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作 者:李惠翔[1] 王尧河[1] 高冬玲[1] 张宏新[1] 张云汉[1]
机构地区:[1]河南医科大学病理学教研室
出 处:《临床与实验病理学杂志》1997年第3期224-226,共3页Chinese Journal of Clinical and Experimental Pathology
摘 要:目的:探讨喉癌的发生机理。方法:应用免疫组化LSAB法对30例喉鳞状细胞癌人乳头瘤病毒(HPV)感染、Langerhans细胞(LC)及p53蛋白表达进行了研究。结果:26.7%的病例可以检测到HPV抗原成分。HPV感染的癌旁粘膜内LC数量明显少于无感染者,且形态也发生改变。p53蛋白表达阳性率在HPV感染组(37.5%)明显低于HPV检测阴性组(83.33%)。结论:提示HPV、LC、p53在喉癌发生发展过程中起一定作用,且相互影响,HPV感染引起LC数量减少,局部免疫功能降低,HPV感染还可能通过表达的肿瘤蛋白或其他机制使抑癌基因p53失活,进而导致肿瘤的发生。Purpose To investigate the carcinogenesis of laryngeal carcinoma. Methods HPV infection, Langerhans cell (LC) and p53 protein expression were evaluated in 30 cases of squamous cell carcinoma of laryhx by LSAB immunohistochemical technique. Results HPV antigen positivity rate was 26 7%. The amount of LCs in pericarcinoma mucosa with HPV infection was much less than that without HPV infections, and LC changed morphologically. Positivity rate of p53 expression in HPV infected group (37 5%) was significantly lower than that in no HPV infected group (83 33%). Conclusions HPV, LC and p53 gene play a role in carcinogenesis and development of laryngeal carcinoma, and interact on each other. HPV infection may result in LC diminishment and deficiency of the local immune function. HPV can make p53 gene inactivation through expression certain kind of tumor protein so that it come out carcinogenesis.
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