期刊文献+

脑膜瘤组织中组织蛋白酶异常表达及其诊断价值研究

The Abnormal Expression of Cathepsin in Meningioma and its Diagnostic Value
下载PDF
导出
摘要 目的探索组织蛋白酶B与抑制因子于脑膜瘤组织中的表达及临床诊断价值。方法选取2018年1月-2020年1月本院收治的100例脑膜瘤患者肿瘤组织标本,按免疫组织化学分析法,分析组织蛋白酶B与抑制因子于脑膜瘤组织中的表达及临床诊断价值。结果脑瘤膜分类中,良性75例,非典型性14例,恶性11例,从疾病侵袭性来看,侵袭硬脑膜与颅骨的有53例,未造成侵袭的有47例。从表达上来看,差异较大是良、恶性脑膜瘤、良恶性脑膜瘤与非典型性脑膜瘤(P<0.05)。结论恶性脑膜瘤患者的组织蛋白酶B水平明显要比良性者高,有希望成为辨别肿瘤性质的重要依据,组织蛋白酶异常表达能够清晰展现病灶的发展,有助于良恶性的判断,脑膜瘤良恶性的准确诊断下,患者的疾病治疗可得到及时的控制,这对患者的病情预后大有裨益。 Objective To explore the expression and clinical diagnostic value of cathepsin B and inhibitors in meningiomas.Methods From January 2018 to January 2020,100 tumor tissue specimens from meningioma patients were collected.According to immunohistochemical analysis,the expression of cathepsin B and inhibitors in meningiomas and their clinical diagnostic value were analyzed.Results In the classification of meningeal membranes,75 were benign,14 were atypical,and 11 were malignant.From the perspective of disease aggressiveness,53 cases invaded the dura mater and skull,and 47 cases did not cause invasion.From the expression point of view,the big difference is between benign and malignant meningioma,benign and malignant meningioma and atypical meningioma(P<0.05).Conclusion The cathepsin B level of patients with malignant meningioma is significantly higher than that of benign ones.It is hoped to become an important basis for distinguishing the nature of tumors.Abnormal expression of cathepsin can clearly show the development of lesions,which is helpful for the judgment of benign and malignant meningioma.Under the accurate diagnosis of benign and malignant meningioma,the patient’s disease treatment can be controlled in time.The prognosis of the disease is of great benefit.
作者 李立 谭超华 周灿宦 蔡晓燕 LI Li;TAN Chaohua;ZHOU Canhuan;CAI Xiaoyan(Department of Pathology,Taishan People's Hospital,Taishan,Guangdong,529200)
出处 《智慧健康》 2022年第32期206-209,共4页 Smart Healthcare
关键词 组织蛋白酶B 抑制因子 脑膜瘤 异常表达 诊断 效果 Cathepsin B Inhibitory factor Meningioma Abnormal expression Diagnosis Effect
  • 相关文献

参考文献10

二级参考文献40

共引文献39

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部