Purpose:  To determine early changes in gene expression that drive gastric cancer development in the landscape of CLDN18 loss using RNAseq.;	Results:  Although claudin-18 is a tight junction protein and should regulate paracellular permeabiity and/or ion flux across the mucosa, we showed this protein is rather a potent tumor suppressor that regulates cellular signaling and differentiation pathways in gastric epithelial cells.;	Methods: Stomach neck region mRNA profiles of 7-day-old wild-type (WT) and claudin-18 knockout (CLDN18/) mice were generated by deep sequencing, in triplicate, using the Illumina HiSeq2000 sequencing system. The resulting sequences were mapped to the Mouse genome (mm10) using STAR aliger and P-values were adjusted using the Benjamini-Hochberg procedure (J R Statist Soc B  1995;57:289-300).;	Conclusions:  Loss of claudin-18 promotes gastric cancer development by modulating the expression program of gastric epithelial cells, including cellular signaling and differentiation pathways that are required for mucosal homeostasis. SOURCE: Susan,J,Hagen (shagen@bidmc.harvard.edu) -  Beth Israel Deaconess Medical Center

Pluto Bioinformatics

GSE93774: Quantitative Transcriptome Analysis of the Stomach Neck Mucosa from Control vs Claudin (CLDN)-18 knockout mice.