应用免疫组织化学检测EphA2及其调节基因HoxA1、C-myc在喉癌组织中的表达及相互关系  被引量:3

EXPRESSION AND RELATIONS OF EphA2,HoxA1 AND C-myc IN LARYNGEAL CARCINOMA WITH IMMUNOHISTOCHEMICAL STAINING

在线阅读下载全文

作  者:石栋梁[1] 杜涛[2] 习国平[1] 

机构地区:[1]河北省邯郸市第三医院耳鼻咽喉-头颈外科,河北邯郸056001 [2]河北省邯郸市第二医院内窥镜室,河北邯郸056001

出  处:《河北医科大学学报》2014年第9期1018-1021,共4页Journal of Hebei Medical University

摘  要:目的探讨同源异形盒基因A1(homeobox genes A1,HoxA1)、癌基因(cancer-myc,C-myc)、促红细胞生成素产生肝细胞受体A2(erythropoietin-producing hepatocellular receptor A2,EphA2)与喉癌发生发展的关系,从分子生物学角度探讨喉癌的发病机制。方法 40例喉癌组织及40例癌旁组织,取15例非喉癌患者的喉部正常黏膜组织做对照。所有肿瘤经病理检查证实为鳞状细胞癌,癌旁组织和正常组织取材经病理检查证实为炎症或正常。应用免疫组织化学检测喉癌组织、癌旁组织及喉部正常黏膜组织中EphA2、HoxA1、C-myc阳性表达率。结果 EphA2、HoxA1、C-myc在喉癌组织中的阳性表达率分别高于癌旁组织和正常喉黏膜组织,而癌旁组织与正常喉黏膜组织间的表达差异无统计学意义。结论 EphA2蛋白、HoxA1蛋白、C-myc蛋白在喉癌中的表达与喉癌的发生、发展有关。OcjectiVe The study eXplored the relation of homeoboX genes A1( HoXA1 ),cancer-myc(C-myc)and erythropoietin-producing hepatocellular receptor A2(EphA2)with laryngeal carcinoma for the genesis mechanism of laryngeal carcinoma at the level of molecular biology. Methods Forty laryngeal carcinoma fresh samples were analyzed and meanwhile 40 para-carcinoma tissues and 15 normal laryngeal mucosa samples were also studied as controls. All tumor tissues were confirmed to be squamous-cell carcinoma;the para-carcinoma tissues and normal mucosa were confirmed to be inflammatory or normal mucosa pathologically. The eXpression of EphA2,HoXA1 and C-myc protein were measured in laryngeal carcinoma, para-carcinoma tissues and normal larynneal mucosa tissues with the immunohistochemical staining. Results The eXpressions of EphA2,HoXA1,C-myc in laryngeal carcinoma tissues were significantly higher than those of para-carcinoma and in normal laryngeal mucosa tissues,respectively. There was no significant difference between the eXpressions of para-carcinoma and normal laryngeal mucosa tissues. Conclusion The eXpressions of EphA2,HoXA1 and C-myc contribute to the carcinogenesis and development of laryngeal carcinoma.

关 键 词:喉肿瘤 基因表达 免疫组织化学 

分 类 号:R739.65[医药卫生—肿瘤]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象