The allelic frequency distributions showed that the variant T allele of MMP2 promoter 1306 conferred lower oral cancer susceptibility than the wild-type C allele (odds ratio=0.61, 95% confidence interval=0.50-0.75, p=1.1E-6).
The aim of this study was to estimate the relationship of glutathione S-transferases (GST)P1, GSTA1, GSTM1, and GSTT1 gene polymorphisms to oral cancer risk.
The AG and GG genotypes of IL10A-1082G, together with smoking and areca chewing habits, synergistically contribute to individual susceptibility for oral cancer.
Tobacco use, the major etiological factor for oral cancer is known to generate free radicals resulting in alterations in antioxidant enzymes like, glutathione-S-transferase (GST), glutathione reductase, superoxide dismutase, catalase, and glutathione peroxidase as well as lipid peroxidation and total thiol.
This case-control study focused on the interactions between oral cancer risk factors and genetic polymorphisms of cytochrome P-450 (CYP) 2E1 and glutathione S-transferase (GST) M1 and GSTT1.
Our findings suggest that presence of GSTM1 and/or GSTT1 null genotypes along with variant alleles of CYP1A1 may be the risk alleles for oral cancer susceptibility in Pashtun population.
GSTM1 null alone or associated with CYP1A1 increased the risk of head and neck cancer; the CYP2E1PstI mutated allele increased the risk for only oral cancer.
The prevalence of the GSTM1 null genotypes was 29/87 (33.3%) and 21/40 (52.5%) in controls and oral cancer cases, respectively but the differences were not significant (OR=2.2; 95%CI=0.96-5.1; p=0.06).
Among these 14 variants, 9 variants were reported to be significantly associated with the risk of oral cancer (CYP1A1-MspI, CYP2E1-RsaI/PstI, MTHFR-C677T, p73-G4C14-to-A4T14, XRCC1-Arg194Trp, CYP1A1-Ile462Val, GSTM1-±, and NAT2 slow vs rapid).
A significant risk increase for oral cancer was observed among subjects with the homozygous CYP1A1 (m2/m2) genotype (OR=3.8, 95% CI=1.9-7.7), but not the GSTM1 null genotype (OR=0.7, 95% CI=0.4-1.3).