Evidence map›Paper›PMID 24119614›Full record

ArticleBMC medical genomics2013

Transcriptome signatures in Helicobacter pylori-infected mucosa identifies acidic mammalian chitinase loss as a corpus atrophy marker.

Intawat Nookaew, Kaisa Thorell, Kuntal Worah, Shugui Wang, Martin Lloyd Hibberd, Henrik Sjövall, Sven Pettersson, Jens Nielsen, Samuel B Lundin

Open access · goldAbstract read
In one paragraph

Article in BMC medical genomics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 2 pooled it
2.9field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 2 countries.

Intawat NookaewDepartment of Microbiology and Immunology, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. samuel.lundin@gu.se.
Kaisa Thorell
Kuntal Worah
Shugui Wang
Martin Lloyd Hibberd
Henrik Sjövall
Sven Pettersson
Jens Nielsen
Samuel B Lundin
Chalmers University of Technology · SEUniversity of Gothenburg · SEGenome Institute of Singapore · SGKarolinska Institutet · SENational Cancer Centre Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe 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.

methodsBiopsies 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.

resultsUsing 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.

conclusionsTranscriptome 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.

Indexed as

TranscriptomeAdultAgedAged, 80 and overBiomarkersBlood VesselsChitinasesEnergy MetabolismFemaleGastric MucosaGastritis, AtrophicHelicobacter pyloriHumansMaleMiddle AgedOligonucleotide Array Sequence AnalysisBiomarkersCHIA protein, humanChitinases

Identifiers

PMID24119614
PMCPMC4015281
OpenAlexW2116719366

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.