ArticleWorld journal of gastroenterology2008
Alteration of sister chromatid exchange frequencies in gastric cancer and chronic atrophic gastritis patients with and without H. pylori infection.
Article in World journal of gastroenterology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed, 10 citations in OpenAlex.
- The mutual interactions among Helicobacter pylori, chronic gastritis, and the gut microbiota: a population-based study in Jinjiang, Fujian.Frontiers in microbiology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo determine, by counting sister chromatid exchange (SCE) frequencies, whether genetic impairment and DNA damage have an effect on the pathogenesis of gastric cancer (GC).
methodsAnalysis of SCE is a cytogenetic technique used to show DNA damage as a result of an exchange of DNA fragments between sister chromatids. We analyzed SCE frequency in 24 patients with GC, 26 patients with chronic atrophic gastritis (CAG), and 15 normal controls. The presence of H. pylori was confirmed by urease test, toluidine-blue stain and hematoxylin-eosin stain.
resultsSCE was significantly increased in H. pylori-negative GC patients, and in H. pylori-negative CAG patients compared with controls (7.41 +/- 1.36 and 6.92 +/- 1.20, respectively, vs 5.54 +/- 0.8, P < 0.001). There was no difference in the SCE frequency between H. pylori-negative GC patients and H. pylori-negative CAG patients (P > 0.05). On other hand, the SCE frequencies in H. pylori-positive GC patients were higher than those in H. pylori-positive CAG patients (9.20 +/- 0.94 vs 7.93 +/- 0.81, P < 0.01). Furthermore, H. pylori-positive GC patients had a higher SCE frequency than H. pylori-negative GC patients (9.20 +/- 0.94 vs 7.41 +/- 1.36, P < 0.001). Similarly, a significant difference was detected between H. pylori-positive CAG patients and H. pylori-negative CAG patients (7.93 +/- 0.81 vs 6.92 +/- 1.20, P < 0.05).
conclusionWe suggest the increased SCE in patients reflects a genomic instability that may be operative in gastric carcinogenesis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.