AIM: To evaluate the association and interaction among human 8-oxoguanine DNA glycosylase 1 (hOGG1) genotypic polymorphism, smoking status and lung cancer risk in Taiwan. MATERIALS AND METHODS: The gene for hOGG1 was analyzed via polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in 358 patients with lung cancer and 716 healthy controls recruited from the China Medical Hospital. RESULTS: The hOGG1 codon 326 genotypes were not differently distributed between the lung cancer and control groups (p=0.0809). However, the C allele of hOGG1 codon 326 was significantly (p=0.0198) more frequently found in controls than in cancer patients. We further analyzed the joint effect of genetics and smoking on lung cancer risk and found an interaction between hOGG1 codon 326 genotypes and smoking status. The hOGG1 codon 326 C allele-bearing genotypes were significantly associated with lung cancer risk only in the smoker group (p=0.0132), but not in the non-smoker group (p=0.06588). CONCLUSION: Our results provide evidence that the C allele of hOGG1 codon 326 may have a joint effect with smoking on the development of lung cancer.
AIM: To evaluate the association and interaction among human 8-oxoguanine DNA glycosylase 1 (hOGG1) genotypic polymorphism, smoking status and lung cancer risk in Taiwan. MATERIALS AND METHODS: The gene for hOGG1 was analyzed via polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in 358 patients with lung cancer and 716 healthy controls recruited from the China Medical Hospital. RESULTS: The hOGG1 codon 326 genotypes were not differently distributed between the lung cancer and control groups (p=0.0809). However, the C allele of hOGG1 codon 326 was significantly (p=0.0198) more frequently found in controls than in cancerpatients. We further analyzed the joint effect of genetics and smoking on lung cancer risk and found an interaction between hOGG1 codon 326 genotypes and smoking status. The hOGG1 codon 326 C allele-bearing genotypes were significantly associated with lung cancer risk only in the smoker group (p=0.0132), but not in the non-smoker group (p=0.06588). CONCLUSION: Our results provide evidence that the C allele of hOGG1 codon 326 may have a joint effect with smoking on the development of lung cancer.