Serum Pepsinogen Levels,<i>Helicobacter pylori</i>CagA Status, and Cytokine Gene Polymorphisms Associated with Gastric Premalignant Lesions in Costa Rica

Con, Sergio A.; Con-Wong, Reinaldo; Con-Chin, Gil R.; Con-Chin, Vicky G.; Takeuchi, Hiroaki; Valerín, Ana L.; Echandi, Guillermo; Mena, Fernando; Brenes, Fernando; Yasuda, Nobufumi; Araki, Keijiro; Sugiura, Tetsuro

doi:10.1158/1055-9965.epi-07-0215

Cited by 24 publications

(23 citation statements)

References 42 publications

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“…In particular, IL-1β is important in initiating and amplifying the inflammatory response to H pylori infection, resulting in severe inflammation possibly leading to atrophic and metaplastic changes in the gastric mucosa. An association between cytokine polymorphisms in IL-1β and IL-1RN, and gastric premalignant lesions was previously reported in a Costa Rican population [33] , while carriers of IL-1β+3954_T/C and IL-1RN*2/L had an increased risk for developing gastric cancer in another Costa Rican study [34] . Likewise, our results showed that the prevalence of the proinflammatory genotypes IL-1β+3954_T/C and IL-1RN*2/L was significantly higher in gastric cancer cases than in non-cancer cases, supporting the association of polymorphisms within IL-1β and IL-1RN and gastric cancer in the Costa Rican population.…”

Section: Discussionmentioning

confidence: 55%

Role of bacterial and genetic factors in gastric cancer in Costa Rica

Con¹,

Takeuchi²,

Con-Chin³

et al. 2009

WJG

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AIM:To evaluate several risk factors for gastric cancer (GC) in Costa Rican regions with contrasting GC incidence rate (GCIR). METHODS:According to GCIR, 191 Helicobacter pylori (H pylori )-positive patients were classified into groups A (high GCIR, n = 101) and B (low GCIR, n = 90). Human DNA obtained from biopsy specimens was used in the determination of polymorphisms of the genes coding for interleukin (IL)-1β and IL-10 by PCR-RFLP, and IL-1RN by PCR. H pylori DNA extractions obtained from clinical isolates of 83 patients were used for PCR-based genotyping of H pylori cagA , vacA and babA2 . Human DNA from gastric biopsies of 52 GC patients was utilized for comparative purposes. RESULTS:Cytokine polymorphisms showed no association with GCIR variability. However, gastric atrophy, intestinal metaplasia and strains with different vacA genotypes in the same stomach (mixed strain infection) were more frequently found in group A than in group B, and cagA and vacA s1b were significantly associated with high GCIR (P = 0.026 and 0.041, respectively). IL-1β+3954_T/C (OR 2.1, 1.0-4.3), IL-1RN*2/L (OR 3.5, 1.7-7.3) and IL-10-592_C/A (OR 3.2, 1.5-6.8) were individually associated with GC, and a combination of these cytokine polymorphisms with H pylori vacA s1b and m1 further increased the risk (OR 7.2,. C O N C L U S I O N :A l t h o u g h a p r o i n f l a m m a t o r y cytokine genetic profile showed an increased risk for developing GC, the characteristics of H pylori infection, in particular the status of cagA and vacA genotype distribution seemed to play a major role in GCIR variability in Costa Rica.

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Section: Discussionmentioning

confidence: 55%

Role of bacterial and genetic factors in gastric cancer in Costa Rica

Con¹,

Takeuchi²,

Con-Chin³

et al. 2009

WJG

Self Cite

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“…After excluding 59 articles, we were left with a total of fifteen studies (21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35). From each study, we extracted information on publication year, country, race/ethnicity, description of sampling procedures including selection criteria, sample size, prevalence of H. pylori infection, outcome studied, reference group, criteria for histologic classification, polymorphisms studied, genotyping method, and respective quality control.…”

Section: Systematic Review and Meta-analysismentioning

confidence: 99%

Association Between Cytokine Gene Polymorphisms and Gastric Precancerous Lesions: Systematic Review and Meta-analysis

