DNMT3b Promoter Polymorphism and Risk of Gastric Cancer in the Korean Population.
- Author:
Sung Geun KIM
1
;
Hun JUNG
;
Sin Sun KIM
;
Kyung Hwa JEON
;
Kyo Young SONG
;
Jin Jo KIM
;
Hyung Min JIN
;
Wook KIM
;
Cho Hyun PARK
;
Seung Man PARK
;
Keun Woo LIM
;
Seung Nam KIM
;
Hae Myung JEON
Author Information
- Publication Type:Original Article
- Keywords: Gastric cancer; DNMT3b; Methylation; Gene polymorphism; Cancer risk suscotability
- MeSH: Alleles; Carcinogenesis; Case-Control Studies; DNA; DNA Methylation; Epigenomics; Genes, Tumor Suppressor; Genotype; Helicobacter Infections; Heterozygote; Homozygote; Humans; Methylation; Polymerase Chain Reaction; Polymorphism, Restriction Fragment Length; Stomach Neoplasms*
- From:Journal of the Korean Gastric Cancer Association 2007;7(1):9-15
- CountryRepublic of Korea
- Language:Korean
- Abstract: PURPOSE: DNA methylation is an important epigenetic factor in tumorigenesis. We hypothesized that polymorphism of the promoter of the DNA methyltransferase 3b (DNMT3b) genes, which are responsible for regulating the methylation status of tumor suppressor genes, are associated with increased risk of gastric cancer. MATERIALS AND METHODS: In this hospital-based case-control study, to determine the role of this polymorphism of the promoter of DNA methyltransferase 3b (DNMT3b) genes in gastric cancer, we genotyped 176 cases and 70 control subjects. To determine the genotype, we used a polymerase chain reaction restriction fragment length polymorphism assay. We compared alleles and genotypes between the two groups and revealed an association of DNMT3b promoter polymorphism with increased risk of gastric cancer in the Korean population. RESULTS: Genotype frequencies were 14.8% (Cytosine-Cytosine), 71.6% (Cytosine-Thymine), and 13.6% (Thymine- Thymine) in the case patients and 40.0% (Cytosine-Cytosine), 42.9% (Cytosine-Thymine), and 17.1% (Thymine-Thymine) in the control subjects, respectively. Compared with CC homozygotes, CT heterozygotes had a 4.523-fold increased risk (OR, 2.13; 95% CI, 2.324~8.803), and the TT homozygotes had a 2.154-fold elevated risk (OR, 1.42; 95% CI, 0.899~5.165). For the T variant genotype (CT+TT), there was a 3.846-fold increased risk (OR, 1.88; 95% CI, 2.040~7.251). However, no significance was observed in the genotype distributions of both polymorphisms according to histopathology, stage of stomach cancer. The Ssame results were observed with Helicobacter infection. CONCLUSION: DNMT3b promoter polymorphism, especially the T variant genotype, is associated significantly with thean increased risk of gastric cancer.
