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    Genetic susceptibility to hepatocellular carcinoma in chromosome 22q13.31, findings of a genome-wide association study

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    Author
    Wang, Zhanwei
    Budhu, Anuradha S.
    Shen, Yi
    Wong, Linda Lou
    Hernandez, Brenda Y.
    Tiirikainen, Maarit
    Ma, Xiaomei
    Irwin, Melinda L.
    Lu, Lingeng
    Zhao, Hongyu
    Lim, Joseph K.
    Taddei, Tamar
    Mishra, Lopa
    Pawlish, Karen
    Stroup, Antoinette
    Brown, Robert
    Nguyen, Mindie H.
    Koshiol, Jill
    Hernandez, Maria O.
    Forgues, Marshonna
    Yang, Hwai I.
    Lee, Mei Hsuan
    Huang, Yu Han
    Iwasaki, Motoki
    Goto, Atsushi
    Suzuki, Shiori
    Matsuda, Koichi
    Tanikawa, Chizu
    Kamatani, Yoichiro
    Mann, Dean
    Guarnera, Maria
    Shetty, Kirti
    Thomas, Claire E.
    Yuan, Jian Min
    Khor, Chiea Chuen
    Koh, Woon Puay
    Risch, Harvey
    Wang, Xin Wei
    Yu, Herbert
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    Date
    2021-11-27
    Journal
    JGH Open
    Publisher
    Wiley-Blackwell
    Type
    Article
    
    Metadata
    Show full item record
    See at
    https://doi.org/10.1002/jgh3.12682
    Abstract
    Background and Aim: Chronic hepatitis C virus (HCV) infection, long-term alcohol use, cigarette smoking, and obesity are the major risk factors for hepatocellular carcinoma (HCC) in the United States, but the disease risk varies substantially among individuals with these factors, suggesting host susceptibility to and gene–environment interactions in HCC. To address genetic susceptibility to HCC, we conducted a genome-wide association study (GWAS). Methods: Two case-control studies on HCC were conducted in the United States. DNA samples were genotyped using the Illumian microarray chip with over 710 000 single nucleotide polymorphisms (SNPs). We compared these SNPs between 705 HCC cases and 1455 population controls for their associations with HCC and verified our findings in additional studies. Results: In this GWAS, we found that two SNPs were associated with HCC at P < 5E-8 and six SNPs at P < 5E-6 after adjusting for age, sex, and the top three principal components (PCs). Five of the SNPs in chromosome 22q13.31, three in PNPLA3 (rs2281135, rs2896019, and rs4823173) and two in SAMM50 (rs3761472, rs3827385), were replicated in a small US case-control study and a cohort study in Singapore. The associations remained significant after adjusting for body mass index and HCV infection. Meta-analysis of multiple datasets indicated that these SNPs were significantly associated with HCC. Conclusions: SNPs in PNPLA3 and SAMM50 are known risk loci for nonalcoholic fatty liver disease (NAFLD) and are suspected to be associated with HCC. Our GWAS demonstrated the associations of these SNPs with HCC in a US population. Biological mechanisms underlying the relationship remain to be elucidated. © 2021 The Authors.
    Keyword
    genome-wide association study
    liver cancer
    nonalcoholic fatty liver disease
    PNPLA3
    SAMM50
    Identifier to cite or link to this item
    http://hdl.handle.net/10713/17313
    ae974a485f413a2113503eed53cd6c53
    10.1002/jgh3.12682
    Scopus Count
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