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Ogawa E Takenaka K Katakura H Adachi M Otake Y Toda Y Kotani H Manabe T Wada H Tanaka F 《Annals of surgical oncology》2008,15(2):547-554
Purpose Aurora-A, also known as STK15/BTAK, is a member of the protein serine/threonine kinase family, and experimental studies have
revealed that Aurora-A plays critical roles in cell mitosis and in carcinogenesis. However, no clinical studies on Aurora-A
expression in non-small-cell lung cancer (NSCLC) have been reported. Thus, the present study was conducted to assess the clinical
significance of Aurora-A status.
Experimental Design A total of 189 consecutive patients with resected pathologic (p-)stage I-IIIA, NSCLC were retrospectively reviewed, and immunohistochemical
staining was used to detect Aurora-A expression.
Results Aurora-A expression was negative in 31 patients (16.4%); among Aurora-A positive patients, 124 patients showed pure diffuse
cytoplasmic Aurora-A expression and the other 34 patients showed perimembrane Aurora-A expression. Perimembrane Aurora-A tumors
showed the highest proliferative index (PI) (mean PIs for negative, diffuse cytoplasmic, and perimembrane tumors: 49.2, 41.7,
and 63.5, respectively; P < .001). Five-year survival rates of Aurora-A negative, diffuse cytoplasmic, and perimembrane patients were 67.8%, 66.7%,
and 47.6%, respectively, showing the poorest postoperative survival in perimembrane patients (P = .033). Subset analyses revealed that perimembrane Aurora-A expression was a significant factor to predict a poor prognosis
in squamous cell carcinoma patients, not in adenocarcinoma patients. A multivariate analysis confirmed that perimembrane Aurora-A
expression was an independent and significant factor to predict a poor prognosis.
Conclusions Perimembrane Aurora-A status was a significant factor to predict a poor prognosis in correlation with enhanced proliferative
activity in NSCLC. 相似文献
2.
《Expert opinion on therapeutic targets》2013,17(2):187-200
Introduction: Based on its role as a mitotic regulatory kinase, overexpressed and associated with aneuploidy in cancer, small-molecule inhibitors have been developed for Aurora-A (AURKA) kinase. In preclinical and clinical assessments, these agents have shown efficacy in inducing stable disease or therapeutic response. In optimizing the use of Aurora-A inhibitors, it is critical to have robust capacity to measure the kinase activity of Aurora-A in tumors.Areas covered: We provide an overview of molecular mechanisms of mitotic and non-mitotic activation of Aurora-A kinase, and interaction of Aurora-A with its regulatory partners. Typically, Aurora-A activity is measured by use of phospho-antibodies targeting an autophosphorylated T288 epitope. However, recent studies have identified alternative means of Aurora-A activation control, including allosteric regulation by partners, phosphorylation on alternative activating residues (S51, S98), dephosphorylation on inhibitory sites (S342) and T288 phosphorylation by alternative kinases such as Pak enzymes. Additional work has shown that the relative abundance of Aurora-A partners can affect the activity of Aurora-A inhibitors, and that Aurora-A activation also occurs in interphase cells.Expert opinion: Taken together, this work suggests the need for comprehensive analysis of Aurora-A activity and expression of Aurora-A partners in order to stratify patients for likely therapeutic response. 相似文献
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Aurora-A激酶家族是一组新近发现的调节中心体、微管功能的丝氨酸/苏氨酸激酶,在细胞中心体的成熟、纺锤体的建立以及染色体的正常分离过程中起着重要的调控作用。Aurora激酶家族包括 相似文献
4.
Vassilis Samaras Angeliki Stamatelli Efstathios Samaras Christos Arnaoutoglou Marianthi Arnaoutoglou Ioanna Stergiou Paraskevi Konstantopoulou Vassilis Varsos Andreas Karameris Calypso Barbatis 《Pathology, research and practice》2009,205(11):765-773
In the present study, we carried out a comparative immunohistochemical analysis of aurora-A and aurora-B expression in 40 patients with primary glioblastomas, and attempted to identify any associations with Ki-67 index and the patients’ clinical features. The impact of various treatment modalities and proliferative activity on patient outcome was also assessed.Immunohistochemistry was carried out using formalin-fixed and paraffin-embedded tissue sections.Aurora-A expression was higher in tumors with high Ki-67 expression (p=0.01) and was positively, though marginally, related to aurora-B expression (p=0.085). Aurora-B expression was not linked to Ki-67 expression (p=0.182). Lower aurora-A immunohistochemical expression, chemotherapy administration, and tumor localization in one lobe of the brain implied a greater probability of patient survival in univariate analysis (p=0.044, p=0.008, p=0.041, respectively). Ki-67 and aurora-B immunoreactivities were not associated with patient survival (p=0.918 and p=0.539, respectively).To our knowledge, for the first time, the association between aurora-A and aurora-B expression, the correlation of aurora-A with Ki-67 index, and the prognostic impact of aurora-A expression were assessed in glioblastomas. Although we addressed a prognostic connotation of aurora-A, we presume that aurora-A and aurora-B play a complicated role within glioblastomas. Further examinations of larger series are required, so that definite conclusions can be drawn. 相似文献
5.
