Is the Association Between <i>Helicobacter pylori</i> and Gastric Cancer Confined to CagA‐Positive Strains?

Held, Maria; Engstrand, Lars; Hansson, Lars‐Erik; Bergström, Reinhold; Wadström, Torkel; Nyrén, Olof

doi:10.1111/j.1083-4389.2004.00222.x

Cited by 29 publications

(19 citation statements)

References 32 publications

(58 reference statements)

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“…The titer of CagA antibody in patients with gastric cancer was higher than that in people without gastric cancer; similarly, the titer of CagA antibody in high-risk populations was significantly higher than that in low-risk populations (Zhang et al, 1998). Compared with CagA-negative H. pylori strains, CagA-positive strains dramatically increased the occurrence of severe gastritis and gastric adenocarcinoma (Tokieda et al, 1999;Enroth et al, 2000;Held et al, 2004;Nobuta et al, 2004). These studies indicate that CagA may play an important role in the development of gastric cancer.…”

Section: Introductionmentioning

confidence: 75%

Transformed immortalized gastric epithelial cells by virulence factor CagA of Helicobacter pylori through Erk mitogen-activated protein kinase pathway

et al. 2005

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Section: Introductionmentioning

confidence: 75%

Transformed immortalized gastric epithelial cells by virulence factor CagA of Helicobacter pylori through Erk mitogen-activated protein kinase pathway

et al. 2005

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“…Antibodies solely to the 116-kDa CagA antigen (not fulfilling the criteria for CagA seropositivity according to the manufacturer) were detected in 11 (5%) patients of the whole 215-patient study population, and 2 of them were known to have been previously infected with H. pylori. In studies assessing the impact of H. pylori infection on gastric cancer risk (6,5,10,29,35,41,48,50) or on the development of atrophic gastritis (1,4,7,24,36), the different definitions of the criteria for CagA positivity as a sign of a previous contact with H. pylori may give different risk estimations. In our study, among patients for whom it had been more than 5 years since successful H. pylori eradication, the positive EIA serology found only 18 (34%) of the 53 patients with verified past H. pylori infection, but the immunoblot detected 45 (85%) subjects, if CagA positivity according to the manufacturer's criteria were used, and even more, 47 (89%) subjects, if antibodies solely to CagA antigen had been considered; the specificities were 83% and 74%, respectively.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of a Commercial Immunoblot, Helicoblot 2.1, for Diagnosis of Helicobacter pylori Infection

Veijola

Oksanen

Sipponen

et al. 2008

Clin Vaccine Immunol

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The best method to diagnose Helicobacter pylori infection in different clinical situations is controversial. The aim of the study was to assess the performance of a commercial immunoblot, Helicoblot 2.1. The study comprised 215 patients, who were grouped according to the presence of H. pylori infection (assessed by two gastroscopies including histology with a median interval of 7.1 years, enzyme immunoassay [EIA]-based serology, and history of previous H. pylori infections and eradication therapies) into four categories: no H. pylori infection ever, previous infection, ongoing infection, and EIA seropositivity as the only marker of a possible previous infection. The sensitivity of Helicoblot 2.1 to show an ongoing or previous H. pylori infection was 100% and 92%, respectively. Helicoblot 2.1 was negative in only 80% of individuals with no evidence of present or previous infection but in 96% of patients 50 years of age or younger. The current infection marker of the immunoblot was positive in 49% of patients with successful H. pylori eradication therapy. After successful eradication therapy, Helicoblot 2.1 sustained positive results in 87% of patients, and CagA positivity was detected in 87% of patients with follow-up samples for more than 10 years after therapy. Helicoblot 2.1 is a sensitive and, among patients of ages 50 years or younger, a specific test in the primary diagnosis of H. pylori infection. However, it does not discriminate between past and current infections. It can be used in epidemiological studies assessing the role of H. pylori in different late sequelae.

