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作 者:夏娟[1] 李秉琦[2] 曾昕[2] 陈谦明[2] 何园[3] 蔡扬[4]
机构地区:[1]中山大学光华口腔医学院牙周黏膜科,广州510055 [2]四川大学华西口腔医学院口腔黏膜病学研究室 [3]同济大学附属口腔医院口腔内科 [4]贵阳医学院附属医院口腔科
出 处:《中华口腔医学杂志》2005年第2期102-104,共3页Chinese Journal of Stomatology
基 金:国家自然科学基金 ( 30300387;30070815 );国家"十五"攻关项目基金 (2004BA720A28 );教育部回国人员启动基金资助项目
摘 要:目的 了解EMS1基因扩增是否参与口腔黏膜癌变。方法 采用显微解剖技术分别获取正常口腔黏膜上皮,口腔白斑患者的单纯增生,轻、中、重度异常增生上皮和原发性口腔鳞癌组织标本 78例,应用差示PCR反应检测EMS1基因扩增。结果 ①分别有 20 0%的口腔白斑组织, 57 6%的口腔鳞癌组织观察到EMS1扩增;②在口腔黏膜癌变进程中,EMS1扩增开始于中度异常增生黏膜,在伴有淋巴结转移的口腔鳞癌组织中其扩增率有显著增高(P=0 015)。结论 EMS1基因扩增与口腔黏膜癌变的演进相平行,似是口腔黏膜癌变的早期分子事件。Objective To investigate the amplification of EMS1 gene in the carcinogenesis of oral mucosa.Methods A total of 78 subjects, including 30 patients with oral leukoplakia (OLK), 33 with oral squamous cell carcinoma (OSCC), and 15 healthy controls, were studied. By using microdissection method, we obtained normal mucosa, hyperplastic epithelia, mild dysplastic epithelia, moderate dysplastic epithelia, severe dysplastic epithelia and primary OSCC tissue. Then we analyzed EMS1 amplification by using differential PCR. Results EMS1 amplification began from moderate dysplastic epithelia and occurred in 20 0% OLK cases and 57 6% OSCC cases. In the progress of OSCC, no gene amplification was observed in normal tissues, non dysplastic OLK and mild dysplastic OLK, while in the cases with metastasis, amplification frequency increased significantly ( P =0 015).Conclusions EMS1 amplification parallels with the progress of oral carcinogenesis, indicating their potential roles in oral carcinogenesis.
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