ArticleDigestive diseases and sciences2004
The association between cagA+ H. pylori infection and distal gastric cancer: a proposed model.
Article in Digestive diseases and sciences, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Gender Differences in Patients with Gastric Adenocarcinoma.Journal of clinical medicine · 2024Article
- Sex Disparity in Patients with Gastric Cancer: A Systematic Review and Meta-Analysis.Journal of oncology · 2022Review
- HP-CagA+ Regulates the Expression of CDK4/CyclinD1 viaInternational journal of molecular sciences · 2019Article
- Molecular Evidence of Helicobacter Pylori Infection in Prostate Tumors.Current urology · 2015Article
- Latest insights into the effects of Helicobacter pylori infection on gastric carcinogenesis.World journal of gastroenterology · 2006Review
Corrections and comments
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Authors and funding
3 authors.
Funding
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Abstract
Cytotoxin-associated gene A (cagA)+ infection is associated with an increased risk of distal gastric cancer. The aim was to determine the effect of Helicobacter pylori (HP) on gastric mucus thickness, hydrophobicity, and PGE2 and their relation to colonization density. Ninety-nine patients were recruited (69 HP- and 30 HP+: 10 cagA+, 18 cagA-, 2 undetermined) and six biopsies were obtained from each patient. Mucus thickness, hydrophobicity, PGE2, and colonization density were determined. HP status was assessed by histology and culture; cagA+ was determined by PCR. In age- and sex-matched patients, PGE2 was greater in PH+ than HP- (P = 0.04), with cagA+ having higher PGE2 than HP- patients (P = 0.031). No differences were observed in mucus thickness (P = 0.717) or hydrophobicity (P = 0.27) between HP+ and HP- patients. However, cagA+ showed a nonsignificant trend of increase in mucus thickness (P = 0.784) and hydrophobicity (P = 0.30) compared to cagA- and HP- patients. cagA+ colonization density was weakly correlated with increased thickness (r = 0.333, P = 0.381), whereas cagA- density was inversely correlated with thickness (r = -0.805, P = 0.0001). A model suggesting the possible changes induced by cagA+ infection is proposed which explains the high association of cagA+ with distal gastric cancer. If supported by large multicenter studies, this could form the basis for the development of new therapies directed at the mucous layer to eradicate HP and thus reduce the risk of gastric cancer.
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