In the present study we investigated the association of deletion polymorphisms in <i>GSTT1/GSTM1</i> genes and single nucleotide polymorphisms (SNPs) in the <i>TNF-</i>α gene at positions -308/-238 with the risk and outcome in MM and sensitivity to bortezomib under <i>in vitro</i> conditions.
Individuals who carried polymorphisms for GSTT1 null and/or high activity microsomal epoxide hydrolase (mEH 113YY+139HR or 113YY+139RR or 113YH+139RR) and/or low activity NAD(P)H:quinone oxidoreductase 1 (NQO1 187PS/SS) were 1.65, 2.49 and 13 times more likely to have MM (P(trend)=0.001).
Individuals who carried polymorphisms for GSTT1 null and/or high activity microsomal epoxide hydrolase (mEH 113YY+139HR or 113YY+139RR or 113YH+139RR) and/or low activity NAD(P)H:quinone oxidoreductase 1 (NQO1 187PS/SS) were 1.65, 2.49 and 13 times more likely to have MM (P(trend)=0.001).
NQO1 and GSTT1 polymorphisms were recently reported as risk factors for multiple myeloma and GSTP1 genotype was found to be a prognostic marker for therapy outcome in multiple myeloma.
These results were different from those of a previous report on Caucasians which suggested the association of the GSTT1 polymorphism with an increased MM risk and no association of CYP1A1 with the MM risk.