Helicobacter pylori Infection and Gastric Lymphoma

Parsonnet, Julie; Hansen, Svein; Rodriguez, Larissa; Gelb, Arnold B.; Warnke, Roger A.; Jellum, Egil; Orentreich, Norman; Vogelman, Joseph H.; Friedman, Gary D.

doi:10.1056/nejm199405053301803

Cited by 1,993 publications

(1,390 citation statements)

References 23 publications

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“…Our finding that all gastric cancer cases had evidence of H. pylori infection is different from other published studies, where the proportion tends to be lower. For example, the studies by Parsonnet et al 36 and Nomura et al 37 reported seroprevalence rates of 84% and 94%, respectively. The difference between our study and others may reflect the fact that all our cases had the earlier presentation or diagnosis of cancer in this closely screened population compared to the West, where patients tend to present with advanced and metastatic disease.…”

Section: Discussionmentioning

confidence: 99%

Association between serum pepsinogens and polymorphismof PTPN11 encoding SHP‐2 among Helicobacter pylori seropositive Japanese

Goto

Ando

Yamamoto

et al. 2005

Intl Journal of Cancer

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Helicobacter pylori (H. pylori) plays a crucial role in the development of gastric atrophy and cancer, and cagA‐positive strains, which are universal in Japan, increase the risk of these outcomes substantially. The CagA protein is injected from attached H. pylori into gastric epithelial cells and undergoes Src‐dependent tyrosine phosphorylation and activation of the eukaryotic phosphatase SHP‐2. The CagA/SHP‐2 interactions elicit cellular changes that increase the risk of carcinogenesis. We investigated the association of a frequent single nucleotide polymorphism (SNP; JST057927; G‐to‐A) in the PTPN11 gene that encodes SHP‐2 with gastric atrophy and gastric cancer in Japan. Gastric atrophy was assessed by measuring serum pepsinogen I and II levels. The subjects comprised 454 healthy controls (126 males; mean age, 58.4) and 202 gastric cancer cases (134 males and 68 females; mean age, 66.7). All gastric cancer cases and 250 (55%) controls were H. pylori seropositive; 179 (89%) of the gastric cancer cases had gastric atrophy compared to 137 (55%) of the H. pylori seropositive controls (p < 0.001). Among HP seropositive controls compared to the common PTPN11 G/G genotype, the odds ratio of atrophy was nonsignificantly reduced with the G/A genotype (0.70; 95% CI = 0.39–1.25) and significantly reduced with the A/A genotype (0.09; 95% CI = 0.01–0.72). Lower risk for gastric atrophy had a gene‐dose association with the A allele (p = 0.01, trend test). There was a clear deficiency of the A/A genotype in those with atrophy compared to those without (1 subject in the gastric atrophy group vs. 8 in the group without). Cancer cases differed from controls in frequencies of PTPN11 G/A genotype only because of a higher prevalence of atrophy among the cancer cases. The G/A SNP in the PTPN11 gene appears to be a risk factor for gastric atrophy in subjects infected with cagA‐positive H. pylori. This may explain why only a proportion of CagA‐positive individuals develop gastric atrophy and gastric cancer, even though infection with cagA strains is universal in Asian countries such as Japan. The functional consequences of the G/A polymorphism remain to be elucidated. © 2005 Wiley‐Liss, Inc.

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Section: Discussionmentioning

confidence: 99%

Association between serum pepsinogens and polymorphismof PTPN11 encoding SHP‐2 among Helicobacter pylori seropositive Japanese

Goto

Ando

Yamamoto

et al. 2005

Intl Journal of Cancer

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“…Evidence from epidemiological studies suggests a relative risk for subsequent development of gastric carcinoma of 3-6 in H. pyloriinfected persons (Nomura et al, 1991;Parsonnet et al, 1991;Eurogast Study Group, 1993). The impracticability of preventive treatment of all H. pylori-infected individuals implies an urgent need to identify patients who are at increased risk for the development of gastric carcinoma.…”

