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- Simán, Henrik, et al.
(author)
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Association between Helicobacter pylori and gastric carcinoma in the city of Malmo, Sweden. A prospective study
- 1997
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In: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 1502-7708 .- 0036-5521. ; 32:12, s. 1215-1221
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Journal article (peer-reviewed)abstract
- BACKGROUND: We have investigated the association between Helicobacter pylori and gastric carcinoma through a nested case-control study in a single city. METHODS: From a cohort of 32,906 residents recruited from 1974 through 1992, 56 cases of gastric adenocarcinoma and 224 matched controls were selected. The mean interval between serum collection and diagnosis was 5.7 years. Frozen serum or plasma samples were analysed for IgG antibodies against H. pylori with an enzyme-linked immunosorbent assay. RESULTS: The overall seropositivity prevalence in gastric cancer cases was 82%, compared with 49% in controls, giving an odds ratio (OR) of 5.0 (95% confidence interval (CI), 2.2-11.5). Partial gastrectomy because of peptic ulcer 5 to 36 year before diagnosis of gastric cancer could be a confounding factor. With exclusion of 10 such cases, H. pylori seropositivity among cases was 78%, as compared with 50% in matched controls (OR, 3.9; 95% CI, 1.7-9.2). Tumours of the cardia were not associated with H. pylori (OR, 0.92; 95% CI, 0.23-3.7), which is in contrast to tumours of the fundus, corpus, and antrum, which were significantly associated (OR, 11.1; 95% CI, 2.4-71.8). This difference in location was significant (P < 0.01). CONCLUSION: There is a significant association between prior infection with H. pylori and later development of gastric carcinoma, and the association is related to noncardia gastric cancer.
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| 2. |
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| 3. |
- Simán, Henrik, et al.
(author)
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Helicobacter pylori and CagA seropositivity and its association with gastric and oesophageal carcinoma.
- 2007
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In: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 1502-7708 .- 0036-5521. ; 42:8, s. 933-940
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Journal article (peer-reviewed)abstract
- Objective. Helicobacter pylori infection is an established risk factor for non-cardia gastric adenocarcinoma. Infection with H. pylori strains harbouring the cagA pathology island may augment this association. H. pylori infection may at the same time reduce the risk for oesophageal carcinoma. However, prospective data on the association between CagA seropositivity and gastric or oesophageal carcinomas are limited. The purpose of this study was to investigate whether CagA seropositivity among H. pylori seropositive subjects is associated with gastric or oesophageal carcinomas. Material and methods. A nested case-control study was performed in the Malmo Preventive Medicine cohort consisting of 32,906 middle-aged subjects. Tumour cases were identified by the Swedish National Cancer Registry. The Western blot method Helicoblot 2.1 was used to detect H. pylori and CagA seropositivity. Results. Non-cardia gastric adenocarcinoma was associated with H. pylori seropositivity, odds ratio 17.8 (95% CI: 4.2 - 74.8; 67 cases). The odds ratio for CagA seropositivity among H. pylori seropositive subjects was 9.7 ( 95% CI: 1.5 - infinity). No significant associations were found between cardia gastric adenocarcinoma and H. pylori or CagA seropositivity among H. pylori seropositive subjects; odds ratios were 1.5 ( 95% CI: 0.51 - 4.8) and 2.7 ( 95% CI: 0.38 - infinity), respectively ( 24 cases). Oesophageal adenocarcinoma and oesophageal squamous cell carcinoma were not significantly associated with H. pylori seropositivity or with CagA seropositivity among H. pylori seropositive subjects; the odds ratios associated with oesophageal adenocarcinoma were 0.46 ( 95% CI: 0.07 - 2.6) and 0.38 ( 95% CI: 0.02 - 24), respectively. Corresponding odds ratios for oesophageal squamous cell carcinoma were 0.44 ( 95% CI: 0.15 - 1.2; 37 cases) and 2.0 ( 95% CI: 0.24 - infinity), respectively. Conclusions. CagA seropositivity among H. pylori seropositive subjects is a risk factor for non-cardia gastric adenocarcinoma.
