Subgroup analyses by ethnicity showed there was also no association between GSTP1 Ile105Val</span> polymorphism and glioma</span> risk in mixed populations under recessive model (OR = 1.199, 95%CI = 0.928-1.549, Pheterogeneity = 0.060, P = 0.166) and Caucasian populations (OR = 1.097, 95%CI = 0.885-1.360, Pheterogeneity = 0.186, P = 0.398).
The combined results based on all studies showed that there was no association between any of the GST variants and the risk of glioma (for GSTM1: pooled OR = 1.03; 95 % CI, 0.92-1.15; for GSTT1: pooled OR = 1.12; 95 % CI, 0.90-1.40; for GSTP1 I105V: pooled OR = 0.92; 95 % CI, 0.64-1.31 and for GSTP1 A114V: pooled OR = 1.14; 95 % CI, 0.97-1.34).
The genotype #GA# for rs1695 was recognized to be a protective genotype forglioma (OR, 0.67; 95% CI, 0.47-0.96; P = 0.027), while the genotype #AG# for rs2853676 was shown to be a risk genotype for glioma (OR, 1.50; 95% CI, 1.05-2.15; P = 0.025).
There was evidence of supermultiplicativity of the joint effect of GSTP1 I105V and CYP2E1 RsaI variants on both glioma and acoustic neuroma, even following adjustment of estimates toward a common prior distribution using hierarchical regression models.
The combined results based on all studies showed that there was no association between any of the GST variants and the risk of glioma (for GSTM1: pooled OR = 1.03; 95 % CI, 0.92-1.15; for GSTT1: pooled OR = 1.12; 95 % CI, 0.90-1.40; for GSTP1 I105V: pooled OR = 0.92; 95 % CI, 0.64-1.31 and for GSTP1 A114V: pooled OR = 1.14; 95 % CI, 0.97-1.34).