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.
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).