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| 4. |
- Simán, Henrik, et al.
(author)
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Helicobacter pylori infection is associated with a decreased risk of developing oesophageal neoplasms
- 2001
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In: Helicobacter. - : Wiley. - 1083-4389 .- 1523-5378. ; 6:4, s. 310-316
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Journal article (peer-reviewed)abstract
- Background. The role of Helicobacter pylori infection in the development of oesophageal malignancies was investigated through a multivariate conditional logistic regression analysis in a nested case-control study. Methods. Blood samples and a questionnaire on smoking and alcohol habits were collected from a cohort of 32,906 city residents during a health-screening programme between 1974 and 1992. Forty-four cases of oesophageal cancer and 149 matched controls were selected. The mean interval between screening and cancer diagnosis was 11.9 years. H. pylori seropositivity was determined by an enzyme-linked immunosorbant assay measuring IgG. Occupation was included in the statistical analysis as an indicator of socio-economic status. Results. Helicobacter pylori seropositivity was present in 10 of the cases (22.7%) and 67 of the controls (45.0%). In a multivariate model, vith adjustment for occupation, tobacco and alcohol consumption, the odds ratio for developing in oesophageal malignancy when infected with H. pylori was 0.29 (95% confidence interval (CI): 0.12-0.67). Current smokers had an odds ratio of 17.3 (95% Cl: 3.0-99.4) and the odds ratio for ex-smokers was 5.9 (95% CI: 1.15-29.9). High alcohol consumption was no longer significantly, associated with oesophageal neoplasms after tobacco smoking was included into the model, odds ratio 1.22 (95% CI: 0.46-3.2). The protective effect of H. pylori was more pronounced for oesophageal adenocarcinoma (seven cases, odds ratio 0.16, 95% Cl: 0.00-1.06) than for squamous-cell carcinoma (29 cases, odds ratio 0.41, 95% Cl: 0.14-1.2). Conclusions. Helicobacter pylori infection is associated with a decreased risk of developing an oesophageal malignancy. Current smokers and ex-smokers have instead a definite increased risk of oesophageal neoplasms.
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| 5. |
- Simán, Henrik, et al.
(author)
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Tobacco smoking increases the risk for gastric adenocarcinoma among Helicobacter pylori-infected individuals
- 2001
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In: Scandinavian Journal of Gastroenterology. - 1502-7708. ; 36:2, s. 208-213
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Journal article (peer-reviewed)abstract
- BACKGROUND: The importance of tobacco smoking and Helicobacter pylori infection as risk factors in the development of gastric carcinoma was investigated through multivariate conditional logistic regression analysis in a nested case-control study. METHODS: Blood samples and a questionnaire on smoking habits were collected from a cohort of 32,906 city residents during a health screening programme from 1974 to 1992. Fifty-six cases of gastric cancer and 224 matched controls were selected. The mean interval between screening and cancer diagnosis was 5.7 years. H. pylori infection was determined by IgG-serology. Occupation categorized into blue-collar workers, white-collar workers, self-employed and unknown occupation was included in the statistical analysis as an indicator of socio-economic status. RESULTS: The proportion of current smokers was 61% among gastric cancer cases, versus 41% among controls. H. pylori seropositivity was present in 82% of the cases and 49% of the controls. In a multivariate model current smokers had an odds ratio (OR) of 2.2 (95% confidence interval (CI): 1.2-4.2). With different levels of tobacco consumption, smoking less than 20 g tobacco each day gave the OR of 2.1 (95% CI: 0.98-4.4), and the OR when smoking more than 20 g tobacco per day was 2.5 (95% CI: 1.1-5.6). The OR of H. pylori infection was 5.0 (95% CI: 2.2-11.2). Among H. pylori-seropositive citizens, current smoking was associated with an increased risk of 2.3 (95% CI: 1.1-4.7) compared with non-smoking H. pylori-positive persons. CONCLUSIONS: Tobacco smoking and H. pylori are both risk factors in the development of gastric cancer, and tobacco smoking is still a risk factor among H. pylori-infected individuals. The risk of gastric cancer among H. pylori-infected current smokers is 11 times that of non-infected individuals not currently smoking.
