食管癌和Barrett食管中RASSF2启动子甲基化的研究

 目的　研究食管癌和Barrett食管组织的甲基化情况，探讨其发生的表观遗传学分子机制的异同。方法　采用甲基化特异性PCR，对27例手术后食管癌、癌旁正常组织以及18例胃镜活组织检查Barrett食管组织中RASSF2基因的甲基化情况进行检测。结果　RASSF2在食管癌组织中甲基化率（66.7 %，18／27）高于相应癌旁正常组织（22.2 %，6／27）及Barrett食管组织的甲基化率（33.3 %，6／18）（均P＜0.05）。而Barrett食管和癌旁组织之间的甲基化率差异无统计学意义（P＞0.05）。结论　RASSF2高甲基化状态可能是引起食管癌的分子机制，在Barrett食管中需进一步验证。

Hypermethylation of RASSF2 promoter in esophageal carcinoma and Barrett's esophagus

Objective　To explore the molecular mechanism through detecting methylation status in esophageal carcinoma and Barrett's esophagus. Methods　The methylation-specific PCR was employed to detect the expressions of RASSF2 in esophageal carcinoma tissues, adjacent tissues from 27 patients after surgery and Barrett's esophagus tissues from 18 patients after gastroscopic biopsy. Results　The rate of RASSF2 methylation was much higher in esophageal carcinoma (66.7 %, 18/27) than that in adjacent tissues (22.2 %, 6/27) (P < 0.05), and was more frequently than that in Barrett's esophagus (33.3 %, 6/18) (P < 0.05). However, no significant difference of methylation status was observed between Barrett's esophagus and adjacent tissue (P > 0.05). Conclusion　The hypermethylation of RASSF2 may be the molecular mechanism in the development of esophageal carcinoma, and more samples should be used for further experiment in Barrett's esophagus.