当前位置:主页 > 医学论文 > 五官科论文 >

喉癌组织中CD44v5、CD44v6的表达变化及意义

发布时间:2018-04-22 00:36

  本文选题:细胞黏附分子 + CD44v5基因 ; 参考:《辽宁医学院》2012年硕士论文


【摘要】:目的 喉癌恶性程度较高,易发生淋巴转移。恶性肿瘤的发展进程是一个复杂连续的过程,在此过程中,肿瘤细胞与血管及淋巴管基底膜的黏附非常重要。细胞黏附分子CD44v5、CD44v6与许多恶性肿瘤的浸润、转移密切相关,并直接影响患者的预后。本研究通过观察喉癌及癌旁组织中细胞黏附分子CD44v5、CD44v6的表达变化情况来探讨其临床意义。 方法 采用免疫组织化学SP法检测78例喉癌组织及14例癌旁正常组织中CD44v5、 CD44v6表达变化。 RT-PCR法和Western蛋白印迹法鉴定CD44v5、CD44v6的表达情况。采用SPSS13.0统计分析软件处理实验数据,X~2检验、t检验进行分析。 结果 CD44v5在喉癌组织和癌旁组织中均有表达,,以喉癌组织中的阳性表达占优势,两组比较,P<0.05。CD44v5在喉癌中阳性表达率Ⅰ~Ⅱ期明显低于Ⅲ~Ⅳ期,无淋巴结转移者明显低于有淋巴结转移者,且随喉癌组织学分化程度的升高而降低。 CD44v6仅在喉癌组织中有表达,癌旁组织中无表达,两组比较,P<0.05。CD44v6在喉癌中阳性表达率Ⅰ~Ⅱ期明显低于Ⅲ~Ⅳ期,无淋巴结转移者明显低于有淋巴结转移者,且呈随喉癌组织学分化程度的升高而降低的趋势。 结论 CD44v5、CD44v6在喉癌组织中均表达,其中CD44v6表达特异性更高一些。 CD44v5、CD44v6的表达,与喉癌的TNM分期及有无淋巴结转移呈正相关,与组织分化程度呈负相关。CD44v5、CD44v6在喉癌中的高表达与肿瘤的侵袭、淋巴结的转移密切相关,且CD44v6与细胞的分化程度密切相关。
[Abstract]:Purpose Laryngeal carcinoma has a high degree of malignancy and is prone to lymphatic metastasis. The development of malignant tumors is a complex and continuous process in which the adhesion of tumor cells to blood vessels and lymphatic basement membrane is very important. The cell adhesion molecule CD44v5, CD44v6 is closely related to the invasion and metastasis of many malignant tumors, and directly affects the prognosis of the patients. The aim of this study was to investigate the clinical significance of CD44v5 and CD44v6 expression in laryngeal carcinoma and paracancerous tissues. Method Immunohistochemical SP method was used to detect the expression of CD44v5 and CD44v6 in 78 cases of laryngeal carcinoma and 14 cases of adjacent normal tissues. The expression of CD44v5, CD44v6 was identified by RT-PCR and Western Western blot. The SPSS13.0 statistical analysis software was used to process the experimental data. Result The expression of CD44v5 was found in laryngeal carcinoma and paracancerous tissues. The positive expression rate of 0.05.CD44v5 in laryngeal carcinoma was significantly lower in stage 鈪

本文编号:1784845

资料下载
论文发表

本文链接:https://www.wllwen.com/yixuelunwen/wuguanyixuelunwen/1784845.html


Copyright(c)文论论文网All Rights Reserved | 网站地图 |

版权申明:资料由用户1daf6***提供,本站仅收录摘要或目录,作者需要删除请E-mail邮箱bigeng88@qq.com