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.
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:Our aim is to identify frequent genomic aberrations both in ESCC and esophageal dysplasia, and to discover important copy number-driving genes and microRNAs in ESCC. We carried out array-based comparative genomic hybridization (array CGH) on 59 ESCC resection samples and 16 dysplasia biopsy samples. Expression of genes at 11q13.3 was analyzed by real-time PCR and immunohistochemistry (IHC). Integrated analysis was performed to identify genes or microRNAs with copy number-expression correlations. Two group experiment, esophageal dysplasia vs. esophageal squamous cell carcinoma. Biological replicates: 16 dysplasias vs. 59 carcinomas
Project description:This study was designed to identify genes aberrantly expressed in esophageal squamous cell carcinoma (ESCC) cells. Three esophageal squamous cell carcinoma-derived cell lines and one normal human esophageal squamous cell line were analyzed.
Project description:To understand the difference of protein expression between paired esophageal squamous cell carcinoma (ESCC) and adjacent normal tissues, we collected 10 paired ESCC and normal tissues from surgical resected specimems for high-throughput proteomic experiments. From comparative analysis, the dysregulated signaling pathways in ESCC could be uncovered.
