Epigenomic profiling of DNA methylation in paired prostate cancer versus adjacent benign tissue
Epigenomic profiling of DNA methylation in paired prostate cancer versus adjacent benign tissue
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DOI：
10.1002/pros.23093
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发表时间：
2015-12-01
期刊：
影响因子：
2.8
通讯作者：
Stanford, Janet L.
中科院分区：
文献类型：
--
作者：
Geybels, Milan S.;Zhao, Shanshan;Stanford, Janet L.
DNA甲基化异常可能促进前列腺癌的发生。我们研究了前列腺癌（PCa）与邻近良性组织的表观基因组DNA甲基化谱，以确定甲基化CpG位点的差异。方法选取20例根治性前列腺切除术患者的配对前列腺癌及邻近良性组织标本。表观遗传分析使用Infinium HumanMethylation450 BeadChip完成。考虑配对研究设计和错误发现率q值的线性模型用于评估差异CpG甲基化。分析CpG位点差异最大的基因的mRNA表达水平。结果在前列腺癌与邻近良性组织中共鉴定出2040个差异甲基化的CpG位点（q值）
BackgroundAberrant DNA methylation may promote prostate carcinogenesis. We investigated epigenome-wide DNA methylation profiles in prostate cancer (PCa) compared to adjacent benign tissue to identify differentially methylated CpG sites.MethodsThe study included paired PCa and adjacent benign tissue samples from 20 radical prostatectomy patients. Epigenetic profiling was done using the Infinium HumanMethylation450 BeadChip. Linear models that accounted for the paired study design and False Discovery Rate Q-values were used to evaluate differential CpG methylation. mRNA expression levels of the genes with the most differentially methylated CpG sites were analyzed.ResultsIn total, 2,040 differentially methylated CpG sites were identified in PCa versus adjacent benign tissue (Q-value