论文部分内容阅读
目的 探讨人乳头瘤病毒 16、18型感染与p5 3 ,p2 1ras癌基因协同 ,在大肠癌发生机制中的作用。 方法 采用SP免疫组化技术 ,检测 3 0例大肠腺瘤、10例腺瘤恶变、5 3例大肠腺癌和 3 0例正常大肠粘膜组织中HPV16、18E6,p5 3 ,p2 1ras蛋白并分析其相互关系。 结果 腺瘤、腺瘤恶变和腺癌组中E6,p5 3 ,p2 1ras的阳性表达分别为 3 6.7%、3 3 .3 %、40 .0 % ,60 .0 %、60 .0 %、70 .0 %和 5 4.7%、62 .2 %、71.7%。在腺瘤组中 ,随着上皮不典型性增生程度的加重 ,E6、p5 3、p2 1ras的阳性表达呈逐渐上升的趋势。腺瘤伴不典型性增生Ⅱ～Ⅲ级组中E6、p5 3、p2 1ras阳性表达显著高于腺瘤伴不典型性增生Ⅰ级 (P <0 .0 5 )。此外 ,腺瘤、腺瘤恶变及腺癌组中E6与p5 3 ,E6与 p2 1ras的双阳性表达均具显著相关性 (P <0 .0 5 )。在有淋巴结转移组中 ,E6的阳性表达和E6与 p5 3 ,E6与p2 1ras的双阳性表达均显著高于无淋巴结转移组 (P <0 .0 5 )。结论 本研究结果表明 :高危HPB16、18感染并在p5 3、ras癌基因的协同参与下 ,与本地区大肠癌的发生、发展过程密切相关 ,HPV 16、18感染后所致的 p5 3突变 /失活可能是大肠腺瘤恶变过程中的一个早期事件 ,在腺瘤中同时检测E6、p5 3、p2 1ras蛋白有可能成为大肠癌早期诊断的免疫
Objective To investigate the role of human papillomavirus 16 and 18 infections in synergy with p53 and p21ras oncogenes in the pathogenesis of colorectal cancer. Methods SP immunohistochemical technique was used to detect HPV16, 18E6, p53 and p21ras protein in 30 cases of colorectal adenoma, 10 cases of malignant adenoma, 53 cases of colorectal adenocarcinoma, and 30 cases of normal colorectal mucosa. Relationships. Results The positive expressions of E6, p53, and p21ras in adenomas, adenomas, and adenocarcinomas were 3 7%, 33.3%, 40.0 %, 60.0%, 60.0 %, and 70 respectively. .0 % and 5 4.7%, 62.2 %, 71.7%. In the adenoma group, the positive expression of E6, p53, and p21ras increased gradually with the increase of epithelial dysplasia. The positive expression of E6, p53, and p21ras in adenoma with atypical hyperplasia in II-III group was significantly higher than that in adenoma with atypical hyperplasia (P < 0.05). In addition, there was a significant correlation between double positive expression of E6 and p53, E6 and p21ras (P < 0.05) in adenoma, adenoma, and adenocarcinoma group. In the group with lymph node metastasis, the positive expression of E6 and double positive expression of E6 and p53, E6 and p21ras were significantly higher than those without lymph node metastasis (P < 0.05). Conclusion The results of this study indicate that high-risk HPB16 and 18 infections are closely related to the occurrence and development of colorectal cancer in the region, with the cooperative participation of p53 and ras oncogenes, and p53 mutations caused by HPV 16 and 18 infections. Inactivation may be an early event in the malignant transformation of colorectal adenomas. Simultaneous detection of E6, p53, and p2 1ras proteins in adenomas may serve as an early diagnosis of colorectal cancer.