人乳头状瘤病毒16/18型、p53、p16蛋白在口腔疣状癌中的表达

目的　研究人乳头状瘤病毒 16 / 18型、p5 3、p16蛋白在口腔疣状癌中的表达状况 ,探讨它们在口腔疣状癌发生发展中的生物学意义。方法　采用SP免疫组化和原位杂交方法分别检测 8例正常口腔粘膜、13例疣状癌、10例高分化鳞癌、10例低分化鳞癌组织中HPV16 / 18E6、p5 3、p16蛋白和HPV16 / 18DNA的表达。结果　 1.疣状癌HPV16 / 18E6蛋白和p5 3蛋白阳性表达率均为 6 9.2 % (9/ 13) ,p16蛋白表达缺失率为 2 3.1% (3/ 13) ,过度表达率为 6 9.2 % (9/ 13) ,平均染色强度与高分化鳞癌和低化分鳞癌组比均有显著性差异 (P <0 .0 5 )。 2 .免疫组化方法检测HPV16 / 18E6蛋白与原位杂交方法检测HPV16 / 18DNA结果有良好的一致性。 3.疣状癌HPV16 / 18E6蛋白与p5 3蛋白、p5 3蛋白与p16蛋白表达之间无相关性 (P <0 .0 5 ) ,而HPV16 / 18E6蛋白与p16蛋白表达之间呈正相关 (P<0 .0 5 )。结论　 1.进一步证实HPV16 / 18型感染是口腔疣状癌的重要致病因子。 2 .疣状癌的发生过程中可能存在p5 3基因突变。 3.p16基因变异在疣状癌的发生中起一定作用 ,用疣状癌中p16蛋白过度表达与HPV16 / 18型感染有关。 4 .HPV16 / 18、p5 3、p16蛋白在疣状癌与高分化鳞癌、低分化鳞癌组织中的表达存在明显差异 ,证实疣状癌是一种独立类型

EXPRESSION OF HUMAN PAPILLOMAVIRUS TYPES 16 AND 18, p53, p16 PROTEIN IN ORAL VERRUCOUS CARCINOMA

Objective To investigate the expression of human papillomavirus types 16 and 18 (HPV16/18), p53, p16 protein in oral verrucous carcinoma (VC) and to reveal their roles in the occurrence and development of VC. Methods Using streptavidin/peroxidase(SP) immunohistochemical technique(IHC) and in situ hybridization(ISH), we studied the expression of HPV16/18 E6, p53, p16 protein and HPV16/18 DNA in 41 archival samples, including 8 normal mucosa, 13 VC, 10 well differentiated squamous cell carcinoma (wdSCC), 10 poorly differentiated squamous cell carcinoma (pdSCC). Results (1) Both HPV16/18 E6 and p53 protein were identified in 69.2%(9/13) of VC. Absence (23.1%, 3/13) and overexpression 69.2%.9/13) of p16 protein were both found in VC. There are significant statistical differences of the mean intensitys between VC and SCC ( P <0.05). (2) Our study showed significant concordence between IHC and ISH results. (3) Significant reciprocal relationship between HPV16/18E6 and p16 protein in VC was observed ( P <0.05). But, there was lack of correlation between HPV16/18E6 and p53 protein in VC( P <0.05). The p16 and p53 protein in VC also had no relationship. Conclusion (1) Our result demonstrate that HPV16/18 infection is an important epiological agent of VC. (2) p53 gene mutations may play an important role in VC carcinogenesis. (3) p16 gene aberrant may involved in the development of VC. p16 protein expression of VC is associated with HPV16/18 infection. (4) Differential expression of HPV16/18, p53,p16 protein among VC and wdSCC, pdSCC indicateed that VC is an independent entity of oral cancer.