目的:通过检测大肠癌、癌旁黏膜与正常黏膜中APE和XRCC1蛋白的表达,探讨大肠癌的发生机制。方法:选取大肠癌手术切除标本185例,其中32例标本取癌旁黏膜组织;正常黏膜组织36例。通过免疫组化方法检测APE和XRCC1蛋白在癌、癌旁黏膜和正常黏膜的表达。结果:大肠癌、癌旁黏膜组APE阳性表达率分别为78.9%(146/185)和81.2%(26/32),两者均明显高于正常黏膜组的61.1%(22/36),χ2值分别为5.23和4.86,P值分别为0.024和0.03,但前两者APE表达差异无统计学意义。大肠癌中APE蛋白表达与患者性别、年龄、肿瘤部位、分化程度、浆膜浸润及淋巴结转移无明显相关关系。大肠癌与癌旁黏膜组XRCC1阳性表达率分别为94.6%(175/185)和87.5%(27/32),两者均明显高于正常黏膜组的27.7%(10/36),χ2值分别为4.43和29.69,P值分别为0.036和0.002,但前两者间差异无统计学意义。大肠癌中XRCC1蛋白表达与患者性别、年龄、肿瘤部位、分化程度、浆膜浸润及淋巴结转移无明显相关关系。大肠癌XRCC1阳性组的APE阳性率为95.8%(136/142),显著高于大肠癌XRCC1阴性组的86.0%(37/43),XRCC1与APE两者表达呈明显正相关关系,r=0.354,P=0.02。大肠癌和癌旁黏膜组的APE和XRCC1蛋白同时表达的阳性率分别为75.8%(140/185)和65.6%(21/32),两组均明显高于正常黏膜组的16.7%(6/36),χ2值分别为46.8和16.17,P值分别为0.001和0.001 5,但癌组与癌旁组间差异无统计学意义。结论:大肠癌和癌旁黏膜中存在APE和XRCC1表达上调。大肠癌发生可能与DNA复制时位点损伤及烷化剂等有毒物质损伤关系密切,同时检测大肠黏膜不同种类DNA修复基因的表达有助于大肠癌的早期诊断。 Objective: To explore the mechanism of colorectal cancer by detecting the expression of APE and XRCC1 protein in colorectal cancer, adjacent mucosa and normal mucosa. Methods: 185 cases of colorectal cancer were selected for surgical resection, of which 32 cases were adjacent mucosa tissues and 36 cases were normal mucosal tissues. The expression of APE and XRCC1 protein in cancer, paracancerous mucosa and normal mucosa were detected by immunohistochemistry. Results: The positive rates of APE in colorectal cancer and adjacent noncancerous mucosa were 78.9% (146/185) and 81.2% (26/32), respectively, which were significantly higher than those in normal mucosa (61.1%, 22/36) The values ​​were 5.23 and 4.86 respectively, P values ​​were 0.024 and 0.03 respectively, but there was no significant difference in APE expression between the two. There was no significant correlation between the expression of APE protein and the gender, age, tumor location, differentiation degree, serosal invasion and lymph node metastasis in colorectal cancer. The positive rates of XRCC1 in colorectal cancer and adjacent mucosa were 94.6% (175/185) and 87.5% (27/32), respectively, which were significantly higher than those in normal mucosa (27.7%, 10/36) respectively 4.43 and 29.69 respectively, with P values ​​of 0.036 and 0.002 respectively, but there was no significant difference between the former two. The expression of XRCC1 protein in colorectal cancer had no significant correlation with gender, age, tumor location, degree of differentiation, serosal invasion and lymph node metastasis. The positive rate of APE in XRCC1 positive group was 95.8% (136/142), which was significantly higher than that in XRCC1 negative group (86.0%, 37/43). There was a positive correlation between XRCC1 and APE (r = 0.354 , P = 0.02. The positive rates of APE and XRCC1 protein expression in colorectal cancer and adjacent noncancerous mucosa tissues were 75.8% (140/185) and 65.6% (21/32), respectively, which were significantly higher than those in normal mucosa (16.7%, 6 / 36), χ2 values ​​were 46.8 and 16.17, P values ​​were 0.001 and 0.001 5, but no significant difference between the cancer group and adjacent non-cancerous group. Conclusion: APE and XRCC1 are up-regulated in colorectal cancer and adjacent mucosa. The occurrence of colorectal cancer may be closely related to the site damage of DNA replication and alkylating agents and other toxic substances, and the detection of different types of DNA repair gene in colorectal mucosa may be helpful for the early diagnosis of colorectal cancer.