天津医药
天津醫藥
천진의약
TIANJIN MEDICAL JOURNAL
2015年
1期
97-101
,共5页
张书卿%张绪亮%张博%洪亮
張書卿%張緒亮%張博%洪亮
장서경%장서량%장박%홍량
E-钙黏蛋白%甲基化%膀胱癌%Meta分析
E-鈣黏蛋白%甲基化%膀胱癌%Meta分析
E-개점단백%갑기화%방광암%Meta분석
E-cadherin%methylation%bladder cancer%Meta-analysis
目的：将既往有关E-钙黏蛋白（CDH1）基因启动子区甲基化与膀胱癌关系的研究进行Meta分析，评估CDH1基因启动子区甲基化与膀胱癌的具体关联。方法参照Cochrane协作网制定的检索策略在国内外相关数据库进行检索，筛选并纳入文献后，提取文献信息：第一作者、文献发表时间、国家、语种、研究设计、样本量、种族、病理亚型、甲基化检测方法、基因甲基化频率等。采用STATA12.0进行Meta分析，计算优势比（OR）及其95%可信区间（95%CI）。结果本Meta分析共计纳入10项病例对照研究，通过检测其中620例膀胱癌组织和341例正常或癌旁组织的CDH1基因甲基化频率，结果发现膀胱癌组织中的甲基化频率明显高于正常或癌旁组织（OR=3.09，95%CI：1.13～8.50，P=0.029）；亚组分析结果显示，在亚洲人群中膀胱癌组织中的甲基化频率明显高于正常或癌旁组织（OR=3.85，95%CI：1.46~10.14，P=0.006），而在欧美人群中未发现此种差异（OR=2.22，95%CI：0.38~12.91，P=0.375）；采用MSP方法检测时，膀胱癌组织与癌旁及正常组织间CDH1基因启动子区甲基化频率存在明显差异（P<0.001），采用Q-MSP方法检测时，两组CDH1基因启动子区甲基化频率无明显差异（P=0.818）。结论 CDH1基因启动子区甲基化可能参与了膀胱癌的发生和发展。
目的：將既往有關E-鈣黏蛋白（CDH1）基因啟動子區甲基化與膀胱癌關繫的研究進行Meta分析，評估CDH1基因啟動子區甲基化與膀胱癌的具體關聯。方法參照Cochrane協作網製定的檢索策略在國內外相關數據庫進行檢索，篩選併納入文獻後，提取文獻信息：第一作者、文獻髮錶時間、國傢、語種、研究設計、樣本量、種族、病理亞型、甲基化檢測方法、基因甲基化頻率等。採用STATA12.0進行Meta分析，計算優勢比（OR）及其95%可信區間（95%CI）。結果本Meta分析共計納入10項病例對照研究，通過檢測其中620例膀胱癌組織和341例正常或癌徬組織的CDH1基因甲基化頻率，結果髮現膀胱癌組織中的甲基化頻率明顯高于正常或癌徬組織（OR=3.09，95%CI：1.13～8.50，P=0.029）；亞組分析結果顯示，在亞洲人群中膀胱癌組織中的甲基化頻率明顯高于正常或癌徬組織（OR=3.85，95%CI：1.46~10.14，P=0.006），而在歐美人群中未髮現此種差異（OR=2.22，95%CI：0.38~12.91，P=0.375）；採用MSP方法檢測時，膀胱癌組織與癌徬及正常組織間CDH1基因啟動子區甲基化頻率存在明顯差異（P<0.001），採用Q-MSP方法檢測時，兩組CDH1基因啟動子區甲基化頻率無明顯差異（P=0.818）。結論 CDH1基因啟動子區甲基化可能參與瞭膀胱癌的髮生和髮展。
목적：장기왕유관E-개점단백（CDH1）기인계동자구갑기화여방광암관계적연구진행Meta분석，평고CDH1기인계동자구갑기화여방광암적구체관련。방법삼조Cochrane협작망제정적검색책략재국내외상관수거고진행검색，사선병납입문헌후，제취문헌신식：제일작자、문헌발표시간、국가、어충、연구설계、양본량、충족、병리아형、갑기화검측방법、기인갑기화빈솔등。채용STATA12.0진행Meta분석，계산우세비（OR）급기95%가신구간（95%CI）。결과본Meta분석공계납입10항병례대조연구，통과검측기중620례방광암조직화341례정상혹암방조직적CDH1기인갑기화빈솔，결과발현방광암조직중적갑기화빈솔명현고우정상혹암방조직（OR=3.09，95%CI：1.13～8.50，P=0.029）；아조분석결과현시，재아주인군중방광암조직중적갑기화빈솔명현고우정상혹암방조직（OR=3.85，95%CI：1.46~10.14，P=0.006），이재구미인군중미발현차충차이（OR=2.22，95%CI：0.38~12.91，P=0.375）；채용MSP방법검측시，방광암조직여암방급정상조직간CDH1기인계동자구갑기화빈솔존재명현차이（P<0.001），채용Q-MSP방법검측시，량조CDH1기인계동자구갑기화빈솔무명현차이（P=0.818）。결론 CDH1기인계동자구갑기화가능삼여료방광암적발생화발전。
Objective To assess the role of E-cadherin (CDH1) promoter methylation in bladder carcinogenesis by meta-analysis. Methods The relevant database were searched by the retrieval strategy of Cochrane network. All included studies were collected following data:the first author’s surname, publication year of article, country, language of publication, design of study, sample size, ethnicity, histological subtypes, methylation detection method and genotype frequencies etc. This meta-analysis was performed using the STATA 12.0 software. The crude odds ratio (OR) with 95%confidence interval (CI) was calculated. Results Ten case-control studies were included in this meta-analysis. The methylation frequency of CDH1 was detected in 620 bladder cancer tissues and 341 normal or cancerous tissues. Results showed that the methylation frequency of CDH1 was significantly higher in bladder cancer tissue than that of normal or cancerous tissue (OR=3.09, 95%CI:1.13~8.50, P=0.029). Furthermore, the ethnicity-stratified analysis revealed that the methylation frequency of CDH1 was significantly higher in bladder cancer tissue of Asian populations than that of normal or cancerous tissue (OR=3.85, 95%CI:1.46~10.14, P=0.006), but no such association was found in Caucasian populations(OR=2.22, 95%CI:0.38-12.91, P=0.375). The subgroup analysis based on the detection methods revealed that there was a statistically significant difference in the methylation frequency of CDH1 between bladder cancer tissue and adjacent tissues and normal tissues under the MSP subgroup (P<0.001), while such association was not observed under the Q-MSP subgroup (P=0.818). Conclusion Pro?moter methylation of CDH1 gene may be involved in the occurrence and development of bladder cancer, which may serve as a biomarker for diagnosis and prognosis of bladder cancer.
