Effects of methylation of P16 gene, polymorphism of GSTM1 gene and environmental factors on susceptibility to lung cancer

[Objective] To study the relationship bwtween the genetic polymorphism of GSTM1 gene, methylation of p16 gene, environment exposure and susceptibility to lung cancer so as to explore the mechansim of lung cancer and perfect the theory of diagnosis, prevention and therapy of lung cancer. [Methods] The case-control study was conducted among 47 lung cancer cases and 94 controls. Methylation of p16 gene was tested in DNA from 47 lung cancer tissues and adjacent nomalignant tissues by MSP;the GSTM1 gene genetic polymorphisms were genotyped with method of PCR-RFLP. [Results] There was a high frequency of dust and toxicant exposure in lung cancer group than in control group (P < 0.01). In lung cancer tissues, the frequency of P16 methylation was 44.7%, significantly higher than that in the nomalignant tissue 17% ( P < 0.01), P16 methylation significantly correlated with smoking. There was no statistical difference of GSTM1 null genotype frequency between case group and control group (P > 0.05). There was a synergistic interaction between dust and tobacco exposure with GSTM1 null genotype; methylation of P16 does not correlate with polymorphism of GSTM1. [Conclusion] This study suggests that dust and toxicant exposure significantly increases the risk of lung cancer. Methylation of P16 gene due to smoking was involved in the progress of lung cancer. There was an elevated risk of lung cancer in GSTM1 null genotype with exposure to dust and tobacco. In this study no interaction between genetics and epigenetics in lung cancer was revealed.