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Jiang DK, Sun J, Cao G, Liu Y, Lin D, Gao YZ, Ren WH, Long XD, Zhang H, Ma XP, Wang Z, Jiang W, Chen TY, Gao Y, Sun LD, Long JR, Huang HX, Wang D, Yu H, Zhang P, Tang LS, Peng B, Cai H, Liu TT, Zhou P, Liu F, Lin X, Tao S, Wan B, Sai-Yin HX, Qin LX, Yin J, Liu L, Wu C, Pei Y, Zhou YF, Zhai Y, Lu PX, Tan A, Zuo XB, Fan J, Chang J, Gu X, Wang NJ, Li Y, Liu YK, Zhai K, Zhang H, Hu Z, Liu J, Yi Q, Xiang Y, Shi R, Ding Q, Zheng W, Shu XO, Mo Z, Shugart YY, Zhang XJ, Zhou G, Shen H, Zheng SL, Xu J, Yu L. Nat Genet. 2012 Dec 16;45(1):72-5. doi: 10.1038/ng.2483. Epub 2012 Dec 16. |
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Source
1] State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, Shanghai, China. [2].
Abstract
To identify genetic susceptibility loci for hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) in the Chinese population, we carried out a genome-wide association study (GWAS) in 2,514 chronic HBV carriers (1,161 HCC cases and 1,353 controls) followed by a 2-stage validation among 6 independent populations of chronic HBV carriers (4,319 cases and 4,966 controls). The joint analyses showed that HCC risk was significantly associated with two independent loci: rs7574865 at STAT4, P(meta) = 2.48 × 10(-10), odds ratio (OR) = 1.21; and rs9275319 at HLA-DQ, P(meta) = 2.72 × 10(-17), OR = 1.49. The risk allele G at rs7574865 was significantly associated with lower mRNA levels of STAT4 in both the HCC tissues and nontumor tissues of 155 individuals with HBV-related HCC (P(trend) = 0.0008 and 0.0002, respectively). We also found significantly lower mRNA expression of STAT4 in HCC tumor tissues compared with paired adjacent nontumor tissues (P = 2.33 × 10(-14)).
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