Gene expression in normal and tumoral esophageal squamous cell lines
ABSTRACT: This study was designed to identify genes aberrantly expressed in esophageal squamous cell carcinoma (ESCC) cells. Overall design: Three esophageal squamous cell carcinoma-derived cell lines and one normal human esophageal squamous cell line were analyzed.
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:This study was designed to identify microRNAs aberrantly expressed in esophageal squamous cell carcinoma (ESCC) cells. Overall design: Three esophageal squamous cell carcinoma-derived cell lines and one normal human esophageal squamous cell line were analyzed.
Project description:Preoperative chemoradiotherapy (CRT) followed by surgery has been proved to improve esophageal squamous cell carcinoma (ESCC) patients’ survival in comparison with surgery alone. However, the outcomes of CRT are heterogeneous, and no clinical or pathological method could predict CRT response. We aim to identify mRNA markers for ESCC CRT-response prediction through gene expression analyses. Gene expression analyses were performed on pretreatment cancer biopsies from 28 ESCCs who received neoadjuvant CRT and surgery and 10 normal esophageal epithelia using Affymetrix U133 Plus 2.0 arrays.
Project description:Human esophageal cancer is the sixth leading cause of cancer death worldwide. More than 90% of esophageal cancer is esophageal squamous cell carcinoma (ESCC). However, the etiological cause of ESCC remains unclear. By using gene expression microarray analysis, we aimed to find whether fungal infection is involved in ESCC development. We identified a wide spectrum of molecular signatures in a fungal infection and ESCC mouse model, including alterations involved in epigenetic regulation, cell cycle control, cell proliferation and survival signaling, and inflammation, which share many similarities with human ESCC. Overall design: Esophagus from Amphotericin B treated KA mouse, ESCC from untreated KA mouse, Esophagus from WT mice
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:A proportion of superficial esophageal squamous cell carcinoma, a type of less invasive esophageal squamous cell carcinoma (ESCC), would have metastasis after esophagectomy or endoscopic resection with poor prognosis. The purpose of this study was to discover the whole-genome copy number alteration (CNA) profiles of superficial ESCC and compare the CNAs of superficial ESCC patients with and without metastasis after surgery. Thirty eight superficial ESCC cases, including 19 cases with metastasis and 19 cases without metastasis within 5 years after surgery, were analyzed CNAs by Affymetrix OncoScan™ FFPE Assay. A 39-gene signature was initially constructed to identify high risk of metastasis in superficial ESCC patients. In addition, amplification of 11q13.3 (FGF4) and deletion of 9p21.3 (CDKN2A) were identified as recurrent CNAs across all 38 superficial ESCC cases. And amplifications of 3p26.33 (SOX2-OT), 8q24.21 (MYC), 14q21.1 (FOXA1) and deletion of 3p12.1 (GBE1) were identified as recurrent CNAs among metastasis cases only. Our study provided a 39-gene signature tool to identified high risk metastasis in superficial ESCC and suggested that amplifications of SOX2-OT, MYC, FOXA1 genes and deletion of GBE1 gene might play a vital role in metastasis among superficial ESCC. Overall design: Copy number analysis of Affymetrix FFPE Oncoscan Array was performed for 38 superficial esophageal squamous cell carcinoma (pT1N0M0) samples, including 19 cases with metastasis after surgery within 5 years after surgery and 19 cases without metastasis.
Project description:We obtained transcriptome profiling (SAGE-seq) of esophageal squamous cell carcinoma (ESCC) and normal tissue specimens by using next generation sequencing. Overall design: Comparison of expression pfofiles between ESCC and normal mucosa.
Project description:We identified a number of deregulated genes through transcriptome analysis on esophageal squamous cell carcinoma (ESCC) and adjacent normal tissues. Our pathway enrichment analysis suggested that deregulated genes were strongly enriched in multiple functionally linked pathways known to be important in tumor cell proliferation (e.g., the p53 pathway and the cell-cycle pathway) and migration (e.g., the Notch pathway, the Wnt/β-catenin pathway). To identify the functional pathways playing important roles in the tumorigenesis of esophageal squamous cell carcinoma, pooled 10 ESCC tissues and pooled 10 adjacent normal tissues were analyzed using gene expression microarrays.
Project description:We obtained methylome profiling (MeDIP-seq) of esophageal squamous cell carcinoma (ESCC) and normal tissue specimens by using next generation sequencing. Overall design: Comparison of DNA methylation pfofiles between ESCC and normal mucosa.
Project description:Esophageal carcinoma is the third most common gastrointestinal malignancy worldwide and is generally unresponsive to therapy. African Americans have an increased risk for esophageal squamous cell cancer (ESCC), the subtype that shows marked variation in geographic frequency. To identify key genes involved in ESC carcinogenesis in African Americans we conducted microarray expression profiling and found a significant dysregulation of genes encoding stress response and drug-metabolizing enzymes, mainly in NRF2 pathway. The involvement of NRF2 mediated oxidative damage represent a key step in the evolution of African American ESCC. Loss of activity of these enzymes would confer increased sensitivity of esophageal cells to xenobiotics, such as alcohol and tobacco smoke, and may account for the high incidence of ESCC in this ethnic group. The differential expression profile also indicates an inflammatory component and tissue regeneration in ESCC tumorigenesis. Together, these findings suggest a remarkable interplay of genetic and environmental factors in the pathogenesis of African American ESCC. Overall design: Fourteen paired Human biopsy specimens collected from African Americans diagnosed with Esophageal Squamous Cell Carcinoma (ESCC). Seven of the fourteen specimens represent ESCC while the remaining represent paired healthy tissue.