涎腺腺样囊性癌p16基因失活机制的研究

Mechanism of p16 Gene Inactivation in Salivary Adenoid Cystic Carcinoma

目的研究p16基因在涎腺腺样囊性癌中的失活机制。方法收集山东大学齐鲁医院及口腔医院口腔颌面外科涎腺腺样囊性癌新鲜标本53例,应用PCR、聚合酶链反应-单链构象多态性分析(PCR_SSCP)及甲基化特异性PCR(MSP)技术检测涎腺腺样囊性癌中p16基因的纯合性缺失、突变及甲基化。结果53个病例中16例(30.2%)纯合性缺失,4例(7.5%)突变,26例(49.1%)高甲基化。结论p16基因在涎腺腺样囊性癌中的主要失活机制是启动子高甲基化和纯合性缺失,而基因突变比较少见。

Objective To study the mechanism of p16 gene inactivation in salivary adenoid cystic carcinoma. Methods 53 cases of freshly excised salivary adenoid cystic carcinomas were studied. Polymerase chain reaction （PCR） and single-stranded conformation polymorphism analysis of polymerase chain reaction products （PCR-SSCP） were used to detect deletion and mutation of p16 gene in salivary adenoid cystic carcinomas. Methylation specific PCR （MSP） was used to detect the methylation status of p16 gene. Results ~ homozygous deletion, mutation and hypermethylation of p16 gene were noted in 16 cases （ 30.2% ） ,4 cases （7.5%） and26 cases （49.1%） respectively in53 cases of salivary adenoid cystic carcinomas. Conclusion The main inactivation mechanisms of p16 gene in salivary adenoid cystic carcinoma were hypermethylation and homozygous deletion. The mutation p16 gene was rare in salivary adenoid cystic carcinoma.