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Epigenomic profiling of primary gastric adenocarcinoma reveals super-enhancer heterogeneity

Gene expression is regulated by enhancers and super-enhancers, which can be identified by chromatin profiling. Here, the authors surveyed gastric cancer samples and cell lines to identify enhancer elements exhibiting somatic alterations.

Wen Fong Ooi
Manjie Xing
Patrick Tan
ResearchOpen Access28 Sept 2016
Nature Communications

Volume: 7, P: 1-17
Cross-species chromatin interactions drive transcriptional rewiring in Epstein–Barr virus–positive gastric adenocarcinoma

Genome-wide analysis of 3D chromatin topologies across gastric cancers suggests that Epstein–Barr virus infection may induce the epigenetic rewiring of EBV-positive tumors through human–viral chromatin interactions, a phenomenon termed ‘enhancer infestation’.

Atsushi Okabe
Kie Kyon Huang
Atsushi Kaneda
Research27 Jul 2020
Nature Genetics

Volume: 52, P: 919-930
Nanoscale chromatin profiling of gastric adenocarcinoma reveals cancer-associated cryptic promoters and somatically acquired regulatory elements

Epigenetic alterations alter chromatin structure and gene expression and are known contributors to cancer development. Here, Muratani et al.profile multiple epigenetic chromatin marks in primary gastric cancers and identify hundreds of altered promoters and enhancers that drive the gene expression program in these malignancies.

Masafumi Muratani
Niantao Deng
Patrick Tan
Research10 Jul 2014
Nature Communications

Volume: 5, P: 1-14
HoxC5 and miR-615-3p target newly evolved genomic regions to repress hTERT and inhibit tumorigenesis

The expression of telomerase catalytic subunit hTERT is frequently upregulated in many cancers. Here, the authors show HoxC5 and miR-615-3p can negatively regulate hTERT to impede tumorigenesis by targeting the newly evolved cis-regulatory genomic elements of hTERT.

TingDong Yan
Wen Fong Ooi
Shang Li
ResearchOpen Access08 Jan 2018
Nature Communications

Volume: 9, P: 1-15
Mutation hotspots at CTCF binding sites coupled to chromosomal instability in gastrointestinal cancers

The impact of non-coding somatic mutations in gastric cancer is unknown. Here, using whole genome sequencing data from 212 gastric tumors, the authors identify recurring mutations at specific CTCF binding sites that are common across gastrointestinal cancers and associated with chromosomal instability.

Yu Amanda Guo
Mei Mei Chang
Anders Jacobsen Skanderup
ResearchOpen Access18 Apr 2018
Nature Communications

Volume: 9, P: 1-14

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Epigenomic profiling of primary gastric adenocarcinoma reveals super-enhancer heterogeneity

Cross-species chromatin interactions drive transcriptional rewiring in Epstein–Barr virus–positive gastric adenocarcinoma

Nanoscale chromatin profiling of gastric adenocarcinoma reveals cancer-associated cryptic promoters and somatically acquired regulatory elements

HoxC5 and miR-615-3p target newly evolved genomic regions to repress hTERT and inhibit tumorigenesis

Mutation hotspots at CTCF binding sites coupled to chromosomal instability in gastrointestinal cancers

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Epigenomic profiling of primary gastric adenocarcinoma reveals super-enhancer heterogeneity

Cross-species chromatin interactions drive transcriptional rewiring in Epstein–Barr virus–positive gastric adenocarcinoma

Nanoscale chromatin profiling of gastric adenocarcinoma reveals cancer-associated cryptic promoters and somatically acquired regulatory elements

HoxC5 and miR-615-3p target newly evolved genomic regions to repress hTERT and inhibit tumorigenesis

Mutation hotspots at CTCF binding sites coupled to chromosomal instability in gastrointestinal cancers

Search

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