Section: Discussionmentioning

confidence: 99%

“…pylori-infected subjects have an increased risk of gastric cancer (Nomura et al, 1991;Parsonnet et al, 1991;Eurogast Study Group, 1993). However, only a few of them will actually develop gastric carcinoma later in life.…”

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confidence: 99%

Severe expression of corpus gastritis is characteristic in gastric cancer patients infected with Helicobacter pylori

Miehlke

Hackelsberger²,

Meining³

et al. 1998

Br J Cancer

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Summary In 50 Helicobacterpylori-infected gastric carcinoma patients the corpus gastritis was significantly higher than in matched H. pyloripositive control subjects (P < 0.01). Atrophy and intestinal metaplasia (IM) occurred significantly more often in the antrum of carcinoma patients (P < 0.01). The odds ratio for gastric carcinoma was 8.85 for high-grade corpus gastritis and 8.04 when atrophy in the antrum was present.

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“…This organism is a human gastric pathogen associated with peptic ulcer disease and gastritis (Blaser, 1987;Dick, 1990), which may predispose to gastric cancer (Nomura et al, 1991;Parsonnet et al, 1991). Several factors associated with pathogenesis have been identified, including urease (Cussac et al, 1992), flagellins (Leying et al, 1992;Haas et al, 1993;Suerbaum et al, 1993), the vacuolating toxin VacA (Cover et al, 1994;Telford et al, 1994), and the cytotoxin-associated protein CagA (Covacci et al, 1993;Tummuru et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

Transcriptional analysis of the divergent cagAB genes encoded by the pathogenicity island of Helicobacter pylori

Spohn

Beier

Rappuoli

et al. 1997

Molecular Microbiology

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SummaryHelicobacter pylori strains isolated from most patients with peptic ulcer disease and adenocarcinoma express the vacuolating toxin VacA and contain a pathogenicity island named cag. The cag pathogenicity island codes for more than 40 putative proteins with features similar to bacterial secretion systems. One of these proteins, CagA, is an immunodominant antigen with unknown function encoded by the cagA gene. In the present study, we have analysed the functional promoter elements of the H. pylori cagA gene as well as of the divergently transcribed cagB gene. Primer extension analyses identified a single 5Ј end of the cagA mRNA, while two initiation sites were mapped in the case of the cagB mRNA. The promoters deduced upstream of these start points of transcription contained conserved ¹10 regions but no ¹35 regions with respect to the Escherichia coli 70 consensus sequence. Nevertheless, they could be activated in E. coli and in vitro by purified E. coli RNA polymerase. Deletion analyses indicated that the cagA and cagB genes are transcribed by overlapping promoters and that full activation requires sequences up to ¹70 and ¹96 respectively. Instead, basal transcription is likely to be mediated by ¹10 extended promoter-like sequences. RNA polymerase is able to bind the ¹40 to ¹60 region of the cagA promoter, and its binding is mediated by the ␣-subunit. This region resembles the UP elements of prokaryotic promoters in location, sequence and mechanism of interaction with the RNA polymerase. We discuss the features of these promoters and propose that they could represent a class of minimum promoters, which ensures a basic level of transcription, while full activation requires regulatory elements or a defined promoter context.

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Helicobacter pylori Infection and Gastric Lymphoma

Abstract: Non-Hodgkin's lymphoma affecting the stomach, but not other sites, is associated with previous H. pylori infection. A causative role for the organism is plausible, but remains unproved.

Cited by 1,993 publications

References 23 publications

Association between serum pepsinogens and polymorphismof PTPN11 encoding SHP‐2 among Helicobacter pylori seropositive Japanese

Association between serum pepsinogens and polymorphismof PTPN11 encoding SHP‐2 among Helicobacter pylori seropositive Japanese

Severe expression of corpus gastritis is characteristic in gastric cancer patients infected with Helicobacter pylori

Transcriptional analysis of the divergent cagAB genes encoded by the pathogenicity island of Helicobacter pylori

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