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Helicobacter pylori has been associated with the development of two malignant diseases: gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphoma. Although the cag pathogenicity island, especially the cagA gene, has been linked with adenocarcinoma, few data concerning H. pylori pathogenic factors involved in low-grade gastric MALT lymphoma are available. The goal of this study was to analyze the prevalence of and correlation between genes coding for seven H. pylori virulence factors (cagA, cagE, vacA, iceA, babA, hopQ, and oipA) and two novel adhesins (sabA and hopZ) by comparing a collection of 43 H. pylori strains isolated from patients with low-grade gastric MALT lymphoma to 39 strains isolated from age-matched patients with gastritis only. Our results show that taken individually, none of the nine genes tested can be considered associated with MALT strains and allow us to conclude that MALT pathogenesis is not linked with more proinflammatory H. pylori strains. We demonstrated that in patients infected with strains harboring the iceA1 allele, sabA functional status, and hopZ "off" status, the odds of developing a MALT lymphoma were 10 times higher. However, the low prevalence of such strains (10 of 43 MALT strains) renders this triple association a low-sensitivity marker for MALT strains. Our data confirmed that H. pylori virulence factors are correlated with one another. If the involvement of H. pylori in MALT lymphoma is well established, the pathomechanism by which gastric lymphoma occurs remains to be identified.Helicobacter pylori infection is the essential etiological factor of type B chronic gastritis and peptic ulcer disease (29,35). It is also the first bacterium discovered to be involved in the development of malignant diseases: i.e., gastric carcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphoma (14,21,40). Following H. pylori colonization, inflammation occurs. Untreated gastritis may persist for years with different grades of severity. In some individuals, immunological stimulation induces lymphoid follicles in the gastric mucosa and provides the background for MALT lymphoma development (11), the polyclonal lymphoid hyperplasia evolving further toward a monoclonal lymphoid population (36). The reasons for this evolution, which is accompanied by genetic abnormalities, remain to be elucidated (33, 37). MALT lymphoma induction and growth are probably antigen driven, and it has been shown that H. pylori could be the trigger (18,23,24,26). Moreover, there is a demonstrated causal association between H. pylori infection and MALT-type lymphoma development, because it is possible to cure this cancer by eradicating H. pylori, suggesting that bacterial virulence factors exist and are associated with the disease development. H. pylori is the cause of approximately 80% of MALT lymphomas (8,57).Among the factors that may be linked to the outcome of infection, bacterial virulence factors such as cytotoxins and the cag pathogenicity island (PAI) have been extensively ...

Colorectal cancer (CRC) is posing an increasingly important burden on the health care system, with western countries seeing a growing incidence of the disease. Except for germline DNA mutations which have been attributed to less than 5% of patients, little is known about the main causes of CRC. However, environment factors such as food, lifestyle and medication are now suspected to have a major influence on inducing cancers. Today, exhaustive quantitative and qualitative evaluation of all environmental factors is not possible. Various environment-induced diseases have been characterized based on colon microflora, also called microbiota, analyses. Growing data have shown specific changes in microflora (i.e. dysbiosis) in the stools of patients with colon cancer or those adherent to the colonic mucosa. Thus, it appears that microbiota may be considered a platform offering host and environment interactions for studying CRCs. The hypothesis that colon cancer might be a bacteria-related disease is suggested and perspectives are discussed.

H. pylori eradication rates were similar (approximately 80%) with all three regimens. Metronidazole resistance reduced efficacy; increasing the dose of metronidazole appeared not to overcome the problem or significantly improve the outcome. Treatment failure was generally associated with either prestudy or acquired metronidazole resistance. These findings are of importance when attempting H. pylori eradication in communities with high levels of metronidazole resistance.

SUMMARYAim: To compare the efficacy of different regimens in patients in whom previous Helicobacter pylori eradication therapy has failed. Methods: In this study named StratHegy patients (n ¼ 287) were randomized to receive one of three empirical triple therapy regimens or a strategy based on antibiotic susceptibility. The empirical regimens were omeprazole, 20 mg b.d., plus amoxicillin, 1000 mg b.d., and clarithromycin, 500 mg b.d., for 7 days (OAC 7 ), clarithromycin, 500 mg b.d., for 14 days (OAC 14 ) or metronidazole, 500 mg b.d., for 14 days (OAM 14 ). In the susceptibility-based strategy, patients with clarithromycin-susceptible strains received OAC 14 , whilst the others received OAM 14 . The 13 C-urea breath test was performed before randomization and 4-5 weeks after eradication therapy.Results: In the intention-to-treat analysis, the eradication rates for empirical therapies were as follows: OAC 7 , 47.4% (27/57); OAC 14 , 34.5% (20/58); OAM 14 , 63.2% (36/57); it was 74.3% (84/113) for the susceptibilitybased treatment (P < 0.01 when compared with OAC 7 and OAC 14 ). In patients receiving clarithromycin, the eradication rates were 80% for clarithromycin-susceptible strains and 16% for clarithromycin-resistant strains; in patients receiving OAM 14 , the eradication rates were 81% for metronidazole-susceptible strains and 59% for metronidazole-resistant strains. Conclusions: Eradication rates of approximately 75% can be achieved with second-line triple therapy based on antibiotic susceptibility testing. If susceptibility testing is not available, OAM 14 is an appropriate alternative.

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