摘要：
Objective: 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 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 and TNM staging. hTere was also no signiifcant difference (P>0.05) between MSH2 missing expression and the lesion location. However, there was some difference (P0.05) between MLH1, PMS2, MSH2, MSH6 missing expression and Pgp, GSTπ, TopoⅡ expression. Nevertheless, the differences existed between MLH1, PMS2, MSH2, MSH6 missing expression and Ki-67 expression (P50% (+) were 6.1%, 4.1%, 8.2%, 6.1%, respectively. MLH1, PMS2, MSH2, MSH6 missing expression and Ki-67 expression was negatively correlated (correlation coefficientr=−0.969,r=−0.464,r=−0.143,r=−0.344,P50%(+)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(P0.05)。MLH1、PMS2、MSH2、MSH6缺失表达与Ki-67表达有一定差异性(P50%(+)的MLH1、PMS2、MSH2、MSH6缺失表达率分别为6.1%、4.1%、8.2%、6.1%。MLH1、PMS2、MSH2、MSH6缺失表达与Ki-67表达呈负相关(相关系数分别为r=−0.969、r=−0.464、r=−0.143、r=−0.344， P<0.05)。结论：错配修复基因MLH1、PMS2、MSH6基因缺失表达发生右半结肠几率相对较高，其次依次是左半结肠、直肠。MLH1、PMS2、MSH2、MSH6缺失表达与Ki-67表达呈负相关。
