Helicobacter pylori–gastrin link in MALT lymphoma

Abstract

There is accumulating evidence linking gastric infection with the spiral bacterium, Helicobacter pylori, to the cause of various gastric pathologies including gastritis, gastro-duodenal ulcerations and gastric cancers and lymphomas. 1±5 We demonstrated recently that gastric cancer is closely linked to H. pylori infection; approximately 92% of cancer patients were H. pyloriseropositive and 68% of them were H. pylori CagAseropositive. 6 Our study con®rmed recent retrospective studies presented by Danesh in his review on H. pylori infection and gastric cancer, showing that this infection SUMMARY Background: There is accumulating evidence for the role of Helicobacter pylori in the development of gastric cancer as well as of lymphomas that arise in mucosaassociated lymphoid tissue (MALT). We reported recently that gastric cancer patients show high prevalence of cagA-positive H. pylori and express gastrin and gastrin receptors enabling them to stimulate tumour growth in autocrine fashion. Aims: Since the H. pylori infection is considered to be more strongly associated with MALT lymphoma than with gastric cancer, we decided to determine the gastrin and its receptors' mRNA expression and gastrin content in this tumour as well as the release of this hormone both into plasma and gastric lumen. Twenty MALT lymphoma patients were compared with 100 age-and gendermatched controls with similar dyspeptic symptoms. Results: The overall H. pylori seropositivity in MALT lymphoma was about 90% and CagA positivity was 70%, compared to 56% and 33%, respectively, in controls. The serum gastrin in MALT lymphoma was

Gastric ghrelin in relation to gender, stomach topographyand Helicobacter pylori in dyspeptic patients

“…The cagA gene is present in about 60%-70% of H pylori strains. It is associated with prominent inflammatory and atrophic changes and increases the risk (3-6 times) of developing a peptic ulcer, gastric adenocarcinoma and lymphoma [29][30][31][32] . H pylori infection results in an increase in proliferative activity and affects the apoptotic processes of the glandular epithelium of the gastric mucosa.…”

Implication of Peroxisome Proliferator-Activated Receptor γ and Proinflammatory Cytokines in Gastric Carcinogenesis: Link to Helicobacter pylori-Infection

“…The question remains whether the hypergastrinemia in H. pylori positive GC was caused merely by the infection or by the accompanying increase in mucosal levels of cytokines which were shown previously to contribute to hypergastrinemia (38,39). We conclude that 1) H. pylori infection is associated with increased PPARg expression in the gastric mucosa and that this might reflect an induction of one of the protective mechanisms limiting the extent of gastric mucosal injury induced by this germ; 2) PPARg is expressed at higher levels in GC itself than at its margin and in both the PPARg levels are higher than in normal gastric mucosa of healthy controls; 3) Gastric mucosal tissue levels of proinflammatory cytokines are highly elevated in GC H. pylori infected patients, suggesting that cancerogenic action of H. pylori may be related to augmented inflammatory reaction in the infected mucosa; 4) Treatment of GC cells with specific PPARg ligands suppresses the proliferation rate of the cells and induces apoptosis in dose-dependent manner possibly due to the downregulation of antiapoptotic Bcl-2 and upregulation of Bax; and 5) Based on our present results and previous reports of amelioration of GC after treatment with ligands of PPARg and with specific antiinflammatory COX-2 inhibitors such as rofecoxib 30 , we postulate that PPARg and proinflammatory cytokines are strongly implicated in gastric carcinogenesis and that the specific PPARg ligands and antiinflammatory agents may have therapeutic potential as chemopreventive agents.…”

Helicobacter pylori genotyping in gastric adenocarcinoma and MALT lymphoma by multiplex PCR analyses of paraffin wax embedded tissues

“…30 In addition to iceA1, studies using serological detection methods have postulated that cagA is also a prognostic marker for the risk of developing MALT lymphoma. [31][32][33] However, two reports using PCR based detection of cagA in cultured H pylori isolates found no correlation between cagA and MALT lymphoma. 30 34 Although the in vitro culture of H pylori may lead to altered prevalence rates as a result of strain selection, the loss of genes, or a low culture rate, 35 these data correspond to our findings, confirming that the cagA status is not a prognostic factor for the development of GC or of MALT lymphoma.…”