Project description:The overall goal of this study was to compare gene expression profiles in MOAB-overexpressing PrSC cells and control cells, also to compare gene expression profiles in MAOB-knockdown and control cells.
Project description:ANO1 is located in the 11q13 region that is commonly amplified in head and neck squamous cell carcinoma. However, the exact mechanism of ANO1's involvement in oncogenesis and cancer proliferation remains unclear. In this study, we discovered novel genes which have an interplay in ANO1 cancer signalling pathways and were significantly differentially expressed upon ANO1 knockdown. All cell lines were cultured in three dimensional collagen I, a matrix that closely resembles tumor microenvironment. The aim of this study was to reveal novel mediators and pathways in ANO1 cancer cell signalling, and therefore gain insight on novel molecules that can present potent therapeutic targets.
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: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.
