Helicobacter pylori cagA status and gastric mucosa-associated lymphoid tissue lymphoma: a systematic review and meta-analysis
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Masoud Keikha1, Amirhossein Sahebkar2,3, Yoshio Yamaoka4,5
1Department of Microbiology and Virology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Background:
Recent studies have investigated the role of Helicobacter pylori infection in the development of gastric mucosa-associated lymphoid tissue (MALT) lymphoma. It is estimated that approximately 0.1% of people infected with H. pylori develop gastric MALT lymphoma. However, the role of the CagA antigen, the highest causative agent of H. pylori, in increasing the risk of gastric MALT lymphoma remains unclear and controversial. A systematic review and meta-analysis were conducted to evaluate the effect of cagA status on the development of gastric MALT lymphoma.
Methods:
All articles evaluating the status of the cagA gene in the development of gastric MALT lymphoma were collected using systematic searches in online databases, including PubMed, Scopus, Embase, and Google Scholar, regardless of publication date. The association between cagA and gastric MALT lymphoma was assessed using the odds ratio (OR) summary. In addition, a random-effects model was used in cases with significant heterogeneity.
Results:
A total of 10 studies met our inclusion criteria, among which 1860 patients participated. No association between cagA status and the development of MALT lymphoma (extranodal marginal zone B-cell lymphoma) was found in this study (OR 1.30; 0.906-1.866 with 95% CIs; I2: 45.83; Q-value: 12.92). Surprisingly, a meaningful association was observed between cagA status and diffuse large B-cell lymphoma (OR 6.43; 2.45-16.84 with 95% CIs). We also observed an inverse association between vacA and gastric MALT lymphoma risk (OR 0.92; 0.57-1.50 with 95% CIs).
Conclusions:
It seems that the infection with cagA-positive H. pylori strains does not have a meaningful effect on the gastric MALT lymphoma formation, while translocated CagA antigen into the B cells plays a crucial role in the development of diffuse large B-cell lymphoma.
Insights
Helicobacter pylori CagA antigen status does not influence gastric MALT lymphoma risk. However, CagA antigen translocation into B cells is crucial for diffuse large B-cell lymphoma development.
Area of Science:
- Gastroenterology
- Oncology
- Infectious Diseases
Background:
- Helicobacter pylori infection is linked to gastric mucosa-associated lymphoid tissue (MALT) lymphoma.
- The specific role of the CagA antigen in H. pylori regarding MALT lymphoma risk is debated.
- A small percentage (0.1%) of H. pylori-infected individuals develop gastric MALT lymphoma.
Purpose of the Study:
- To systematically review and meta-analyze the association between CagA antigen status and gastric MALT lymphoma development.
- To clarify the controversial role of CagA in H. pylori-related gastric MALT lymphoma.
- To investigate the impact of CagA status on other B-cell lymphomas.
Main Methods:
- Systematic literature search across PubMed, Scopus, Embase, and Google Scholar.
- Meta-analysis using odds ratio (OR) to assess the association between CagA status and gastric MALT lymphoma.
- Random-effects model employed for significant heterogeneity.
Main Results:
- Ten studies involving 1860 patients were included.
- No significant association was found between CagA status and gastric MALT lymphoma (OR 1.30; 95% CIs: 0.906-1.866).
- A significant association was observed between CagA status and diffuse large B-cell lymphoma (OR 6.43; 95% CIs: 2.45-16.84).
Conclusions:
- CagA-positive H. pylori infection does not appear to significantly impact gastric MALT lymphoma formation.
- Translocation of the CagA antigen into B cells plays a critical role in the pathogenesis of diffuse large B-cell lymphoma.
- Further research may elucidate the precise mechanisms involved in CagA's role in lymphomagenesis.
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