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Transcription factor EHF interacting with transcription coactivator AJUBA (JUB) aggravates malignancy of gastroesophageal adenocarcinoma [ChIP-seq]

ABSTRACT: Transcriptional dysregulation of genes is a hallmark of tumors and can be pharmacologically developed in cancer. However, little is known about the interaction or transcriptional cooperativity between TF and transcription cofactor in gastroesophageal adenocarcinoma (GEA).

ORGANISM(S): Homo sapiens

PROVIDER: GSE207554 | GEO | 2024/06/05

REPOSITORIES: GEO

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Transcription factor EHF interacting with transcription coactivator AJUBA (JUB) aggravates malignancy of gastroesophageal adenocarcinoma [ATAC-seq]

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Transcription factor EHF interacting with transcription coactivator AJUBA (JUB) aggravates malignancy of gastroesophageal adenocarcinoma.

Project description:This SuperSeries is composed of the SubSeries listed below.

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Transcription factor EHF interacting with transcription coactivator AJUBA (JUB) aggravates malignancy of gastroesophageal adenocarcinoma.

Project description:Transcription factor EHF interacting with transcription coactivator AJUBA (JUB) aggravates malignancy of gastroesophageal adenocarcinoma.

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Transcription factor EHF interacting with transcription coactivator AJUBA (JUB) aggravates malignancy of gastroesophageal adenocarcinoma [ATAC-seq]

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Transcription factor EHF interacting with transcription coactivator AJUBA (JUB) aggravates malignancy of gastroesophageal adenocarcinoma [ChIP-seq]

Project description:Transcription factor EHF interacting with transcription coactivator AJUBA (JUB) aggravates malignancy of gastroesophageal adenocarcinoma [ChIP-seq]

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Genomic profiling of gastroesophageal adenocarcinoma

Project description:We aimed to characterize the genomic profiles of adenocarcinomas in the gastroesophageal junction in relation to cancers in the esophagus and the stomach. Profiles of gains/losses as well as gene expression profiles were obtained from 27 gastroesophageal adenocarcinomas using 32k high-resolution array-based comparative genomic hybridization (aCGH) and 27k oligo gene expression arrays and putative target genes were validated in an extended series. Adenocarcinomas in the distal esophagus and the gastroesophageal junction showed strong similarities with the most common gains at 20q13, 8q24, 1q21-q23, 5p15, 13q34, and 12q13, whereas different profiles with gains at 5p15, 7p22, 2q35, and 13q34 characterized gastric cancers. CDK6 and EGFR were identified as putative target genes in cancers of the esophagus and the gastroesophageal junction with upregulation in one quarter of the tumors. Gains/losses and gene expression profiles show strong similarity between cancers in the distal esophagus and the gastroesophageal junction with frequent upregulation of CDK6 and EGFR, whereas gastric cancer displays distinct genetic changes. These data suggest that molecular diagnostics and targeted therapies can be applied to adenocarcinomas of the distal esophagus and gastroesophageal junction alike. Three types of gastroesophageal adenocarcinomas; 7 distal esophageal (EA) tumors, 9 junctional (JA) and 7 proximal stomach cancers (GA) was genomically profiled using tiling 32k BAC-arrays. Two replicates of tumors IDs 1-EA-CGH (replicate 1-EA-CGH-2), 12-EA-CGH (replicate 12-EA-CGH-2) and 18-EA-CGH (replicate 18-EA-CGH-2). Reference samples consist of a pool of male DNA (Promega, Madison, WI, USA).

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