Search

The interaction of genetic and environmental factors can determine individual susceptibility to various cancers. We studied the influence of NAT2 and codon 72 p53 polymorphisms on 151 patients with lung cancer and an equal number of matched population controls. Polymorphisms of NAT2 and p53 were determined by PCR-RFLP techniques. The results were analyzed using logistic regression analysis. A statistically significant relationship between NAT2*5 and NAT2*6 alleles and lung cancer risk was observed. In addition, the population with slow acetylator alleles for NAT2*5 and NAT2*6 had a significantly higher risk of lung cancer compared with rapid acetylator alleles both in smokers and nonsmokers. The combined genotype of heterozygous arginine ( Arg)/proline ( Pro), Pro/Pro, and slow acetylator alleles of NAT2*5 and NAT2*6 showed higher, although not significant, risk of lung cancer compared with Arg/Arg and rapid acetylator alleles of NAT2*5 and NAT2*6. In conclusion, these findings suggest that the influence of NAT2 genotype, alone or in combination with p53 genotype, may confer increased susceptibility to lung cancer. [ABSTRACT FROM AUTHOR]

DNA ligases play an essential role in repair, replication, and recombination of DNA, and catalyzes the formation of a phosphodiester bond at a nick junction on single- and double-strand breaks. We have conducted a hospital-based case–control study to examine the role of polymorphism of DNA repair gene ligase I ( LIGI) in the context of lung cancer risk for north Indian population. One hundred, fifty-one primary lung cancer cases and an equal number of matching hospital controls were collected. The LIGI polymorphism was determined by using the PCR-RFLP method. The association between polymorphisms in the LIGI gene with the risk of lung cancer was estimated by computing odds ratios (ORs) and a 95% confidence interval (CI) using a Multivariate Logistic Regression Analysis. The risk for lung cancer was not associated for individuals featuring LIGI (AC) (OR –0.8, 95% CI = 0.44–1.40) and (AA) (OR –0.8, 95% CI = 0.41–1.80) genotypes. The DNA repair gene ( LIGI) may not be playing an important role in modulating the risk of lung cancer in the north Indian population. [ABSTRACT FROM AUTHOR]