A distinctive set of genes is upregulated during the inflammation-carcinoma sequence in mouse stomach infected by Helicobacter felis.

A distinctive set of genes is upregulated during the inflammation-carcinoma sequence in mouse stomach infected by Helicobacter felis. Research Abstract Details 

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A distinctive set of genes is upregulated during the inflammation-carcinoma sequence in mouse stomach infected by Helicobacter felis. Abstract Text:

Motohiro Kobayashi,Heeseob Lee,Lana Schaffer,Tim J Gilmartin,Steven R Head,Shigeo Takaishi,Timothy C Wang,Jun Nakayama,Minoru Fukuda,

Helicobacter pylori infects over half the population worldwide and is a leading cause of chronic gastritis and gastric cancer. However, the mechanism by which this organism induces inflammation and carcinogenesis is not fully understood. In the present study we used insulin-gastrin (INS-GAS) transgenic mice that fully develop gastric adenocarcinoma after infection of H. pylori-related Helicobacter felis. Histological examination revealed that more than half of those mice developed invasive adenocarcinoma after 8 months of infection. These carcinomas were stained by NCC-ST-439 and HECA-452 that recognize 6-sulfated and non-sulfated sialyl Lewis X. Lymphocytic infiltration predominantly to submucosa was observed in most H. felis-infected mice, and this was associated with the formation of peripheral lymph node addressin (PNAd) on high endothelial venule (HEV)-like vessels detected by MECA-79. Time-course analysis of gene expression by using gene microarray revealed upregulation of several inflammation-associated genes including chemokines, adhesion molecules, surfactant protein D (SP-D), and CD74 in the infected stomach. Immunohistochemical analysis demonstrated that SP-D is expressed in hyperplasia and adenocarcinoma whereas CD74 is expressed in adenocarcinoma in situ and invasive carcinoma. These results as a whole indicate that H. felis induces HEV-like vessels and inflammation-associated chemokines and chemokine receptors, followed by adenocarcinoma formation.

A distinctive set of genes is upregulated during the inflammation-carcinoma sequence in mouse stomach infected by Helicobacter felis. Publishing Authors By Initials

M Kobayashi,H Lee,L Schaffer,TJ Gilmartin,SR Head,S Takaishi,TC Wang,J Nakayama,M Fukuda,

For similar genetic processes: gene expression regulation: up-regulation research abstracts see: genetic processes: gene expression regulation: up-regulation research

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A distinctive set of genes is upregulated during the inflammation-carcinoma sequence in mouse stomach infected by Helicobacter felis. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: The journal of histochemistry and cytochemistry :

VOLUME: 55

Page Numbers: 263-74

Journal Abbreviation: J. Histochem. Cytochem.

ISSN: 0022-1554

DAY: 13

MONTH: 11

YEAR: 2006

A distinctive set of genes is upregulated during the inflammation-carcinoma sequence in mouse stomach infected by Helicobacter felis. Information

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LANGUAGE: eng

NlmUniqueID: 9815334

A distinctive set of genes is upregulated during the inflammation-carcinoma sequence in mouse stomach infected by Helicobacter felis. Keywords Mesh Terms:

KEYWORDS: Up-Regulation

MESH TERMS: pathology

Chemical & Substance for Abstract: A distinctive set of genes is upregulated during the inflammation-carcinoma sequence in mouse stomach infected by Helicobacter felis. Information

Substance Name: Glycosyltransferases

Registry Number: EC 2.4.-

Grant and Affiliation Information for A distinctive set of genes is upregulated during the inflammation-carcinoma sequence in mouse stomach infected by Helicobacter felis.

AFFILIATION: Glycobiology Program, Cancer Research Center, Burnham Institute for Medical Research, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.

Country: United States

AGENCY: United States NIGMS

GRANT: GM-62116

ACRONYM: GM

MEDLINETA: J Histochem Cytochem

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