Project description:Genome wide DNA methylation profiling of esophageal squamous cell carcinoma (ESCC) tumor and adjacent normal samples using the Illumina Infinium MethylationEPIC array to obtain DNA methylation profiles across approximately 850,000 CpGs. Data included pathologically confirmed 108 tumor and 51 normal samples
Project description:We obtained methylome profiling (MeDIP-seq) of esophageal squamous cell carcinoma (ESCC) and normal tissue specimens by using next generation sequencing.
Project description:Background & Aims: Esophageal squamous cell carcinoma (ESCC) is believed to arise from esophageal mucosa through accumulation of both genetic and epigenetic changes. DNA methylation is a critical epigenetic mechanism involved in key cellular processes and its deregulation has been linked to many human cancers, including ESCC. The aim of this study is to examine the global deregulation of methylation states in ESCC and identify potential early biomarkers. Conclusions: This is the first study to address methylation changes in ESCC in a large panel of genes. Methylome analysis is shown as a sensitive and powerful tool to identify molecular players in ESCC. These data should prove to be the reference for future studies identifying potential biomarkers and molecular targets of ESCC. We performed a bead array analysis of more than 800 cancer-related genes in a series of 10 ESCC samples, 10 matched surrounding tissues, and 4 esophageal mucosa from healthy individuals. Pyrosequencing was used for validation of DNA methylation changes in up to 106 patients and 27 controls.
Project description:Background & Aims: Esophageal squamous cell carcinoma (ESCC) is believed to arise from esophageal mucosa through accumulation of both genetic and epigenetic changes. DNA methylation is a critical epigenetic mechanism involved in key cellular processes and its deregulation has been linked to many human cancers, including ESCC. The aim of this study is to examine the global deregulation of methylation states in ESCC and identify potential early biomarkers. Conclusions: This is the first study to address methylation changes in ESCC in a large panel of genes. Methylome analysis is shown as a sensitive and powerful tool to identify molecular players in ESCC. These data should prove to be the reference for future studies identifying potential biomarkers and molecular targets of ESCC.
Project description:Genome wide DNA methylation profiling of tumor and normal samples with esophageal squamous cell carcinoma patients. The Illumina GolodenGate methylation cancer panel I was used to obtain DNA methylation profiles across approximately 1,505 CpGs in esophageal squemous cell carcinoma samples. Samples included normal, tumors and plasma samples with esophageal squamous cell carcinoma, also inculding the plasma samples with cancer-free individual.
Project description:Profiles of esophageal squamous cell carcinoma and normal esophageal normal epithelium normal cell line. Analysis provides validation of novel microRNA targets prediction algorithms. esophageal squamous cell carcinoma:14, normal epithelium cell:2
Project description:Genome wide DNA methylation profiling of tumor and normal samples with esophageal squamous cell carcinoma patients. The Illumina GolodenGate methylation cancer panel I was used to obtain DNA methylation profiles across approximately 1,505 CpGs in esophageal squemous cell carcinoma samples. Samples included normal, tumors and plasma samples with esophageal squamous cell carcinoma, also inculding the plasma samples with cancer-free individual. Bisulfite converted DNA from the 288 samples were hybridised to the Illumina GolodenGate methylation cancer panel I
Project description:To characterize genomic instability in esophageal squamous cell carcinoma, we examined loss of heterozygosity, copy number loss, and copy number gain in ESCC patients from a high-risk region of China. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from microdissected esophageal squamous cell carcinoma samples or peripheral blood samples. Tumor DNA samples were normalized individually to the set of 102 peripheral blood samples. Copy number variations and loss of heterozygosity were determined by a paired analysis of tumor and blood DNA from the same individual.