Project description:Copy number analysis of primary esophageal squamous cell carcinoma (ESCC) from 40 patients in Japan. Integrative analysis of gene expression profiles and genomic alterations obtained from array-CGH and NGS provided us new insight into the pathogenesis of ESCC.
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.
Project description:Characterization of copy number alterations and unbalanced breakpoints in human esophageal squamous cell carcinoma cell lines by array-based comparative genomic hybridization.
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:Copy number analysis of primary esophageal squamous cell carcinoma (ESCC) from 40 patients in Japan. Integrative analysis of gene expression profiles and genomic alterations obtained from array-CGH and NGS provided us new insight into the pathogenesis of ESCC. 40 tumor samples were prepared for aCGH analysis. For genome profiling, labeling and hybridization of genomic DNA onto the Agilent-014693 Human Genome Microarray Kit 244K (Agilent Technologies) was performed according to the manufacturer's instructions.
Project description:Characterization of copy number alterations and unbalanced breakpoints in human esophageal squamous cell carcinoma cell lines by array-based comparative genomic hybridization. Six cell lines
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: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:Analysis of primary esophageal squamous cell carcinoma (ESCC) from 71 patients in japan. Integrative analysis of gene expression profiles and genomic alterations obtained from array-CGH and NGS provided us new insight into the pathogenesis of ESCC
Project description:Esophageal squamous cell carcinoma (ESCC) is one of the most common cancers with high mortality rate. Smoking is one of the established risk factors of ESCC. However, there is limited data on molecular alterations associated with cigarette smoke exposure in esophageal cells. Understanding the effects of cigarette smoke on esophageal squamous epithelial cells at a molecular level would lead to a better understanding of the pathobiology of ESCC which has implications for identification of early biomarkers and therapeutic targets. To investigate the effect of cigarette smoke exposure, we developed a cell line model where Het1A cells (non-neoplastic human esophageal epithelial cells) were chronically treated with cigarette smoke condensate (CSC) for 2 months, 4 months, 6 months and 8 months. We carried out comparative proteomic, phosphoproteomic and whole exome sequencing analyses on CSC treated and untreated cells. Increased cell proliferation and invasion of Het1A cells was observed after chronic exposure to cigarette smoke. Using quantitative proteomic and phosphoproteomic analyses, we identified 56 proteins and 296 phosphoproteins that showed differential expression. Bioinformatics analysis of differentially expressed proteins and phosphoproteins showed enrichment of molecules involved in DNA damage response pathway. Whole exome sequencing (WES) of CSC treated and untreated cells also revealed mutations and copy number alterations in genes associated with DNA damage response. By correlating WES, proteomic and phosphoproteomic results, we observed potential loss of function in HMGN2 and MED1 that were reported as potential tumor suppressors and are known to play important role in DNA damage response. We also observed decreased expression of HMGN2 in tissue section of ESCC. Overexpression of HMGN2 and MED1 lead to decreased proliferative and invasive ability of CSC treated cells. These findings suggest that cigarette smoke affects genes and proteins associated with DNA damage response pathways which might play a vital role in development of ESCC.
