Project description:To investigated the molecular distinction and functional correlation among different histopathological types of gastric neoplasia, the whole genome expression profiling of gastric early-stage carcinoma(EGC) and high-grade and low-grade intraepithelial neoplasia (HGIN and LGIN) were explored. This research will provide biological evidence for the clinical application in different gastric early-stage neoplasia. Overall design: Human gastric tissue samples were collected for the microarray research, which included 19 LGIN, 20 HGIN, 19 EGC and 19 chronic gastritis tissue samples. EGC are confined to mucosa or submucosa by surgery or ESD(Endoscopic Submucosal Dissection).
Project description:Gastric cancer is one of the most aggressive cancers and is the second leading cause of cancer death worldwide. Approximately 40% of global gastric cancer cases occur in China, with peritoneal metastasis being the prevalent form of recurrence and metastasis in advanced disease (>50%). Currently, there are limited clinical approaches for predicting and treatment of peritoneal metastasis, resulting in a 6- month average survival time. By comprehensive genome analysis will uncover the pathogenesis of peritoneal metastasis. Here we describe a comprehensive whole-genome and transcriptome sequencing analysis of one advanced gastric cancer case, including non-cancerous mucosa, primary cancer and matched peritoneal metastatic cancer. The peripheral blood is used as normal control. Overall design: Gastric carcinoma patients and healthy subjects
Project description:Early gastric cancers (EGC) precede advanced gastric cancers (AGC) with a favorable clinical outcome compared to advanced gastric cancers (AGC). To understand the progression mechanisms of EGC to AGC, it is required to disclose the EGC and AGC genomes in terms of the the mutational and evolutionary perspectives. In this study, we performed whole-exome sequencing and copy number profiling of nine microsatellite (MS)-unstable (MSI-H) (5 EGC and 4 AGC) and eight MS-stable (MSS) gastric cancers (4 EGC and 4 AGC). Unexpectedly, we observed no substantial differences in the number, sequence composition and functional consequences (potential driver mutations and affected pathways) of the mutations and CNAs between EGC and AGC genomes in both MSI-H and MSS cases. Gastrectomy tissues from 17 GC patients were used for this study. The hospital pathology department confirmed pathologic features of the GC (e.g., EGC vs. AGC, differentiation, lymph node metastasis and TNM stage). All of the picked areas from tumor and normal areas were frozen, cut, and stained with hematoxylin & eosin (H&E). Two pathologists selected cases with rich tumor cell population (at least 60%), which were subsequently used in the study. Copy number profiling was performed using Agilent 180K platform according to the manufacturer's protocol.
Project description:cfDNA (Cell-free DNA) was extracted from serum exosome of gastric cancer patient. We analyzed cfDNA by aCGH (array comparative genomic hybridization). Overall design: T1 early carcinoma patients versus normal; T3 advanced carcinoma patients versus normal
Project description:Human primary gastric cancer tissue SAGE libraries. Profile of the genes expressed in well and poorly differentiated gastric cancer, early and advanced gastric cancer, scirrhous type gastric cancer, and lymph node metastasis determined through SAGE. Keywords = gastric cancer, histology, early gastric cancer, advanced gastric cancer, lymph node metastasis, scirrhous type gastric cancer Keywords: other
Project description:We profiled the mutations and gene expressions of early and advanced hepatocellular carcinoma (HCC) related with Hepatitis B-viral infection. Integrative analysis was performed with whole-exome sequencing and gene expression profiles of the 12 cases of early and advanced HCCs and paired non-tumoral adjacent liver tissues. 12 HCC Samples
Project description:We tried progression risk prediction of individual gland-forming gastric cancers using genomic DNA copy number profile as a genetic lineage marker. The unsupervised clustering of DNA copy-number profiles of 107 gastric cancer samples, using large-sized (≥ 6 probes) genes, were divided into the loss-rich (A) and gain-rich (B) clusters. The T1/T2-4 ratio was significantly higher in cluster B and in cluster A (P < 0.0007). Small cancers (≤ 2 cm in diameter) were more frequent in cluster B than in cluster A. These 2 clusters were not linked to the frequency of metastasis but to the liability to progression from early to advanced stage; the cluster A may more readily become advanced than cluster B. Our approach suggested that the genetic lineages of early and advanced gland-forming gastric cancers are largely different; the eradication of small cluster B tumors (≤ 2 cm) by the present ESD indication may be valid, but not be effective for reduction of large, aggressive cluster A tumors. Overall design: We used formalin-fixed paraffin embedded tissues from 55 gland-forming invasive gastric cancers with or without LN metastasis. Genomic DNAs extracted from 107 samples that were taken from mucosal, invasive and lymph node parts of tumors were used for array CGH analysis and subsequent hierarchical clustering analysis and penetrance plots
Project description:Increased incidence of oropharyngeal squamous cell carcinoma (OPSCC) is mainly related to Human Papilloma Virus (HPV) infection. As OPSCCs are often diagnosed at an advanced stage, mortality and morbidity remain high. There are no diagnostic biomarkers for early stage detection of OPSCC. Serum from 25 patients with stage I-II OPSCC and 12 disease- individuals were studied with quantitative label-free proteomics using ultra-definition MSE. Statistical analyses were performed to identify proteins most reliably distinguishing early stage OPSCCs from controls. P16 was used as a surrogate marker for HPV. P16-positive and -negative tumours were also analysed separately. With two or more unique proteins per identification, 176 proteins were quantified. A clear separation between patients with early-stage tumours and controls was seen in principal component analysis. Latent structures discriminant analysis identified 96 proteins most reliably differentiating OPSCC patients from controls, with 13 upregulated and 83 downregulated in study cases. The set of proteins was studied further with network, pathway and protein-protein interaction analyses, and found to participate in e.g. lipid metabolism. We identified patients with early stage OPSCC from controls based on their serum proteome, and suggest a protein set for further evaluation as a diagnostic biomarker panel for OPSCC.