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Epigenetic analysis of gastric cancer

ABSTRACT: Genome-wide DNA methylation profiling of gastric tumors and matched gastric non-malignant samples. The Illumina HumanMethylation27 BeadChip was used to obtain DNA methylation profiles across 27,578 CpGs in 203 gastric tumors and 94 matched non-malignant gastric samples. Bisulphite-converted DNA from the 203 gastric tumors and 94 matched gastric non-malignant samples was hybridized to the Illumina HumanMethylation27 BeadChip.

ORGANISM(S): Homo sapiens

SUBMITTER: Patrick Tan

PROVIDER: E-GEOD-30601 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Methylation subtypes and large-scale epigenetic alterations in gastric cancer.

Zouridis Hermioni H Deng Niantao N Ivanova Tatiana T Zhu Yansong Y Wong Bernice B Huang Dan D Wu Yong Hui YH Wu Yingting Y Tan Iain Beehuat IB Liem Natalia N Gopalakrishnan Veena V Luo Qin Q Wu Jeanie J Lee Minghui M Yong Wei Peng WP Goh Liang Kee LK Teh Bin Tean BT Rozen Steve S Tan Patrick P

Science translational medicine 20121001 156

Epigenetic alterations are fundamental hallmarks of cancer genomes. We surveyed the landscape of DNA methylation alterations in gastric cancer by analyzing genome-wide CG dinucleotide (CpG) methylation profiles of 240 gastric cancers (203 tumors and 37 cell lines) and 94 matched normal gastric tissues. Cancer-specific epigenetic alterations were observed in 44% of CpGs, comprising both tumor hyper- and hypomethylation. Twenty-five percent of the methylation alterations were significantly associa ...[more]

PMID: 23076357

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Epigenetic analysis of gastric cancer

Project description:Genome-wide DNA methylation profiling of gastric tumors and matched gastric non-malignant samples. The Illumina HumanMethylation27 BeadChip was used to obtain DNA methylation profiles across 27,578 CpGs in 203 gastric tumors and 94 matched non-malignant gastric samples.

2012-10-24 | GSE30601 | GEO

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Genetic Landscape of Copy Number Alterations in Gastric Cancer

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2014-04-01 | E-GEOD-51105 | biostudies-arrayexpress

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Project description:To identify key tumour supressor miRNAs involed in MALT lymphoma pathogenesis Gastric mucosa-associated lymphoid tissue lymphoma develops in the chronically inflamed mucosa of Helicobacter pylori-infected patients. MicroRNA expression profiling of human MALT lymphoma revealed a 10-fold down-regulation of miR-203, which resulted from promoter hypermethylation and coincided with the dysregulation of the miR-203 target ABL1. Demethylating treatment of lymphoma B-cells led to an increase in miR-203 expression and concomitant ABL1 down-regulation. The lentiviral delivery of miR-203, as well as treatment with various ABL inhibitors, prevented primary MALT lymphoma cell proliferation in vitro. Finally, the treatment of tumor-bearing mice with imatinib induced MALT lymphoma regression in vivo. Our results show that MALT lymphomagenesis is epigenetically induced by miR-203 promoter methylation and identify ABL1 as a novel target for the treatment of this malignancy. 5 human fresh frozen MALT lymphoma samples were analysed and 4 human tonsil tissue samples were used as the non-tumour control

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Project description:Genome-wide mRNA expression profiles of 70 primary gastric tumors from the Australian patient cohort. Like many cancers, gastric adenocarcinomas (gastric cancers) show considerable heterogeneity between patients. Thus, there is intense interest in using gene expression profiles to discover subtypes of gastric cancers with particular biological properties or therapeutic vulnerabilities. Identification of such subtypes could generate insights into the mechanisms of cancer progression or lay the foundation for personalized treatments. Here we report a robust gene-xpression-based clustering of a large collection of gastric adenocarcinomas from Singaporean patients [GSE34942 and GSE15459]. We developed and validated a classifier for the three subtypes in Australian patient cohort. Profiling of 70 primary gastric tumors on Affymetrix GeneChip Human Genome U133 Plus 2.0 Array. All tumors were collected with approvals from Peter MacCallum Cancer Center, Australia; the Research Ethics Review Committee; and signed patient informed consent.

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