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| Status |
Public on Feb 04, 2014 |
| Title |
Transcriptional analysis reveals the molecular details of atrophic gastritis in Helicobacter pylori infected corpus mucosa |
| Organism |
Homo sapiens |
| Experiment type |
Expression profiling by array
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| Summary |
The majority of gastric cancer cases are believed to be caused by chronic infection with the bacterium Helicobacter pylori, and atrophic corpus gastritis is a predisposing condition to gastric cancer development. We aimed to increase understanding of the molecular details of atrophy by performing a global transcriptome analysis of stomach tissue.
Biopsies from patients with different stages of H. pylori infection were taken from both the antrum and corpus mucosa and analyzed on microarrays. The stages included patients without current H. pylori infection, H. pylori-infected without corpus atrophy and patients with current or past H. pylori-infection with corpus-predominant atrophic gastritis.Using clustering and integrated analysis, we found firm evidence for antralization of the corpus mucosa of atrophy patients. This antralization harbored gain of gastrin expression, as well as loss of expression of corpus-related genes, such as genes associated with acid production, energy metabolism and blood clotting. The analyses provided detailed molecular evidence for simultaneous intestinal metaplasia (IM) and spasmolytic polypeptide expressing metaplasia (SPEM) in atrophic corpus tissue. Finally, acidic mammalian chitinase, a chitin-degrading enzyme produced by chief cells, was shown to be strongly down-regulated in corpus atrophy.Transcriptome analysis revealed several gene groups which are related to development of corpus atrophy, some of which were increased also in H. pylori-infected non-atrophic patients. Furthermore, loss of acidic chitinase expression is a promising marker for corpus atrophy.
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| Overall design |
Biopsies from well classified patients with different stages of H. pylori infection were taken from both the antrum and corpus mucosa. These stages included H. pylori un-infected, H. pylori-infected without corpus atrophy and H. pylori-infected with corpus-predominant atrophic gastritis.
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| Contributor(s) |
Nookaew I, Thorell K, Worah K, Wang S, Pettersson S, Sjövall H, Nielsen J, Lundin SB |
| Citation(s) |
24119614 |
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| Submission date |
Feb 18, 2011 |
| Last update date |
Feb 04, 2014 |
| Contact name |
Intawat Nookaew |
| E-mail(s) |
[email protected]
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| Organization name |
University of Arkansas for Medical Sciences
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| Department |
Department of Biomedical Informatics
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| Street address |
4301 W Markham St
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| City |
Little Rock |
| ZIP/Postal code |
72205 |
| Country |
USA |
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| Platforms (1) |
| GPL6255 |
Illumina humanRef-8 v2.0 expression beadchip |
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| Samples (18)
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| GSM677730 |
Helicobacter pylori non-infected, antrum 23A |
| GSM677731 |
Helicobacter pylori non-infected, antrum 49A |
| GSM677732 |
Helicobacter pylori non-infected, corpus 23C |
| GSM677733 |
Helicobacter pylori non-infected, corpus 49C |
| GSM677734 |
Helicobacter pylori infected, antrum 8A |
| GSM677735 |
Helicobacter pylori infected, antrum 9A |
| GSM677736 |
Helicobacter pylori infected, antrum 30A |
| GSM677737 |
Helicobacter pylori infected, corpus 8C |
| GSM677738 |
Helicobacter pylori infected, corpus 9C |
| GSM677739 |
Helicobacter pylori infected, corpus 30C |
| GSM677740 |
Atrophy, antrum 22A |
| GSM677741 |
Atrophy, antrum 44A |
| GSM677742 |
Atrophy, corpus 22C |
| GSM677743 |
Atrophy, corpus 44C |
| GSM677744 |
Atrophy, antrum 48A |
| GSM677745 |
Atrophy, corpus 48C |
| GSM677746 |
Helicobacter pylori non-infected, antrum 35A |
| GSM677747 |
Helicobacter pylori non-infected, corpus 35C |
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| Relations |
| BioProject |
PRJNA137249 |
| Supplementary file |
Size |
Download |
File type/resource |
| GSE27411_non-normalized.txt.gz |
1.6 Mb |
(ftp)(http) |
TXT |
| Processed data included within Sample table |
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