出 处:《临床与病理杂志》2016年第7期956-963,共8页Journal of Clinical and Pathological Research
摘 要:目的:探讨结直肠癌错配修复基因(MLH1,PMS2,MSH2,MSH6)免疫组化表达特点及其与临床病理的关系,以及错配修复基因(MLH1,PMS2,MSH2,MSH6)与结直肠癌中P-糖蛋白(Pgp)、谷胱甘肽-S-转移酶(GSTπ)、DNA拓扑异构酶Ⅱ(TopoⅡ)、细胞增殖抗原Ki-67免疫组化表达关系。方法:回顾性分析2014年2月至2015年12月我院收治的93例结直肠癌患者的临床病理资料,采用免疫组织化学法,检测癌组织中错配修复基因(MLH1,PMS2,MSH2,MSH6)、Pgp、GSTπ、TopoⅡ、Ki-67的表达,分析其表达特点。采用多个样本率(或构成比)的比较(即:R×C表的χ2检验),分析结直肠癌错配修复基因(MLH1,PMS2,MSH2,MSH6)与临床病理的关系及其与Pgp、GSTπ、TopoⅡ、Ki-67免疫组化表达关系。利用Pearson相关分析法分析MLH1、PMS2、MSH2、MSH6与Ki-67表达相关性。结果:错配修复基因MLH1、PMS2、MSH2、MSH6表达缺失阳性率分别占14.0%、17.2%、10.8%、11.8%,Pgp(-)、Pgp (+)、Pgp (++)、Pgp (+++)表达率分别占3.2%、25.8%、51.6%、19.3%。GSTπ(-)、GSTπ(+)、GSTπ(++)、GSTπ(+++)表达率分别占3.3%、16.7%、56.7%、23.3%。TopoⅡ阴性表达及IV级表达未见,TopoⅡⅠ级、Ⅱ级、Ⅲ级表达率分别占19.3%、77.4%、3.2%。Ki-67表达<10%(+)、10-50%(+)、>50%(+)分别占1.3%、25%、50%。错配修复基因MLH1、PMS2、MSH2、MSH6缺失表达与患者的性别、年龄、病理分化、TNM分期无统计学差异(P>0.05)。MSH2缺失表达与发病部位无统计学差异(P>0.05)。MLH1、PMS2、MSH6基因缺失表达与发病部位有一定差异性(P<0.05),发生左半结肠的缺失表达阳性率分别为:10.7%、10.7%、7.1%,右半结肠缺失表达阳性率分别为28.6%、35.7%、25%,直肠缺失表达阳性率为5.4%、8.1%、5.4%。MLH1、PMS2、MSH2、MSH6缺失表达与Pgp、GSTπObjective: To investigate the immunohistochemical expression characteristics of mismatch repair genes (MLH1, PMS2, MSH2, MSH6), and the relationship with clinicopathology features, and the correlation between the immunohistochemical expression of P-glycoprotein (Pgp), glutathione -S- transferase (GSTπ), DNA topoisomeraseⅡ (TopoⅡ), cell proliferation antigen Ki-67 and those four mismatch repair genes in colorectal cancer.Methods:hTe clinicopathology characteristics of 93 cases of colorectal cancer patients in our hospital from 2014/2 to 2015/12 were analyzed retrospectively. Expression features of mismatch repair genes (MLH1, PMS2, MSH2, MSH6), Pgp, GSTπ, TopoⅡ, Ki-67 determined by immunohistochemical staining were analyzed. hTen we used a plurality of sample rate (or constituent ratio) comparisons (i.e.,χ2 test with R×C table) to analyze the relationship between immunohistochemical expression of mismatch repair genes (MLH1, PMS2, MSH2, MSH6) and Pgp, GSTπ, TopoⅡ, Ki-67 in colorectal cancer. Pearson correlation analyses were used to analyze the correlation of the expression between mismatch repair genes (MLH1, PMS2, MSH2, MSH6) and Ki-67.Results:The missing expression rate of mismatch repair genes MLH1, PMS2, MSH2, MSH6 were 14.0%, 17.2%, 10.8%, 11.8%, respectively. The expression rate of Pgp(-), Pgp (+), Pgp (++), Pgp (+++) each accounted for 3.2%, 25.8%, 51.6%, 19.3%. hTe expression rate of GSTπ (-), GSTπ (+), GSTπ (++), GSTπ (+++) accounted for 3.3%, 16.7%, 56.7%, 23.3%. TopoⅡhad no negative and IV level expression, TopoⅡⅠ level,Ⅱ level,Ⅲ level accounted for 19.3%, 77.4%, 3.2%. hTe expression rate of Ki-67 〈10% (+), 10%~50% (+), 〉50% (+) accounted for 1.3%, 25%, 50%, separately. hTere was no statistically signiifcant difference (P〉0.05) between missing expression of mismatch repair genes (MLH1, PMS2, MSH2, MSH6) and gender, age, histological differentiation
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