膀胱移行细胞癌中p16基因的改变  被引量:6

The mechanism of p16 gene inactivation in human bladder transitional cell carcinoma

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作  者:武玉东[1] 吴海[1] 马腾骧[1] 吴长利[1] 

机构地区:[1]天津市泌尿外科研究所

出  处:《中华病理学杂志》1999年第1期39-41,共3页Chinese Journal of Pathology

基  金:天津市卫生局科研基金

摘  要:目的明确p16基因在膀胱移行细胞癌中的改变。方法采用Southern杂交、聚合酶链反应单链构象多态性分析(PCRSSCP)及DNA甲基化分析技术分别检测52例膀胱移行细胞癌中p16基因的缺失、突变及5′CpG岛甲基化。结果52例膀胱移行细胞癌中11例(2115%)存在p16基因的缺失;仅1例肿瘤于p16基因外显子2出现点突变;19例(36.5%)肿瘤发现p16基因5′CpG岛甲基化。结论基因的缺失和5′CpG岛甲基化是p16基因在膀胱移行细胞癌中失活的主要机制。p16基因缺失多见于早期、高分化的肿瘤,而5′CpG岛的甲基化多见于晚期、低分化的肿瘤。Objective To figure out the mechanism of p16 gene inactivation in human bladder transitional cell carcinoma (BTCC). Methods p16 gene was analyzed for genetic alterations by Southern blot analysis, PCR SSCP and DNA methylation analysis in 52 cases of transitional cell carcinoma of bladder. Results p16 gene deletion was found in 11 of 52(21.15%) BTCCs, only one tumor showed point mutation on p16 exon 2, ninteen cases of BTCCs (36.53%) showed p16 gene 5′CpG island methylation. Conclusion There was a statistically significant association between p16 gene deletion and early stage, well differentiated tumors. Additionally, a statistically significant correlation was also noticed between p16 gene 5′CpG island methylation and tumors in late stage with poor cell differentiation.

关 键 词:膀胱肿瘤 移行细胞癌 P16基因 基因突变 

分 类 号:R737.140.2[医药卫生—肿瘤]

 

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