抑癌基因P16和P15在口腔黏膜癌前病变中的甲基化改变  

Methylation of P16 and P15 in oral precancerous lesion

作　　者：付洁[1] 宿颖[1] 蓝爱仙[1] 关晓兵[1] 张辛燕[1] 孙正[1] 

机构地区：[1]首都医科大学附属北京口腔医院黏膜科,北京100050

出　　处：《实用口腔医学杂志》2013年第5期664-667,共4页Journal of Practical Stomatology

基　　金：首都医学发展科研基金资助(编号:2007-3095);北京市卫生系统高层次卫生技术人才资助(编号:2011-3-073)

摘　　要：目的:探讨口腔黏膜癌前病变组织中抑癌基因P16、P15启动子甲基化与患者病理学及人口学资料的关系。方法:收集2008年以来就诊于首都医科大学附属北京口腔医院黏膜科口腔白斑87例和口腔癌39例,20例正常口腔黏膜为对照,采用内切酶消化法和实时定量PCR的方法对P16和P15甲基化状态进行研究。结果:正常口腔黏膜中,P16、P15启动子区处于未甲基化状态,口腔白斑中P16和P15甲基化阳性率分别为41.38%和44.83%,与正常对照相比显著增高(P<0.001);口腔鳞癌P16和P15甲基化阳性率分别为20.51%和23.08%,与正常对照相比明显增高(P<0.05)。P16、P15启动子甲基化与患者性别、年龄、病变部位、性质、类型、吸烟等因素无相关性。结论:抑癌基因P16和P15启动子甲基化可能是口腔黏膜白斑和早期癌变的标志物。Objective： To study the relationship of the promoter methylation of tumor suppressor genes P16 and P15 in oral precan- cerous lesion with the pathologic and demographic data. Methods： Promoter methylation of P16 and P15 was detected in 87 cases of oral mucosa leukoplakia and 39 cases of oral squamous cell carcinoma（OSCC） tissues using methylation sensitive enzyme and methy- lation dependent enzyme digestion. 20 cases of normal oral mucosa were used as the controls. Results： No promoter methylation of P16 and P15 was found in the controls. In leukoplakia tissues, hypermethylation of P16 and P15 was 41.38% and 44.83% of the cases respectively（vs control, P 〈 0. 001 ）. In oral squamous carcinoma,hypermethylation of P16 and P15 was 20.51% and 23.08% of the cases respectively（vs control, P 〈 0.05 ）. No correlation was found between the methylation and the gender, age, smoking, lesion site, pathology and types of the patients. Conclusion： Promoter methylation of P16 and P15 may be biomarkers of early oral carcinogenesis.

关 键 词：口腔白斑 甲基化 P16 P15 

分 类 号：R781.5[医药卫生—口腔医学]