Herein, we investigated the relationship of three GSTs polymorphisms (GSTT1 deletion, GSTM1 deletion, GSTP1 rs1695) as well as GSTP1 promoter region DNA methylation and HCC risk with a particular focus on the interaction with OCPs exposure among 90 HCC cases and 99 controls in a Chinese population.
The results suggested there was no association between GSTP1 Ile105Val polymorphism and hep</span>atocellular carcinoma</span> ri</span>sk under all genetic models (for ValVal vs. IleIle, OR = 0.79, 95 %CI 0.48-1.29, P = 0.341; for IleVal vs. IleIle, OR = 1.05, 95 %CI 0.84-1.30, P = 0.678; for the dominant model, OR = 0.91, 95 %CI 0.68-1.20, P = 0.498; and for the recessive model, OR = 0.76, 95 %CI 0.47-1.24, P = 0.269).
Two SNPs (GSTO2: rs7085725 and GSTP1: rs4147581) were significantly associated with overall survival in HCC patients (P = 0.035 and 0.042, respectively).
With a recursive partitioning approach, we also demonstrated that significant gene-gene interactions between <i>ERCC1</i> rs3212986, <i>CYP17A1</i> rs743572, <i>GST-P1</i> rs1138272</span>, and the previously described <i>UGT1A7</i>*3 predictive marker, played a role in the complex trait of HCC susceptibility.