Evidence map›Paper›PMID 15259072›Full record

ArticleWorld journal of gastroenterology2004

Increased oxidative DNA damage, inducible nitric oxide synthase, nuclear factor kappaB expression and enhanced antiapoptosis-related proteins in Helicobacter pylori-infected non-cardiac gastric adenocarcinoma.

Chi-Sen Chang, Wei-Na Chen, Hui-Hsuan Lin, Cheng-Chung Wu, Chau-Jong Wang

Open access · hybridAbstract read
In one paragraph

Article in World journal of gastroenterology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
5.1field-weighted citation impact, top 5% 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

17 citing papers in PubMed, 51 citations in OpenAlex.

  1. Trial
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  13. Upregulation of cIAP2 in regenerating colonocytes in ulcerative colitis.Virchows Archiv : an international journal of pathology · 2007
    Article
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  15. Review
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  17. Review
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

5 authors at 2 institutions in 1 country.

Chi-Sen ChangInstitute of Biochemistry, College of Medicine, Chung Shan Medical University, No. 110, Sec. 1, Chien Kuo North Road, 402 Taichung, Taiwan, China.
Wei-Na Chen
Hui-Hsuan Lin
Cheng-Chung Wu
Chau-Jong Wang
Chung Shan Medical University · TWTaichung Veterans General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimSeveral epidemiological studies have demonstrated a close association between Helicobacter pylori (H pylori) infection and non-cardiac carcinoma of the stomach. H pylori infection induces active inflammation with neutrophilic infiltrations as well as production of oxygen free radicals that can cause DNA damage. The DNA damage induced by oxygen free radicals could have very harmful consequences, leading to gene modifications that are potentially mutagenic and/or carcinogenic. The aims of the present study were to assess the effect of H pylori infection on the expression of inducible nitric oxidative synthase (iNOS) and the production of 8-hydroxy-deoxyguanosine (8-OHdG), a sensitive marker of oxidative DNA injury in human gastric mucosa with and without tumor lesions, and to assess the possible factors affecting cell death signaling due to oxidative DNA damage.

methodsIn this study, 40 gastric carcinoma specimens and adjacent specimens were obtained from surgical resection. We determined the level of 8-OHdG formation by HPLC-ECD, and the expression of iNOS and mechanism of cell death signaling (including nuclear factor-kappaB(NFkappaB), MEKK-1, Caspase 3, B Cell lymphomal leukemia-2 (Bcl-2), inhibitor of apoptosis protein (IAP) and myeloid cell leukemia-1 (Mcl-1)) by Western-blot assay.

resultsThe concentrations of 8-OHdG, iNOS, NFkappaB, Mcl-1 and IAP were significantly higher in cancer tissues than in adjacent non-cancer tissues. In addition, significantly higher concentrations of 8-OHdG, iNOS, NFkappaB, Mcl-1 and IAP were detected in patients infected with H pylori compared with patients who were not infected with H pylori. Furthermore, 8-OHdG, iNOS, NFkappaB, Mcl-1 and IAP concentrations were significantly higher in stage 3 and 4 patients than in stage 1 and 2 patients.

conclusionChronic H pylori infection induces iNOS expression and subsequent DNA damage as well as enhances anti-apoptosis signal transduction. This sequence of events supports the hypothesis that oxygen-free radical-mediated damage due to H pylori plays a pivotal role in the development of gastric carcinoma in patients with chronic gastritis.

Indexed as

DNA DamageHelicobacter pyloriAdenocarcinomaAdultAgedAged, 80 and overApoptosisFemaleHelicobacter InfectionsHumansMaleMiddle AgedNF-kappa BNitric Oxide SynthaseNitric Oxide Synthase Type IIOxidation-ReductionNF-kappa BNitric Oxide SynthaseNitric Oxide Synthase Type IINOS2 protein, humanProteins

Identifiers

PMID15259072
PMCPMC4724973
OpenAlexW1607494622

What OpenQuestion holds

Textmetadata
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.