Open Access Research article

Lack of association between gene polymorphisms of Angiotensin converting enzyme, Nod-like receptor 1, Toll-like receptor 4, FAS/FASL and the presence of Helicobacter pylori-induced premalignant gastric lesions and gastric cancer in Caucasians

Juozas Kupcinskas1, Thomas Wex2*, Jan Bornschein2, Michael Selgrad2, Marcis Leja3, Elona Juozaityte4, Gediminas Kiudelis1, Laimas Jonaitis1 and Peter Malfertheiner2

Author Affiliations

1 Department of Gastroenterology, Lithuanian University of Health Sciences, Eiveniu 2, 50009 Kaunas, Lithuania

2 Clinic of Gastroenterology, Hepatology and Infectious Diseases, Otto von Guericke University, Leipziger Str. 44, 39120 Magdeburg, Germany

3 Faculty of Medicine, University of Latvia, Digestive Diseases Center, Hospital Lizeners, 6 Linezera iela, LV1006 Riga, Latvia

4 Department of Oncology, Lithuanian University of Health Sciences, Eiveniu 2, 50009 Kaunas, Lithuania

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BMC Medical Genetics 2011, 12:112  doi:10.1186/1471-2350-12-112

Published: 24 August 2011



Several polymorphisms of genes involved in the immunological recognition of Helicobacter pylori and regulating apoptosis and proliferation have been linked to gastric carcinogenesis, however reported data are partially conflicting. The aim of our study was to evaluate potential associations between the presence of gastric cancer (GC) and high risk atrophic gastritis (HRAG) and polymorphisms of genes encoding Angiotensin converting enzyme (ACE), Nod-like receptor 1 (NOD1), Toll-like receptor 4 (TLR4) and FAS/FASL.


Gene polymorphisms were analyzed in 574 subjects (GC: n = 114; HRAG: n = 222, controls: n = 238) of Caucasian origin. ACE I/D (rs4646994), NOD1 796G>A (rs5743336), TLR4 3725G>C (rs11536889), FAS 1377G>A (rs2234767), FAS 670A>G (rs1800682) and FASL 844T>C (rs763110) were genotyped by different PCR approaches and restriction fragment length polymorphism analysis.


Frequencies of genotypes in our study are similar to the data reported on subjects of Caucasian ethnicity. There was a tendency for NOD1 796G/G genotype to be associated with increased risk of HRAG (62.4% vs. 54.5% in controls, p = 0.082). FAS 670G/G genotype was more frequent in HRAG when compared to controls, 23.9% and 17.2% respectively, however it failed to reach significance level (p = 0.077). We did not find any significant associations for all polymorphisms in relation to GC or HRAG. NOD1 796G>A and TLR4 3725G>C gene polymorphisms were also not associated with Helicobacter pylori infection.


ACE, NOD1, TRL4 and FAS/FASL gene polymorphisms are not linked with gastric carcinogenesis in Caucasians, and therefore they should not be considered as potential biomarkers for identifying individuals with higher risk for GC.