical behaviour of GBMs. Aurora B expression levels were markedly correlated with a shortened survival. Aurora B expression was not directly related to age, tumour proliferation status or to several common molecular changes found in GBMs. These results suggest that Aurora B may be a prognostic feature of impaired survival and a novel therapeutic target in some patients.

摘要

染色体异常和基因组不稳定是肿瘤发生的常见特征及可能的驱动因素。最近,已鉴定出几种对正确染色体分离至关重要的有丝分裂蛋白。极光激酶家族成员已被确定在有丝分裂中发挥重要作用;过表达会诱导多细胞性并促进多倍体形成。由于非整倍体是恶性胶质瘤尤其是胶质母细胞瘤(GBM)的常见特征,我们检测了25例前瞻性收集的GBM,以评估该家族一个成员极光B的过表达可能在GBM临床行为中所起的作用。极光B的表达水平与生存期缩短显著相关。极光B的表达与年龄、肿瘤增殖状态或GBM中发现的几种常见分子变化无直接关系。这些结果表明,极光B可能是生存受损的一个预后特征,并且是部分患者的一个新治疗靶点。