论文部分内容阅读
目的：探讨细菌L型可能致癌的机理。方法;用革兰染色和免疫级化染色技术对69例鼻咽癌、20例鼻咽粘膜慢性炎症进行细菌L型检测，同时对L型阳性和阴性组织的PCNA、P21、P53表达进行对比分析。结果;鼻咽癌组的L型检出率为79.7％，与慢性炎症组（75.0％）无显著性差异（P＞0.05），但鼻咽癌组的PCNA、p21、p53表达部显著高于L型阴性组（P＜0.01）。表明L型感染与鼻咽癌的PCNA、p21、p53过度表达存在着相关性及L型感染的组织处于高增殖状态。结合提示L型感染参与了ras原癌基因激活和p53抑癌基因的失活。基因突变可能是L型致癌作用的机制之一。
Objective: To explore the mechanism of bacterial L-type carcinogenesis. METHODS: Gram-negative and immunohistochemical staining techniques were used to detect bacterial L-forms in 69 cases of nasopharyngeal carcinoma and 20 cases of chronic inflammation of nasopharyngeal mucosa. The expression of PCNA, P21 and P53 in L-positive and negative tissues were also analyzed. . Results: The L-type detection rate was 79.7% in the nasopharyngeal carcinoma group and was not significantly different from the chronic inflammation group (75.0%) (P>0.05). However, the PCNA, p21, and p53 expression levels in the nasopharyngeal carcinoma group were significantly higher than those in the chronic inflammation group (75.0%). L-negative group (P <0.01). It was shown that there was a correlation between L-type infection and PCNA, p21, and p53 overexpression in nasopharyngeal carcinoma and L-infected tissue was in a hyperproliferative state. The combination suggests that L-type infection is involved in ras proto-oncogene activation and inactivation of the p53 tumor suppressor gene. Gene mutations may be one of the mechanisms of L-type carcinogenesis.