Peleteiro

Lunet²,

Carrilho³

et al. 2010

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Polymorphisms within interleukin-1 (IL1) and tumor necrosis factor α (TNFA) gene clusters are associated with an increased risk of gastric cancer. However, their role in gastric precancerous lesions remains poorly understood. Our objective was to perform a meta-analysis of studies addressing the association between IL1B-511, IL1RN variable number of tandem repeat, and TNFA-308 gene polymorphisms and gastric precancerous lesions, including original data from Portugal and Mozambique. Published studies on the association between these cytokine gene polymorphisms and gastric precancerous lesions were identified by systematic review, and estimates of the association were combined using random-effects meta-analysis taking into account new data obtained from Portuguese volunteer shipyard workers (n = 215) and Mozambican dyspeptic patients (n = 96) who underwent endoscopic and pathologic evaluation following the same protocol. Odds ratio (OR) estimates for intestinal metaplasia were 2.83 [95% confidence interval (95% CI), 1.15-6.96] for the IL1RN*22 genotype, 1.86 (95% CI, 1.03-3.36) for IL1B-511 T carriers, and 0.59 (95% CI, 0.12-3.04) for the TNFA-308*AA genotype in the Portuguese sample. All Mozambican subjects with intestinal metaplasia were T carriers for IL1B-511 and none had the 2 allele for IL1RN. In meta-analysis, IL1RN*22 genotype was associated with an increased risk of gastric precancerous lesions (22 The IL1RN*22 genotype seems to consistently increase the risk of gastric precancerous lesions, supporting a role for this polymorphism in the early stages of gastric carcinogenesis.

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“…Nonetheless, those patients who had undergone surgery for gastric malignancy would have exhibited precancerous lesions such as atrophic gastritis and IM, and the possibility of Elroy Patrick Weledji anastomotic recurrence is higher than for the patients who had undergone benign gastric surgery (38,49,52). At present, there are no other recognized good markers of gastric dysplasia or cancer and residual premalignant (type III) IM may be the only marker for anastomotic recurrence of gastric cancer (38,(53)(54)(55). Micro RNAs are currently being evaluated as a specific diagnostic and prognostic marker (55).…”

Section: Gastric Remnantmentioning

confidence: 99%

“…A 100% infection results in 6-fold increase in incidence of gastric cancer (14,37). The H. pylori that carry the Cag A gene product cytotoxin associated vacuolating antigen A (Vac A) also causes gastric B-cell mucosa-associated lymphoid tissue (MALT) lymphoma (38). Despite the fact that the stomach does not normally have any lymphoid tissue like the terminal ileal Peyer's patches from which lymphoid malignancy could arise, recent studies have demonstrated that up to 90% of the gastric MALT type lymphoma were associated with H. pylori infection.…”

Section: Helicobacter Pylorimentioning

confidence: 99%

“…Gastric polyps may be associated with familial adenomatous polyposis (FAP) but they are more commonly sporadic. Malignant change may occur in 40% of those neoplastic adenomas greater than 2 cm (61) The gastroduodenal polyps associated with FAP have an increased risk of malignant transformation to duodenal and periampullary carcinoma (61,62) Gastric epithelial dysplasia Dysplasia may occur in an epithelium which shows intestinal metaplasia and may be flat, depressed or polypoid (38,62). The natural history (mild/ moderate/ severe dysplasia is not a relentless march to carcinoma.…”

Section: Gastric Polypsmentioning

confidence: 99%

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The Pathogenesis of Gastric Carcinoma

Weledji¹

2018

SGO

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Gastric cancer is one of the leading causes of cancer mortality in the world. Gastric adenocarcinomas account for more than 95% of gastric tumours, and these epithelial tumours result from the accumulation of multiple genetic defects which leads to uncontrolled growth. The most plausible pathway for gastric carcinoma indicates that the underlying mechanisms may be different for the diffuse and intestinal types of tumour. The distinct subtypes -proximal, diffuse and distal gastric cancer that are different from a histological and epidemiological standpoint, can also distinguished by gene expression data. The disease classification of the epithelial tumours may lead to different treatment paradigms for individual gastric cancer subtypes. The changes present can be classified as consisting of abnormalities in DNA content, the karyotype (including allele loss), oncogene and tumour suppressant gene expression (or deletion), cell cycle regulation and DNA repair genes. This article reviewed the biological/ molecular differences of the gastric carcinoma subtypes, the risk factors and precursors of gastric carcinoma and the implications on early diagnosis and response to adjuvant treatment. Despite the heterogeneity of multiple somatic alterations in the neoplastic lesion, the implication of a molecular classification is its exploitation to identify prognostic and predictive biomarkers and to identify targets for therapy.

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Serum Pepsinogen Levels,Helicobacter pyloriCagA Status, and Cytokine Gene Polymorphisms Associated with Gastric Premalignant Lesions in Costa Rica

Cited by 24 publications

References 42 publications

Role of bacterial and genetic factors in gastric cancer in Costa Rica

Role of bacterial and genetic factors in gastric cancer in Costa Rica

Association Between Cytokine Gene Polymorphisms and Gastric Precancerous Lesions: Systematic Review and Meta-analysis

The Pathogenesis of Gastric Carcinoma

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