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Chronic inflammation is a risk factor for gastric carcinogenesis after Helicobacter pylori eradication [miRNA]

ABSTRACT: Chronic inflammation is a risk factor for gastric carcinogenesis after Helicobacter pylori eradication [miRNA]

PROVIDER: PRJNA787225 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17168300.fastq.gz	Fastqsanger.gz
	SRR17168301.fastq.gz	Fastqsanger.gz
	SRR17168302.fastq.gz	Fastqsanger.gz
	SRR17168303.fastq.gz	Fastqsanger.gz
	SRR17168304.fastq.gz	Fastqsanger.gz

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Chronic inflammation is a risk factor for gastric carcinogenesis after Helicobacter pylori eradication [miRNA]

Project description:Even after endoscopic treatment of early gastric adenocarcinoma (GAC) and eradication of Helicobacter pylori (H. pylori), some patients develop a metachronous recurrence (MR), the mechanism of which is still unknown. To elucidate the mechanism and risk factors for MR, we analyzed gene expression at multiple locations of the gastric mucosa, considering the heterogeneity of gastric mucosal damage caused by H. pylori infection and investigated the mechanism and risk factors for MR.

2022-12-31 | GSE190455 | GEO

Chronic inflammation is a risk factor for gastric carcinogenesis after Helicobacter pylori eradication [RNA-seq]

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Chronic inflammation is a risk factor for gastric carcinogenesis after Helicobacter pylori eradication

Project description:Chronic inflammation is a risk factor for gastric carcinogenesis after Helicobacter pylori eradication

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Helicobacter pylori-mediated Epigenetic Dysregulation of FOXD3 Tumor-suppressive Cascade In Gastric Carcinogenesis [MMASS]

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Helicobacter pylori-mediated Epigenetic Dysregulation of FOXD3 Tumor-suppressive Cascade In Gastric Carcinogenesis [ChIP]

Project description:Forkhead box (Fox) proteins constitute an evolutionarily conserved family of transcriptional regulators whose deregulations lead to tumorigenesis. However, their regulation and function in gastric cancer are unknown. Promoter hypermethylation occurs during Helicobacter pylori (H pylori)-induced gastritis, but whether the deregulated genes contribute to the multi-step gastric carcinogenesis remains unclear. FOXD3 was found to be hypermethylated in a mouse model of H pylori infection and possess tumor-suppressive functions in gastric cancer cell lines. In order to characterize the direct targets of FOXD3 that confer its actions, we performed ChIP-chip in N87 gastric cancer cell line which express low level of FOXD3 in the nuclei of a sub-population of cells. Promoter hypermethylation occurs during Helicobacter pylori (H pylori)-induced gastritis, but whether the deregulated genes contribute to the multi-step gastric carcinogenesis remains unclear. We used MethylCap-microarray to identify hypermethylated genes in a mouse model of H pylori infection.

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Efficacy Study of Helicobacter Pylori Eradication in Patients Undergoing Subtotal Gastrectomy for Gastric Cancer

Project description:Helicobacter pylori (H. pylori) is associated with gastric cancer in epidemiological studies.Gastric atrophy and intestinal metaplasia caused by H. pylori are considered as precancerous lesions, but whether H. pylori eradication improves these lesions is controversial.The primary objective of this study is to evaluate whether Helicobacter pylori eradication improves glandular atrophy and intestinal metaplasia which are known to be precancerous condition in patients undergoing subtotal gastrectomy for gastric cancer.

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Helicobacter pylori-mediated Epigenetic Dysregulation of FOXD3 Tumor-suppressive Cascade In Gastric Carcinogenesis [ChIP]

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Chronic inflammation is a risk factor for gastric carcinogenesis after Helicobacter pylori eradication [RNA-seq]

Project description:Chronic inflammation is a risk factor for gastric carcinogenesis after Helicobacter pylori eradication [RNA-seq]

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Helicobacter pylori-mediated Epigenetic Dysregulation of FOXD3 Tumor-suppressive Cascade In Gastric Carcinogenesis [MMASS]

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DNA methylation profiles in gastric mucosa samples with low, intermediate and high cancer risk

Project description:DNA methylation profiles were compared between gastric mucosae samples without Helicobacter pylori (HP) infection (low risk : G1), those with HP eradication without gastric cancer (intermediate risk : G2), and those with HP eradication with gastric cancer (high risk : G3).

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