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Gene eRandomized Controlled Trial of the Gastrin Receptor Antagonist Netazepide in Patients with Barrett’s Esophagus

ABSTRACT: Gene eRandomized Controlled Trial of the Gastrin Receptor Antagonist Netazepide in Patients with Barrett’s Esophagus

PROVIDER: PRJNA655179 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12384300_1.fastq.gz	Fastqsanger.gz
	SRR12384300_2.fastq.gz	Fastqsanger.gz
	SRR12384301_1.fastq.gz	Fastqsanger.gz
	SRR12384301_2.fastq.gz	Fastqsanger.gz
	SRR12384302_1.fastq.gz	Fastqsanger.gz

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HOXA13 in etiology and oncogenic potential of Barrett’s esophagus [EPC2]

Project description:Barrett’s esophagus in gastrointestinal reflux patients constitutes a columnar epithelium with distal characteristics, prone to progress to esophageal adenocarcinoma. HOX genes are known mediators of position-dependent morphology. Here we show HOX collinearity in the adult gut while Barrett’s esophagus shows high HOXA13 expression in stem cells and their progeny. HOXA13 overexpression appears sufficient to explain both the phenotype (through downregulation of the epidermal differentiation complex) and the oncogenic potential of Barrett’s esophagus. Intriguingly, employing a mouse model that contains a reporter coupled to the HOXA13 promotor we identify single HOXA13-positive cells distally from the physiological esophagus, which is mirrored in human physiology, but increased in BE. Additionally, we observe that HOXA13 expression confers a competitive advantage to cells. We thus propose that Barrett’s esophagus and associated esophageal adenocarcinoma is the consequence of expansion of this gastro-esophageal HOXA13-expressing compartment following epithelial injury.

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Cloning Barrett’s esophagus stem cells

Project description:Barrett’s esophagus is a precancerous lesion that confers a significant risk of esophageal adenocarcinoma. Strategies for selective eradication of Barrett’s have been stymied by our inability to identify the Barrett’s stem cell. Here we employ novel technologies to clone patient-matched stem cells of Barrett’s, gastric, and esophageal epithelium. Genomic analyses of Barrett’s stem cells reveal a patient-specific mutational spectrum ranging from low somatic variation similar to patient-matched gastric epithelial stem cells to ones marked by extensive heterozygous alteration of genes implicated in tumor suppression, epithelial planarity, and epigenetic regulation. Transplantation of transformed Barrett’s stem cells yields tumors with hallmarks of esophageal adenocarcinoma, whereas transformed esophageal stem cells yield squamous cell carcinomas. Thus Barrett’s develops from cells distinct from local eponymous epithelia, emerges without obvious driver mutations, and likely progresses through and from the generation of dominant clones. These findings define a stem cell target for preemptive therapies of a precancerous lesion.

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HOXA13 in etiology and oncogenic potential of Barrett’s esophagus [BAR-T]

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HOXA13 in etiology and oncogenic potential of Barrett’s esophagus [KH2 mESC diff]

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HOXA13 in etiology and oncogenic potential of Barrett’s esophagus [KH2 mESC non diff]

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Gene eRandomized Controlled Trial of the Gastrin Receptor Antagonist Netazepide in Patients with Barrett’s Esophagus

Project description:A randomized, double-blind, placebo-controlled trial of netazepide (YF476) in patients with BE without dysplasia was performed. Gene expression before and after treatment with netazepide and with a placebo was measured with RNASeq

2021-12-22 | GSE155665 | GEO

Profiling of circulating microRNAs in patients with Barrett’s esophagus and esophageal adenocarcinoma

Project description:miRNAs were extracted from plasma samples of healthy volunteers, patients with Barrett’s esophagus and patients with esophageal adenocarcinoma. We used the Serum / Plasma Focus miRNA PCR panel (Exiqon, Denmark) to quantitate miRNA presence in the different patient groups.

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Global Phospho-Proteomic Profiling of Pathway-Level Molecular Alterations in Barrett’s Esophagus

Project description:In the present study, we applied deep, quantitative mass-spectrometry to clinical samples (Barrett’s esophagus and matched adjacent normal biopsies) to gain a mechanistic understanding of the molecular pathways associated with disease progression. From our rich LC/MS profiles, we identified a robust proteomic signature that was able to correctly classify independent samples on disease status. Projection of this same signature against EAC tumor profiles was strongly predictive of survival outcomes, while subsequent comparative analysis with published BE transcriptomic profiles provided independent evidence in support of these results. Further, our phosphoproteomic analysis revealed signaling pathways specifically and significantly altered in BE relative to paired controls, providing some mechanistic insights into the cellular dysregulation of key components of specific processes that likely drives disease progression.

2022-08-11 | PXD023293 | Pride

Esophageal tissue and serum microRNAs changed in the progression of Barrett’s esophagus in mice

Project description:Circulating microRNAs (miRNAs) are promising biomarkers for the early detection of cancers. This assay aimed to address potential circulating miRNAs to monitor the progression from Barrett’s esophagus to esophageal adenocarcinoma (EAC).

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