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“…[15][16][17] Furthermore, a CagA-positive infection has been shown to be associated with a more intensive inflammation than a CagA-negative infection. 18,19 Thus it seems that an IgA response, perhaps via its association to CagA-positive H. pylori infection, could be regarded as an indicator of an increased risk of noncardia gastric cancer.…”

Section: Immunoglobulin Class Amentioning

confidence: 99%

Helicobacter pylori IgA and IgG antibodies, serum pepsinogen I and the risk of gastric cancer: Changes in the risk with extended follow‐up period

Knekt

Teppo

Aromaa

et al. 2006

Intl Journal of Cancer

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The prediction of Helicobacter pylori antibodies immunoglobulin A (IgA) and immunoglobulin G (IgG) and serum pepsinogen I (PG I) on gastric cancer occurrence was studied in a nested case-control study, based on 225 incident cancer cases and 435 matched controls from a Finnish cohort followed from 1966-1991. The odds ratio of noncardia gastric cancer between infected and noninfected persons was 3.12 (95% confidence interval (CI) 5 1.97-4.95) for elevated IgA and 2.88 (CI: 1.63-5.07) for elevated IgG antibodies. The odds ratio between low and high PG I was 2.24 (CI: 1.43-3.49). The strength of association was significant for IgA antibodies during the total follow-up, but for IgG antibodies this was only true for follow-up periods of 15 years or more. IgA antibodies were significantly associated with all registered histological subtypes apart from intestinal type adenocarcinoma. The highest gastric cancer risk was found among individuals with simultaneously elevated IgA and IgG antibodies and low PG I with an odds ratio of 10.9 (CI: 4.31-27.7) in comparison with those who were negative for both antibodies and had normal PG I. Elevated IgA and IgG antibodies and low PG I were not associated with cancers of the gastric cardia. The findings support the hypothesis that H. pylori infection is a cause of noncardia gastric cancer. Although elevated H. pylori IgA and IgG antibodies and low PG I independently could predict the occurrence of noncardia gastric cancer, their power to do so varied with the stage and length of the follow-up period and it increased when they were applied in combination. ' 2006 Wiley-Liss, Inc.Key words: gastric cancer; H. pylori; IgA antibodies; IgG antibodies; pepsinogen I Chronic infection with Helicobacter pylori leads to chronic gastritis, which may progress to atrophy, intestinal metaplasia and finally to noncardia gastric cancer. 1,2 This hypothesis is in line with results from prospective serologic studies that have shown higher incidence of noncardia gastric cancer in subjects with H. pylori infection, verified by specific IgG antibodies, than in noninfected ones. 3 Practically, all helicobacter-infected subjects have immunoglobulin G (IgG) antibodies, whereas immunoglobulin A (IgA) antibodies are found in approximately two-thirds of infected subjects. 4 Of infected individuals, 2-3% show an elevated IgA antibody level alone. 4 In a 13-year gastric cancer follow-up of the Finnish Mobile Clinic Health Examination cohort, we demonstrated an elevated risk of the disease in persons with H. pylori antibodies of the IgA class and in those with a low serum pepsinogen I (PG I) level. Unexpectedly, however, H. pylori antibodies of the IgG class were not significantly related to the risk of gastric cancer in this cohort characterized by high prevalence of helicobacter infection also in control subjects. 5 We have now conducted a new study for a follow-up period that has been extended up to 24 years within the same study population, to clarify whether the impact of high IgA and IgG antibodies and l...

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Is the Association Between Helicobacter pylori and Gastric Cancer Confined to CagA‐Positive Strains?

Abstract: Although patients with antibodies to CagA have the greatest risk of developing gastric cancer, those with CagA-negative infections run a significantly greater risk than uninfected persons.

Cited by 29 publications

References 32 publications

Transformed immortalized gastric epithelial cells by virulence factor CagA of Helicobacter pylori through Erk mitogen-activated protein kinase pathway

Transformed immortalized gastric epithelial cells by virulence factor CagA of Helicobacter pylori through Erk mitogen-activated protein kinase pathway

Evaluation of a Commercial Immunoblot, Helicoblot 2.1, for Diagnosis of Helicobacter pylori Infection

Helicobacter pylori IgA and IgG antibodies, serum pepsinogen I and the risk of gastric cancer: Changes in the risk with extended follow‐up period

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