Association between P(16INK4a) promoter methylation and non-small cell lung cancer: a meta-analysis.
Association between P(16INK4a) promoter methylation and non-small cell lung cancer: a meta-analysis.
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DOI：
10.1371/journal.pone.0060107
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Zhou Q
中科院分区：
文献类型：
--
作者：
Gu J;Wen Y;Zhu S;Hua F;Zhao H;Xu H;You J;Sun L;Wang W;Chen J;Zhou Q
肿瘤细胞启动子区 CpG 岛的异常甲基化在癌变过程中发挥着重要作用。积累的证据表明 P16INK4a 基因启动子高甲基化与非小细胞肺癌（NSCLC）有关，表明它可能是该疾病的潜在生物标志物。本研究的目的是通过总结已发表的研究来评估癌组织和自体对照之间 P16INK4a 基因启动子甲基化的频率。通过检索Medline、EMBSE和CNKI数据库，采用系统检索策略筛选出公开发表的有关P16INK4a基因启动子甲基化与NSCLC的研究。通过荟萃分析方法计算肺癌组织与自体对照中 P16INK4A 启动子甲基化的汇总几率。本次荟萃分析纳入了 34 项研究，包括 2 652 名 NSCLC 患者、5 175 个样本。一般来说，肺癌组织中P16INK4A启动子甲基化频率为17%~80%（中位数44%），自体对照中P16INK4A启动子甲基化频率为0~80%（中位数15%），这表明癌组织中的甲基化频率远高于自体样本。我们还在研究中发现肿瘤组织和自体对照的 P16INK4A 启动子甲基化频率之间存在强烈且显着的相关性（相关系数 0.71，95% CI：0.51–0.83，P<0.0001）。随机效应模型下，与对照组相比，癌组织中 P16INK4A 启动子甲基化的汇总优势比为 3.45（95% CI：2.63-4.54）。癌组织中P16INK4a启动子甲基化频率远高于自体对照，表明启动子甲基化在NSCLC的癌变过程中发挥着重要作用。肿瘤组织和自体样本的 P16INK4A 启动子甲基化之间存在强而显着的相关性，这证明了它是一种有前景的 NSCLC 生物标志物。
Aberrant methylation of CpG islands acquired in tumor cells in promoter regions plays an important role in carcinogenesis. Accumulated evidence demonstrates P16INK4a gene promoter hypermethylation is involved in non-small cell lung carcinoma (NSCLC), indicating it may be a potential biomarker for this disease. The aim of this study is to evaluate the frequency of P16INK4a gene promoter methylation between cancer tissue and autologous controls by summarizing published studies. By searching Medline, EMBSE and CNKI databases, the open published studies about P16INK4a gene promoter methylation and NSCLC were identified using a systematic search strategy. The pooled odds of P16INK4A promoter methylation in lung cancer tissue versus autologous controls were calculated by meta-analysis method. Thirty-four studies, including 2 652 NSCLC patients with 5 175 samples were included in this meta-analysis. Generally, the frequency of P16INK4A promoter methylation ranged from 17% to 80% (median 44%) in the lung cancer tissue and 0 to 80% (median 15%) in the autologous controls, which indicated the methylation frequency in cancer tissue was much higher than that in autologous samples. We also find a strong and significant correlation between tumor tissue and autologous controls of P16INK4A promoter methylation frequency across studies (Correlation coefficient 0.71, 95% CI:0.51–0.83, P<0.0001). And the pooled odds ratio of P16INK4A promoter methylation in cancer tissue was 3.45 (95% CI: 2.63–4.54) compared to controls under random-effect model. Frequency of P16INK4a promoter methylation in cancer tissue was much higher than that in autologous controls, indicating promoter methylation plays an important role in carcinogenesis of the NSCLC. Strong and significant correlation between tumor tissue and autologous samples of P16INK4A promoter methylation demonstrated a promising biomarker for NSCLC.
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DOI：
10.1073/pnas.93.18.9821
发表时间：
1996-09-03
影响因子：
11.1
作者：
Herman, JG;Graff, JR;Baylin, SB
通讯作者：
Baylin, SB
影响因子：
11.5
作者：
Guo, MZ;House, MG;Brock, MV
通讯作者：
Brock, MV
影响因子：
4.5
作者：
Hong YS;Roh MS;Kim NY;Lee HJ;Kim HK;Lee KE;Kwak JY;Kim JY
通讯作者：
Kim JY
DOI：
10.1073/pnas.95.20.11891
发表时间：
1998-09-29
影响因子：
11.1
作者：
Belinsky, SA;Nikula, KJ;Herman, JG
通讯作者：
Herman, JG
影响因子：
2.4
作者：
Georgiou, Elisavet;Valeri, Rozalia;Kouidou, Sofia
通讯作者：
Kouidou, Sofia