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作 者:罗刚[1] 董俊英[2] 陈谦明[3] 李秉琦[3] 杨晓瑜[1]
机构地区:[1]广东省口腔医院.南方医科大学附属口腔医院,广东广州510280 [2]广东省深圳牙科医疗中心,广东深圳518001 [3]四川大学华西口腔医学院,四川成都610041
出 处:《热带医学杂志》2011年第8期893-896,共4页Journal of Tropical Medicine
基 金:广东省医学科学技术研究基金(A2008109);广东省科技计划项目(2010B031600118)
摘 要:目的研究CCND1基因在口腔黏膜癌前损害及癌变中的变化规律,以期明确该基因在口腔癌发生发展中的作用。方法选取正常口腔粘膜,上皮单纯增生,轻、中、重度上皮异常增生和口腔粘膜鳞状细胞癌及其相应转移淋巴结石蜡组织标本共55例,提取DNA,采用差示PCR技术检测CCND1基因的扩增,并通过直接序列分析验证差示PCR产物的确切性。结果差示PCR扩增显示,上皮单纯增生组无CCND1基因扩增倍率,与正常粘膜基本一致,差异无统计学意义(P=5.645)。上皮异常增生组19例中7例出现CCND1基因的扩增,平均扩增倍率为正常粘膜组的4.2倍,与上皮单纯增生组差异有统计学意义(P<0.01);在上皮异常增生各组中,以重度异常增生最高,但组间差异无统计学意义(P>0.05)。肿瘤组16例中9例出现CCND1扩增,平均扩增倍率为6.2倍,与上皮单纯增生组和异常增生组的差异均有统计学意义(P<0.01);转移癌和非转移癌的扩增率和平均扩增倍数的差异均无统计学意义(P>0.05)。结论 CCND1基因的扩增与口腔粘膜癌前损害的发生发展相关。Objective Based on our previous studies on the deregulation of cell cycle in oral carcinogenesis,this study is aimed to investigate the roles of CCND1 in oral carcinogenesis.Methods A total of 55 formalin-fixed and paraffin-embedded samples were obtained from patients with hyperkerotosis (6),oral premalignant lesions (OPLs,19),oral squamous cell carcinomas (OSCCs,16),and normal healthy controls (7),together with local lymph nodes (7) of patients with metastatic OSCCs.The amplification of CCND1 was evaluated using a differential polymerase chain reaction (DDPCR) followed by a direct PCR-DNA sequencing to confirm the accuracy of the PCR product.Results The results of DDPCR manifested that the group of hyperkerotosis doesn't have CCND1 amplification,the same as normal mucosa(P=5.645).While the average amplification multiplying factor of OPLs was 4.2 times to normal mucosa,it was difference from the group of hyperkerotosis(P0.01).The average amplification multiplying factor of OSCCs was 6.2,it was significantly different from those of OPLs and normal mucosa,but there was no significant difference between metastatic OSCCs and non-metastatic OSCCs(P0.05).DNA sequencing confirmed the accuracy of the PCR.Conclusion These results suggest that the amplification of CCND1 may contribute to the development and progression of oral carcinogenesis.
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