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作 者:李志强[1,2] 袁先厚[1,2] 吴志敏[1] 郭志旺[1] 俞苏寰[1,2] 江普查[1] 文志华[1,2]
机构地区:[1]武汉大学中南医院神经外科,湖北武汉430071 [2]武汉大学中南医院神经肿瘤研究室,湖北武汉430071
出 处:《中国神经肿瘤杂志》2008年第3期193-196,共4页Chinese Journal of Neuro-Oncology
基 金:湖北省卫生厅科研基金(JX1B019);武汉大学科研基金(301270064)
摘 要:背景与目的:非受体酪氨酸蛋白激酶家族成员FAK和Pyk2具有高度同源性,对肿瘤细胞增殖和侵袭具有重要的调控作用,但其是否参与肿瘤血管生成过程尚不明确。本研究旨在探讨FAK和Pyk2在脑星形细胞肿瘤中表达与血管生成的关系。方法:应用免疫组化法检测58例脑星形细胞肿瘤中FAK、Pyk2和血管内皮生长因子(VEGF)表达,并用CD31标记计数瘤内微血管密度。结果:FAK、Pyk2蛋白主要表达于肿瘤细胞胞浆,Pyk2阳性表达也见于肿瘤血管内皮细胞。在Ⅰ、Ⅱ、Ⅲ、Ⅳ级星形细胞肿瘤中,FAK阳性率分别为20.0%(1/5)、26.7%(4/15)、44.4%(8/18)、50.0%(10/20),Pyk2阳性率分别为40.0%(2/5)、60.0%(9/15)、77.8%(14/18)、85.0%(17/20);FAK和Pyk2阳性表达强度评分在Ⅱ级星形细胞肿瘤与Ⅲ、Ⅳ级星形细胞肿瘤中具有显著差异性(P<0.05)。FAK、Pyk2表达与VEGF和微血管密度呈正相关,相关系数分别为rs=0.423(P=0.001)和rs=0.729(P<0.005)。结论:FAK、Pyk2可能通过与VEGF的相互作用而参与脑星形细胞肿瘤的血管生成过程。BACKGROUND & OBJECTIVE:FAK and Pyk2,two membership with highly homologous of the FAK family of non-receptor tyrosine kinases, are confirmed as key regulators of tumor cell proliferation and migration. The aim of this work was to study the expressions of FAK and Pyk2 in human astrocytic tumors and its relationship with angiogenesis. METHODS: The SP immunohistochemical method was used to measure the expression of FAK, Pyk2 and VEGF proteins in 58 human brain astrocytic tumors, and microvessel density (MVD) was detected by CD31 staining. RESULTS: The location of FAK and Pyk2 positive staining were mainly seen in tumor cytoplasm, and in some tumor microvascular endothelial cells Pyk2 positive staining was also observed. In astrocytic tumors withⅠ、Ⅱ、Ⅲ、Ⅳ grades, the positive rate of FAK is 20.00%(1/5)、26.67% (4/15)、44.44% (8/18)、50.00% (10/20)respectively, those of Pyk2 is 40.00% (2/5)、60.00% (9/15)、77.78% (14/ 18)、85.00%(17/20)respectively. There were significant difference of FAK and Pyk2 expression scores between Ⅱand Ⅲ 、 Ⅳ grades astrocytic tumors (P 〈0.05). FAK and Pyk2 expressions, especially Pyk2, correlatespositively with VEGF expression (rs=0.423, P=0.001; rs=0.729, P〈0.005). CONCLUISON: FAK and Pyk2 plays an important role in astrocytic tumor angiogenesis through regulation to VEGF.
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