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Oral intake of high fat diet and acidic bile salts may develop carcinogenesis at the esophagogastric junction

ABSTRACT: Oral intake of high fat diet and acidic bile salts may develop carcinogenesis at the esophagogastric junction

PROVIDER: PRJNA1101010 | ENA |

REPOSITORIES: ENA

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Oral intake of high fat diet and acidic bile salts may develop carcinogenesis at the esophagogastric junction

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The molecular mechanism and clinical significance of IGF2BP3 in adenocarcinoma of the esophagogastric junction [RIP-seq]

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Gastric and esophagogastric junction adenocarcinoma with infrequent hypermethylation show poor prognosis

Project description:Gastric and esophagogastric junction adenocarcinoma with infrequent hypermethylation show poor prognosis

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Gastric and esophagogastric junction adenocarcinoma with infrequent hypermethylation show poor prognosis

Project description:Background Gastric cancer (GC) was characterized by unique DNA methylation epigenotypes (MEs). Still, MEs, including adenocarcinoma of the esophagogastric junction (AEG) and background non-neoplastic columnar mucosae (NM), are yet to be clarified. Methods We analyzed genome-wide DNA MEs of AEG, GC, and background NM using Infinium 450k beadarray, followed by quantitative pyrosequencing validation. Large-scale data of the Cancer Genome Atlas (TCGA) were additionally reviewed. Results Unsupervised two-way hierarchical clustering using Infinium data of 21 AEG, 30 GC, and 11 NM showed four DNA MEs: extremely high-ME (E-HME), high-ME (HME), low-ME (LME), and extremely low-ME (E-LME). The promoter methylation levels were validated by pyrosequencing in 146 samples. Although almost normal mucosae were clustered into E-LME, gastric or esophagogastric junction mucosae with chronic inflammatory change due to either Helicobacter pylori infection or reflux esophagitis were clustered together into LME, which suggested that the inflammation status determined DNA MEs regardless of the causes. Three cases of Barrett’s-related adenocarcinoma were all clustered into HME. Among 94 patients whose tumors can be clustered into one of four MEs, 11 patients with E-LME cancers showed significantly shorter overall survival than the other MEs, even in multivariate Cox regression estimate. TCGA data also showed enrichment of AEG in HME and a poorer prognosis of E-LME. Conclusions E-LME cases, newly confirmed in this study, would be a unique aggressive subtype not associated with the elevation of DNA methylation levels caused by inflammation. LME could be acquired via chronic inflammation independent of the causes, and AEG frequently showed HME.

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