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抑癌基因P16和P15在口腔黏膜癌前病变中的甲基化改变 被引量:9

Methylation of P16 and P15 in oral precancerous lesion
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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.
出处 《实用口腔医学杂志》 CAS CSCD 北大核心 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)
关键词 口腔白斑 甲基化 P16 P15 Oral leukoplakia Methylation P16 P15
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