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作 者:王营[1] 刘伟 刘广珍[2] 李凤朝[2] 赵玉良[5] 费素娟[1] 王人灏[3] 陈文莉[2] 陈淑敏[2]
机构地区:[1]江苏省徐州医学院附属医院消化科,徐州 221006 [2]江苏省徐州医学院附属医院病理科,徐州 221006 [3]江苏省徐州医学院附属医院普外科,徐州 221006 [4]江苏省徐州市民政医院内科 [5]江苏省徐州市第一人民医院
出 处:《胰腺病学》2007年第3期154-156,共3页Chinese JOurnal of Pancreatology
基 金:江苏省教育厅自然研究项目(04KJD320203)、江苏省徐州市科技局科技计划项目(X2004425-3)
摘 要:目的研究γ-氨基丁酸(GABA)、谷氨酸脱羧酶(GAD)65和GAD67在胰腺癌组织中的表达及其意义。方法收集34例胰腺癌、12例慢性胰腺炎和10例正常胰腺组织标本,应用ABC法检测三者GABA、GAD65和GAD67的表达。结果胰腺癌GABA、GAD65和GAD67表达染色强度分值(2.41±0.49,2,09±0.29,2.10±0.30)及阳性细胞数分值(4.34±0.77,3.0±0.87,3.86±0.76)明显高于慢性胰腺炎(1.55±0.83,1.22±0.63,1.44±0.68;2.77±0.78,2.35±0.83,1.88±0.78)和正常胰腺组织(1.17±0.69,0.83±0.37,1.25±0.62;1.92±0.83,1.60±1.11,1.41±0.74),差异显著(P〈0.05或P〈0.01)。慢性胰腺炎GABA和GAD65的表达明显高于正常胰腺组织(P〈0.05)。低分化腺癌GABA和GAD65明显高于高分化腺癌(P〈0.05)。胰腺癌的GABA与GAD65表达呈正相关(r=0.67,P〈0.01)。结论GABA、GAD65和GAD67的表达与胰腺癌的发生、发展及生物学行为有密切关系,可能是潜在的胰腺癌标志物之一。Objective To study the characteristics of expression of gamma-aminobutyric acid (GABA), glutamic acid decarboxylase (GAD) 65 and GAD 67 enzymatic activities and their clinicopathological significance in the tissues of pancreatic cancer. Methods The immunologic activities of GABA, GAD65 and GAD67 were detected by immunohistochemical method of avidin-biotin complex on formalin-fixed and routine paraffin-embedded sections of specimens of pancreatic cancer (n = 34), chronic pancreatitis (n=12) and normal pancreas (n = 10). Results The scores of GABA, GAD65 and GAD67 (2.41 ± 0.49, 2. 09± 0.29, 2.10 ± 0.30) and the positive cell rates (4.34 ± 0.77, 3.0 ± 0.87, 3.86 ± 0.76) were significantly higher in pancreatic cancer than those of chronic pancreatitis (1. 55 ± 0.83, 1.22 ± 0.63, 1.44 ± 0.68; and 2.77 ± 0.78, 2.35 ± 0.83, 1.88 ± 0.78, respectively) and normal pancreas (1.17±0. 69, 0. 83 ± 0. 37, 1. 25 ± 0. 62;and 1. 92 ± 0.83, 1. 60 ± 1. 11, 1. 41 ± 0. 74, respectively), the difference was statistically significant (P 〈 0. 05 or P 〈 0. 01). The expression of GABA and GAD65 in chronic pancreatitis was higher than that in normal pancreas (P 〈 0. 05). The positive cell rates and scores of GABA and GAD65 were significantly higher in poorly-differentiated adenocarcinoma than those of well-differentiated adenocarcinoma (P 〈 0.05). The scores of GABA and GAD65 was significantly higher in chronic pancreatitis than normal pancreas (P 〈 0.05). A positive correlation was found between the scores of GABA and GAD65 in pancreatic cancer (r = 0.67, P 〈 0.01). Conclusions The active expression of GABA, GAD65 and GAD67 may be related to the carcinogenesis, progression and biological behaviors of pancreatic cancer. They may be potential biological markers for pancreatic cancer.
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