CAJ | 학술논문

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.
목적 연구식관암화Barrett식관조직적갑기화정황,탐토기발생적표관유전학분자궤제적이동.방법 채용갑기화특이성PCR,대27례수술후식관암、암방정상조직이급18례위경활조직검사Barrett식관조직중RASSF2기인적갑기화정황진행검측.결과 RASSF2재식관암조직중갑기화솔(66.7％,18/27)고우상응암방정상조직(22.2％,6/27)급Barrett식관조직적갑기화솔(33.3％,6/18)(균P＜ 0.05).이Barrett식관화암방조직지간적갑기화솔차이무통계학의의(P＞0.05).결론 RASSF2고갑기화상태가능시인기식관암적분자궤제,재Barrett식관중수진일보험증.
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.