Abstract
BackgroundRecent studies have reported associations of DNA repair pathway gene variants and risk of various cancers and precancerous lesions, such as chronic atrophic gastritis (CAG).MethodsA nested case-control study within the German population-based ESTHER cohort was conducted, including 533 CAG cases and 1054 controls. Polymorphisms in eleven DNA repair genes (APEX1, ERCC1, ERCC2/XPD, PARP1 and XRCC1), in CD3EAP/ASE-1 and PPP1R13L were analysed.ResultsNo association was disclosed for any of the analysed polymorphisms. Nor did stratified analyses according to ages < 65 and ≥ 65 years show any significant association with CAG risk.ConclusionsThe results of this large German case-control study do not reveal associations of DNA repair pathway polymorphisms and risk of CAG. On the basis of a large number of CAG cases, they do not support associations of DNA repair pathway SNPs with CAG risk, but suggest the need of larger studies to disclose or exclude potential weak associations, or of studies with full coverage of candidate genes.
Highlights
Recent studies have reported associations of DNA repair pathway gene variants and risk of various cancers and precancerous lesions, such as chronic atrophic gastritis (CAG)
Several changes have been identified as precursors to the intestinal type of gastric carcinoma, representing sequential steps in the precancerous process: non-atrophic gastritis, CAG, metaplasia and dysplasia [1]
Genotype distributions for controls were consistent with Hardy-Weinberg equilibrium (HWE), and the average call rate for the analysed single nucleotide polymorphisms (SNPs) was 97.5%
Summary
Recent studies have reported associations of DNA repair pathway gene variants and risk of various cancers and precancerous lesions, such as chronic atrophic gastritis (CAG). Chronic atrophic gastritis (CAG) is a well-established precursor lesion in the aetiology of intestinal gastric cancer (GC), the most common type of GC [1]. Several changes have been identified as precursors to the intestinal type of gastric carcinoma, representing sequential steps in the precancerous process: non-atrophic gastritis, CAG (gland loss), metaplasia and dysplasia [1]. This progression usually takes decades, providing excellent options for timely detection and intervention at precancerous stages [1,3]. Three molecular mechanisms, by which H. pylori may provoke a loss of genomic integrity and
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