乜新普 《山东医学高等专科学校学报》2009,31(6):408-410
目的探讨有丝分裂调节因子Aurora-A在膀胱癌组织中的表达以及与膀胱癌的生物学行为间的关系。方法对53例膀胱癌及11例正常膀胱黏膜组织用免疫组织化学方法检测其Au-rora-A蛋白表达的情况;同时对不同浸润程度的膀胱癌以及正常膀胱组织各6例用RT-PCR法检测Aurora-A mRNA的表达。结果53例膀胱癌中48例Aurora-A蛋白呈阳性表达(91%),而11例正常膀胱组织中只有4例呈阳性表达(36%),二者比较有统计学意义(P〈0.001)。与正常膀胱组织比较,膀胱癌组织中Aurora-A mRNA增高2.1~5.3倍(P〈0.01)。结论Aurora-A在膀胱癌组织中表达明显增高,与膀胱癌的肌肉浸润有一定的关系。 相似文献
6.
Tao Y Zhang P Frascogna V Lecluse Y Auperin A Bourhis J Deutsch E 《British journal of cancer》2007,97(12):1664-1672
Overexpression of Aurora-A kinase has been correlated with cancer susceptibility and poor prognosis in several human cancers. In this study, we evaluated the effect of inhibition of Aurora-A kinase on cell cycle progression and tumour cell survival after exposure to ionising radiation (IR). Combined IR and Aurora-A inhibition by short interfering RNA (siRNA) or by PHA680632 (a selective Aurora kinase inhibitor with submicromolar activity against Aurora-A) prior to IR led to an enhancement of radiation-induced annexin V positive cells, micronuclei formation, and Brca1 foci formation only in cells with deficient p53. However, the drug brought about additive to sub-additive interaction with radiation with regard to in vitro clonogenic survival. Cell cycle analysis revealed a high >4N DNA content 24 h after PHA680632 exposure. DNA content >4N was reduced dramatically when cells were irradiated combined with PHA680632 simultaneously. In vivo xenografts (p53-/- HCT116) of a mice study showed enhanced tumour growth delay (TGD) after the PHA680632-IR combinatorial treatment compared with IR alone. These results demonstrate that PHA680632 in association with radiation leads to an additive effect in cancer cells, especially in the p53-deficient cells, but does not act as a radiosensitiser in vitro or in vivo. 相似文献
7.
RNA干扰对Aurora-A在人卵巢癌细胞中表达及细胞增殖的影响 总被引:2,自引:0,他引:2
目的: 〖HT5"SS〗探讨应用RNA干扰技术沉默AuroraA基因表达,研究其对人卵巢癌SKOV3细胞增殖的抑制作用。〖HT5W〗方法〖HT5"SS〗: 设计合成两对特异性针对AuroraA基因的Oligo siRNA,转染至SKOV3细胞中,采用RTPCR和Western blot检测AuroraA mRNA和蛋白表达情况,同时利用MTT试验和流式细胞仪观察转染后细胞增殖抑制和凋亡情况。〖HT5W〗结果:〖HT5"SS〗转染Oligo siRNA后,SKOV3细胞AuroraA mRNA表达受抑制(P<0.01),蛋白表达水平降低;细胞增殖的抑制率和细胞凋亡率明显增高(P<005, P<0.01)。〖HT5W〗结论: 〖HT5"SS〗体外合成的特异性针对AuroraA基因的Oligo siRNA对卵巢癌细胞株SKOV3中AuroraA基因表达和细胞增殖均有明显抑制作用,为进一步研究Auroraa基因的功能提供了实验基础。 相似文献
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目的通过检测人脑胶质瘤患者肿瘤组织中Aurora-A基因的表达水平,探讨Aurora-A基因与胶质瘤的关系。方法采用荧光实时定量逆转录聚合酶链式反应(RT-PCR)法,检测了42例人脑胶质瘤组织和20例正常脑组织中Auro-ra-AmRNA表达水平,分析其表达水平与胶质瘤的关系。结果Aurora-AmRNA在胶质瘤组、Ⅰ-Ⅱ级胶质瘤组、Ⅲ-Ⅳ级胶质瘤组及对照组中的表达量分别为1.414±0.157%、0.380±0.067%、2.050±0.144%、0.040±0.004%。统计显示Aurora-AmRNA表达水平在胶质瘤组明显高于对照组(P0.05),且在Ⅰ-Ⅱ级胶质瘤组及Ⅲ-Ⅳ级胶质瘤组中均明显高于对照组(P0.05),同时Aurora-AmRNA表达水平在Ⅲ-Ⅳ级胶质瘤组中显著高于Ⅰ-Ⅱ级胶质瘤组(P0.05)。结论Aurora-A基因在人脑胶质瘤组织中有高表达,说明Aurora-A基因在胶质瘤的发生、发展过程中起重要作用;Aurora-A基因在Ⅲ-Ⅳ级恶性程度高的胶质瘤组织中有更高表达,说明Aurora-A基因可能与胶质瘤的恶性程度存在密切关系。 相似文献
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