脑胶质瘤中ADAM17、EGFR和Ki-67的表达及其与脑胶质瘤恶性程度的关系

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目的探讨不同恶性程度脑胶质瘤组织中解聚素-金属蛋白酶17(ADAM17)、表皮生长因子受体(EGFR)和增殖细胞核抗原(Ki-67)的表达及其与肿瘤分级的关系。方法收集2014年1月至12月神经外科手术切除的人脑胶质瘤新鲜标本40例(脑胶质瘤组f),根据其恶性程度分为低度恶性组f(n=20)和高度恶性组f(n=20),设同期颅脑外伤手术减压的脑组织新鲜标本为对照组f(n=20);免疫印迹法检测新鲜标本ADAM17和EGFR的表达。另收集2010年1月至2013年1月病理科人脑胶质瘤蜡块标本60例(脑胶质瘤组p),分为低度恶性组p(n=23)和高度恶性组p(n=37),设同期颅脑外伤手术减压的脑组织蜡块标本为对照组p(n=9);免疫组化SABC法检测蜡块标本ADAM17、EGFR和Ki-67的表达。分别对不同标本的脑胶质瘤不同恶性程度组织和正常对照组织中ADAM17、EGFR和Ki-67表达情况进行比较。检验水准取α=0.05,采用R×C表χ~2检验分割法时,检验水准校正为α’=0.017。结果新鲜标本的免疫印迹法结果:对照组ADAM17表达极低,EGFR未见表达,ADAM17和EGFR蛋白表达在低度恶性组f(0.32±0.05,0.46±0.07)及高度恶性组f(0.80±0.14,1.16±0.15)均明显增加,且高度恶性组f明显高于低度恶性组f(P均<0.01)。蜡块标本的免疫组化SABC法结果:(1)对照组p ADAM17蛋白以弱阳性表达为主,脑胶质瘤组p ADAM17以阳性和强阳性表达为主;ADAM17蛋白阳性表达率脑胶质瘤组p明显高于对照组p(80.0%vs 22.2%,P<0.01),高度恶性组p明显高于低度恶性组p(94.6%vs 56.5%,P<0.017)。(2)EGFR蛋白在对照组脑组织中无表达,脑胶质瘤中以阳性和强阳性表达为主。EGFR阳性表达率脑胶质瘤组p明显高于对照组p(60.0%vs 0,P<0.01),高度恶性组p明显高于低度恶性组p(73.0%vs 39.1%,P<0.017)。(3)9例对照组Ki-67均为阴性表达;Ki-67阳性表达率脑胶质瘤组p明显高于对照组p(63.3%vs 0,P<0.01),高度恶性组p明显高于低度恶性组p(86.5%vs 26.1%,P<0.017)。结论 ADAM17、EGFR和Ki-67在脑胶质瘤中表达增加,且随着恶性程度的增高表达水平明显增高,高表达的ADAM17和EGFR与脑胶质瘤细胞增殖密切相关。 Objective To investigate the expression of ADAM17, EGFR and Ki-67 in different malignant gliomas and its relationship with tumor grade. Methods Forty patients with glioma resected from January 2014 to December 2014 were enrolled in this study. Glioma group f (n = 20) and height (n = 20) were divided into two groups according to their malignancy: The malignant group f (n = 20) was established as the control group f (n = 20). The fresh specimens of fresh specimens of ADAM17 and EGFR were detected by immunoblotting. Sixty patients (glioma group, p) were collected from January 2010 to January 2013, and were divided into low grade group (n = 23) and high grade group (p n = 37). The brain tissue samples of paraffin-embedded sections undergoing craniocerebral trauma during the same period were selected as control group (n = 9). Immunohistochemical SABC method was used to detect the expression of ADAM17, EGFR and Ki-67. The expression of ADAM17, EGFR and Ki-67 in different malignant gliomas and normal control tissues of different specimens were compared. When the inspection level is taken as α = 0.05, the test level is corrected to α ’= 0.017 when using the R × C table χ ~ 2 test. Results The results of Western blotting showed that ADAM17 expression in control group was extremely low and EGFR was not expressed. The expression of ADAM17 and EGFR protein in low malignant group (f = 0.32 ± 0.05, 0.46 ± 0.07) and high malignant group (f ± 0.80 ± 0.14 , 1.16 ± 0.15), respectively, which were significantly higher than those in the low-grade group (P <0.01). The results of immunohistochemical SABC assay of paraffin blocks: (1) The expression of p ADAM17 protein in the control group was mainly weakly positive while the expression of p ADAM17 in glioma group was mainly positive and strongly positive. The positive expression rate of ADAM17 protein was significant The expression of p in tumor group was significantly higher than that in control group (80.0% vs 22.2%, P <0.01). The expression of p in high grade group was significantly higher than that in low grade group (94.6% vs 56.5%, P <0.017). (2) There was no expression of EGFR protein in the brain tissue of control group, mainly positive and strong positive expression in gliomas. The positive rate of EGFR in glioma group p was significantly higher than that in control group p (60.0% vs 0, P <0.01), and in highly malignant group p was significantly higher than that in low grade malignancy group p (73.0% vs 39.1%, P <0.017) . (3) The expression of Ki-67 in 9 cases was negative, Ki-67 positive expression rate in glioma group was significantly higher than that in control group (63.3% vs 0, P <0.01) In low grade malignancy group p (86.5% vs 26.1%, P <0.017). Conclusion The expression of ADAM17, EGFR and Ki-67 is increased in gliomas, and the expression of ADAM17, EGFR and Ki-67 is significantly increased with the increase of malignant degree. The high expressions of ADAM17 and EGFR are closely related to the proliferation of glioma cells.
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