[p53 Codon 72 and 16-bp duplication polymorphisms of gastric cancer in Koreans].

BACKGROUND/AIMS: p53 gene plays an important role in cell cycle control in response to DNA damage which may increase the probability of mutations leading to carcinogenesis. The role of p53 gene polymorphisms [codon 72 (exon 4) and 16-bp duplication (intron 3)] as potential markers indicating cancer risk remains inconclusive, and the data on gastric cancer are very limited. The aim of this study was to assess the role of p53 gene polymorphisms in the risk of gastric cancer and in the determination of genetic susceptibility to gastric cancer in Koreans. METHODS: We analysed p53 genotypes using a polymerase chain reaction-based restriction fragment length polymorphism assay in a population-based case-control study in 120 gastric cancer patients and 145 cancer-free controls in Koreans. RESULTS: There was no specific genotype of p53 gene polymorphism in the gastric cancer patients compared to cancer-free controls. In p53 codon 72 and 16-bp duplication polymorphisms, the frequency and distribution of genotypes showed no statistical significance (p=0.7125 and p=0.1659). There was no difference in genotype by histologic subtypes, location of lesion, and age. However, the genotypic distribution in the patient subgroups with a history of heavy cigarette smoking of p53 16-bp duplication polymorphism were significantly different from those of cancer-free controls (p=0.0079). CONCLUSIONS: The p53 codon 72 and 16-bp duplication polymorphisms were not associated with the increased risk of gastric cancer and did not seem to contribute to gastric cancer susceptibility among Koreans. It is possible that p53 16-bp duplication polymorphism modulates the risk of smoking-induced gastric cancer development in Koreans. In order to clarify the associations between specific genotypes and gastric cancer risk, the evaluations of these polymorphisms in other ethnic backgrounds with larger number of patients would be needed.

[Association between insulin, insulin resistance, and gallstone disease in Korean general population].

BACKGROUND/AIMS: Diabetes is one of the risk factors of gallstone diseases. Many studies found a positive association between insulin and gallstones in individuals with diabetes. However, this association is unclear in non-diabetes. So we conducted a case-control study for the evaluation of the association between gallstone diseases and fasting serum insulin level, insulin resistance in non-diabetic Korean general population. METHODS: This study was a prospective case-control study on 118 Korean subjects which included clinical examination, abdominal ultrasound, and blood chemistries. Serum fasting insulin level were determined by radioimmunoassay and concentrations of cholesterol, glucose, and triglycerides by standard enzymatic colorimetric methods. Insulin resistance was determined by the homeostasis model assessment (HOMA-IR). Body mass index (BMI), percentage of body fat, and waist hip ratio were also measured. RESULTS: We studied 118 subjects with no clinical evidence of diabetes mellitus and serum glucose <126 mg/dL. Compared with controls (n=89), cases (n=29) had higher levels of serum insulin, glucose, triglyceride levels, and BMI. In t-test and chi-square test for variables, the association between gallstone disease and serum insulin, HOMA-IR index, and BMI were statistically significant (p<0.05). In multiple logistic regression analysis, gallstone disease risk increased with the level of serum insulin (p=0.024, odds ratio=1.376) and HOMA-IR index (p=0.013, odds ratio=2.006). CONCLUSIONS: We suggest that hyperinsulinemia and insulin resistance could be associated with gallstone formation in individuals without clinical diagnosis of diabetes mellitus and with normal serum glucose level.