p53 Codon 72 and 16-bp Duplication Polymorphisms of Gastric Cancer in Koreans.
- Author:
Jung Mi KIM
1
;
Oh Young LEE
;
Chun Geun LEE
;
Sung Joon KWON
;
Kyung Suk KIM
;
Won MOON
;
Dong Hee KOH
;
Hang Lak LEE
;
Byoeng Chul YOON
;
Ho Soon CHOI
;
Joon Soo HAHM
;
Min Ho LEE
;
Dong Hoo LEE
Author Information
1. Department of Internal Medicine, Hanyang University College of Medicine, Seoul, Korea. leeoy@hanyang.ac.kr
- Publication Type:Original Article ; English Abstract
- Keywords:
Gastric cancer;
p53;
Polymorphism
- MeSH:
Adult;
Aged;
Case-Control Studies;
Codon;
Data Interpretation, Statistical;
Female;
*Genes, p53;
Genetic Predisposition to Disease;
Genotype;
Heterozygote;
Homozygote;
Humans;
Korea;
Male;
Middle Aged;
*Polymorphism, Restriction Fragment Length;
Stomach Neoplasms/*genetics/pathology;
Tandem Repeat Sequences/*genetics
- From:The Korean Journal of Gastroenterology
2007;50(5):292-298
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
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.
