The risk of lung and urinary bladder cancers was reported to be increased in individuals who carried high risk genotypes in either cytochrome P450 (CYP)1A1, CYP2E1 or glutathione S-transferase (GST)M1, and the combined genotype of both CYP1A1 and GSTM1 enzymes have an enhanced tendency of risk to lung cancer more significantly.
We conducted a case-control study to assess the risk of lung cancer in relation to genetic polymorphisms of the detoxifying enzymes glutathione-S-transferase mu1 (GSTM1) and N-acetyl transferase 2 (NAT2), focusing on never-smokers, women, and older people.
The levels of expressions and catalytic activities of cytochrome P450 (CYP1A1) and glutathione-S-transferase class mu (GSTM1) enzymes in lungs and their metabolic balance may be an important determinant host factor underlying lung cancer.
This hypothesis has been examined in case control studies and while data in some diseases such as lung cancer are conflicting, an increasing body of evidence suggests the importance of several glutathione S-transferase polymorphisms.
Gene deletion at the glutathione S-transferase mu locus (GSTM1) has previously been associated with increased risk for environmentally-induced cancers (e.g. smoking-related lung cancer).
Because of this, the null polymorphism in the GSTM1 gene (coding for the glutathione S-transferase class mu enzyme) has been studied widely as a possible source of inherited susceptibility to smoking-related lung cancer.
Polymorphisms of the CYP1A1 and glutathione S-transferase genes associated with susceptibility to lung cancer in relation to cigarette dose in a Japanese population.
A synergistic increase in susceptibility to lung cancer was found when combining genotyping of CYP1A1 and the Mu-class of glutathione S-transferase (GST1).