Article

P53 codon 72 polymorphism and the risk of lung cancer in a Korean population

Department of Preventive Medicine, Chonnam National University Medical School, Gwangju 501-746, South Korea.
Lung cancer (Amsterdam, Netherlands) (Impact Factor: 3.96). 02/2011; 73(3):264-7. DOI: 10.1016/j.lungcan.2010.12.017
Source: PubMed

ABSTRACT

The aim of this study was to assess whether p53 codon 72 polymorphism is associated with an increased risk of lung cancer (LC) in a South Korean population. We conducted a population-based, large-scale, case-control study including 3939 patients with LC and 1700 controls. P53 codon 72 polymorphism was determined by real-time polymerase chain reaction (PCR). The frequencies of p53 codon 72 polymorphisms (Arg/Arg, Arg/Pro, and Pro/Pro) in LC were 37.0%, 46.2%, and 16.7%, respectively; frequencies in the controls were 43.2%, 45.6%, and 11.2%, respectively (p<0.01). The Arg/Pro and Pro/Pro genotype were significantly associated with increased risk of LC (odds ratio (OR)=1.22, 95% confidence interval (CI)=1.06-1.14 and OR=1.83, 95% CI=1.48-2.26, respectively) compared with the Arg/Arg genotype. Risk was compared in different subgroups. The OR of Pro/Pro genotype was significantly higher in small cell lung cancer (SCC) and squamous cell carcinoma (SQC) than in adenocarcinoma (ADC). Higher OR of Pro/Pro genotype was also seen among males. However, relationships between gender, age, smoking, and genotypes were not found. P53 codon 72 polymorphism was associated with an increased risk of LC in this Korean population; the association was especially noteworthy in SQC, SCC, and males.

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    • "To remove the possible confounding effects of cigarette smoking, all participants in our study were female nonsmokers . Consistent with previous studies (Sakiyama et al., 2005; Piao et al., 2011), we found the p53 Arg72Pro polymorphism to be associated with increased lung adenocarcinoma risk. This result is supported by reports that the Pro allele of the p53 Arg72Pro polymorphism, which is less efficient at inducing apoptosis, reduces the tumor suppression function of p53 and increases cancer risk (Thomas et al., 1999). "
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