Project description:The miRNA expression profiles in one pair of hTERT-positive gastric cancer tissue and an hTERT-negative para-cancerous tissue. The para-cancerous tissue is at least 5cm away from the cancer tisse. The expression of hTERT of identified by immunohistochemistry before RNA extraction for miRNA assay. One pair of gastric cancer tissue and para-cancerous tissue(Control). Four replicates per array.
Project description:The lncRNA expression profiles in three pairs of hTERT-positive gastric cancer tissue sand hTERT-negative para-cancerous tissues. The para-cancerous tissue is at least 5cm away from the cancer tissue. The expression of hTERT of identified by immunohistochemistry before RNA extraction for lncRNA assay. LncRNAs/mRNAs in 3 gastric cancer tissue and 3 paired para-cancerous tissue (Control) by microarray using Arraystar Human LncRNA Microarray v2.0
Project description:The lncRNA expression profiles in three pairs of hTERT-positive gastric cancer tissue sand hTERT-negative para-cancerous tissues. The para-cancerous tissue is at least 5cm away from the cancer tissue. The expression of hTERT of identified by immunohistochemistry before RNA extraction for lncRNA assay.
Project description:The miRNA expression profiles in one pair of hTERT-positive gastric cancer tissue and an hTERT-negative para-cancerous tissue. The para-cancerous tissue is at least 5cm away from the cancer tisse. The expression of hTERT of identified by immunohistochemistry before RNA extraction for miRNA assay.
Project description:The study was undertaken to identify microRNAs differently expressed by intestinal type of gastric cancer using miRNA microarray. The miRNA expression in the intestinal type of gastric cancer depending on H. pylori infection suggest that different gastric cancer pathogenesis could be exist between H. pylori-positive and -negative gastric cancer. Total RNA was extracted from cancerous region and non-cancerous regions in formalin fixed paraffin embedded tissues of intestinal type gastric cancer patients who were H. pylori-positive (n=8) or -negative (n=8). Corresponding author: Nayoung Kim, M.D., Department of Internal Medicine, Seoul National University Bundang Hospital (Tel., +82-31-787-7008; e-mail, nayoungkim49@empas.com).
Project description:Biopsies from 24 gastric adenocarcinomas and adjacent normal gastric mucosa were analyzed for from 24 patients following surgical resection of the tumor. Genome-wide DNA methylation profiling of the tumor and matched non-cancerous mucosa was performed and compared to previously performed gene expression, survival and clinicopathological parametres.
Project description:Gastric cancer is a heterogeneous disease. The molecular mechanism behind the development of gastric cancer and the different histological subtypes, are yet not completely clear. A better understanding of this may result in better prevention, early diagnosis and treatment strategies. In this study we analyzed gene expression in tumor, adjacent non-cancerous mucosa biopsies and in age/sex matched samples from healthy individuals.
Project description:Background: Helicobacter pylori has been shown to alter the secretion of gastric hormones that modulate body fat deposition. Since cag-positive H. pylori strains interact intimately with the host gastric epithelial cells and trigger higher inflammation than cag-negative strains, we hypothesized that gastric colonization with H. pylori strains without functional cagA ameliorates obesity and its complications by modulating gastric gene expression and inflammation. Methodology/Principal Findings: To test this hypothesis we examined the effects of gastric colonization on metabolic and inflammatory markers in mice infected with two isogenic strains of H. pylori: 26695 strain 98-325 (cagA+ wild-type) and its cag pathogenicity island (cagPAI) mutant strain 99-305, a knockout made by inserting a chloramphenicol resistance cassette. Only the cagPAI mutant decreased fasting blood glucose levels, improved glucose tolerance and suppressed weight gain in db/db mice and mice with diet-induced obesity. These effects were associated with increased gastric leptin levels, suppressed infiltration of macrophages, enhanced influx of regulatory T cells (Treg) in adipose tissue and suppressed gastric inflammation. Gene set enrichment analyses of gastric mucosal samples identified six differentially modulated pathways, including the Hedgehog signaling pathway that is associated with control of cellular proliferation and gastric carcinogenesis as well as the insulin signaling pathway. Conclusions/Significance: Gastric colonization with cagPAI-negative strains of H. pylori ameliorate obesity and inflammation by modulating gastric gene expression, suggesting that cag-negative H. pylori strains might be beneficial in ameliorating obesity and its co-morbidities. Gastric mucosa from three groups of mice: uninfected, infected with H. pylori 26695 strain 98-325 (cagA+ wild-type) or infected with H. pylori mutant strain 99-305 (lacking cag pathogenicity island; cagA-)
