Abstract
BackgroundRecent 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.MethodsAll 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.ResultsA 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).ConclusionsIt 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.
Highlights
Recent studies have investigated the role of Helicobacter pylori infection in the development of gastric mucosa-associated lymphoid tissue (MALT) lymphoma
In the present meta-analysis, we investigated the association between cagA gene status and gastric MALT lymphoma to determine the role of cytotoxin-associated gene A (CagA) antigen in the development of disease from MALT lymphoma to diffuse large B-cell lymphoma (DLBCL)
The inclusion criteria were as follows: (1) all original, cross-sectional, case–control, and longitudinal articles related to our purpose, (2) studies on the association between cagA gene status and gastric MALT lymphoma; (3) studies based on standard diagnostic methods such as polymerase chain reaction (PCR), ELISA, and conventional microbiology tests; and (4) studies published in English
Summary
Recent studies have investigated the role of Helicobacter pylori infection in the development of gastric mucosa-associated lymphoid tissue (MALT) lymphoma. According to the second hypothesis, CagA is an immunogenic protein that stimulates the production of interleukin 8 (IL-8) and leads to the infiltration of neutrophils in the inflamed area, the production of free radicals, and DNA damage [15,16,17,18] Infection with this bacterium appears to increase the risk of two cancers of the digestive system, including gastric cancer and gastric MALT lymphoma [19]. CagA antigen can induce pro-inflammatory responses such as neutrophil infiltration, production of reactive oxygen species (ROS), and polyclonal activation of B cells, all of which cause gastric damage and genetic instability [35, 36]; the role of CagA in inducing cascade of gastric precancerous lesions remains unclear. In the present meta-analysis, we investigated the association between cagA gene status and gastric MALT lymphoma to determine the role of CagA antigen in the development of disease from MALT lymphoma to DLBCL
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