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| 7. |
- Agudo, Antonio, et al.
(author)
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Polymorphisms in metabolic genes related to tobacco smoke and the risk of gastric cancer in the European prospective investigation into cancer and nutrition
- 2006
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In: Cancer Epidemiology Biomarkers & Prevention. - 1538-7755. ; 15:12, s. 2427-2434
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Journal article (peer-reviewed)abstract
- Metabolizing enzymes, which often display genetic polymorphisms, are involved in the activation of compounds present in tobacco smoke that may be relevant to gastric carcinogenesis. We report the results of a study looking at the association between risk of gastric adenocarcinoma and polymorphisms in genes CYP1A1, CYP1A2, EPHX1, and GSTT1. A nested case-control study was carried out within the European Prospective Investigation into Cancer and Nutrition, developed in 10 European countries. The study includes 243 newly diagnosed cases of histologically confirmed gastric adenocarcinoma and 946 controls matched by center, age, sex, and date of blood collection. Genotypes were determined in nuclear DNA from WBCs. We found an increased risk of gastric cancer for homozygotes for C (histidine) variant in Y113H of EPHX1 (odds ratio, 1.91; 95% confidence interval, 1.19-3.07) compared with subjects with TC/TT. There was also a significant increased risk for smokers carrying at least one variant allele A in Ex7+129C > A (m4) of CYP1A1 and never smokers with null GSTT1 and allele A in the locus -3859G > A of CYP1A2. Most of these genes are involved in the activation and detoxification of polycyclic aromatic hydrocarbons, suggesting a potential role of these compounds in gastric carcinogenesis.
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| 9. |
- Capella, Gabriel, et al.
(author)
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DNA repair polymorphisms and the risk of stomach adenocarcinoma and severe chronic gastritis in the EPIC-EURGAST study
- 2008
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In: International Journal of Epidemiology. - : Oxford University Press (OUP). - 1464-3685 .- 0300-5771. ; 37:6, s. 1316-1325
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Journal article (peer-reviewed)abstract
- Background The contribution of genetic variation in DNA repair genes to gastric cancer (GC) risk remains essentially unknown. The aim of this study was to explore the relative contribution of DNA repair gene polymorphisms to GC risk and severe chronic atrophic gastritis (SCAG). Method A nested case control study within the EPIC cohort was performed including 246 gastric adenocarcinomas and 1175 matched controls. Controls with SCAG (n 91), as defined by low pepsinogen A (PGA) levels, and controls with no SCAG (n 1061) were also compared. Twelve polymorphisms at DNA repair genes (MSH2, MLH1, XRCC1, OGG1 and ERCC2) and TP53 gene were analysed. Antibodies against Helicobacter pylori were measured. Results No association was observed for any of these polymorphisms with stomach cancer risk. However, ERCC2 K751Q polymorphism was associated with an increased risk for non-cardial neoplasm [odds ratio (OR) 1.78; 95 confidence interval (CI) 1.023.12], being ERCC2 K751Q and D312N polymorphisms associated with the diffuse type. ERCC2 D312N (OR 2.0; 95 CI 1.093.65) and K751Q alleles (OR 1.82; 95 CI 1.013.30) and XRCC1 R399Q (OR 1.69; 95 CI 1.022.79) allele were associated with an increased risk for SCAG. Conclusion Our study supports a role of ERCC2 in non-cardial GC but not in cardial cancer. A concordant result was observed for subjects with low PGA levels. XRCC1 allele was associated also with SCAG. This is the first prospective study suggesting that individual variation in DNA repair may be relevant for gastric carcinogenesis, a finding that will require further confirmation validation in larger independent studies.
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