No significant differences in gene and protein expression were detected between the different types of gliomas, suggesting that glioma chemoresistance is probably multifactorial and GSTP1-independent.
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 GSTP1I105V: pooled OR = 0.92; 95 % CI, 0.64-1.31 and for GSTP1A114V: pooled OR = 1.14; 95 % CI, 0.97-1.34).
We identified two tSNPs to be associated with glioma susceptibility (rs1695, GSTP1, P = 0.019; rs2853676, TERT, P = 0.039), which we confirmed using dominant and additive model analyses.
We found no associations between the GSTM3, GSTP1, NQO1, CYP1A1, GSTM1, or GSTT1 polymorphisms and adult brain tumor risk with the possible exception of a weak association between the G-C (Val-Ala) GSTP1 105/114 haplotype and glioma [odds ratio (OR), 0.73; 95% confidence interval (95% CI), 0.54, 0.99], nor was there an interaction between the effects of the GSTM3 or GSTP1 polymorphisms and cigarette smoking.
There was evidence of supermultiplicativity of the joint effect of GSTP1I105V 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 effects of the changes in MTase levels on global genomic DNA methylation and on the methylation status of CpG dinucleotides in the GSTP1 gene were determined in a glioma cell line that overexpresses the GSTP1 gene.