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dc.contributor.authorWang, Zhanwei
dc.contributor.authorBudhu, Anuradha S.
dc.contributor.authorShen, Yi
dc.contributor.authorWong, Linda Lou
dc.contributor.authorHernandez, Brenda Y.
dc.contributor.authorTiirikainen, Maarit
dc.contributor.authorMa, Xiaomei
dc.contributor.authorIrwin, Melinda L.
dc.contributor.authorLu, Lingeng
dc.contributor.authorZhao, Hongyu
dc.contributor.authorLim, Joseph K.
dc.contributor.authorTaddei, Tamar
dc.contributor.authorMishra, Lopa
dc.contributor.authorPawlish, Karen
dc.contributor.authorStroup, Antoinette
dc.contributor.authorBrown, Robert
dc.contributor.authorNguyen, Mindie H.
dc.contributor.authorKoshiol, Jill
dc.contributor.authorHernandez, Maria O.
dc.contributor.authorForgues, Marshonna
dc.contributor.authorYang, Hwai I.
dc.contributor.authorLee, Mei Hsuan
dc.contributor.authorHuang, Yu Han
dc.contributor.authorIwasaki, Motoki
dc.contributor.authorGoto, Atsushi
dc.contributor.authorSuzuki, Shiori
dc.contributor.authorMatsuda, Koichi
dc.contributor.authorTanikawa, Chizu
dc.contributor.authorKamatani, Yoichiro
dc.contributor.authorMann, Dean
dc.contributor.authorGuarnera, Maria
dc.contributor.authorShetty, Kirti
dc.contributor.authorThomas, Claire E.
dc.contributor.authorYuan, Jian Min
dc.contributor.authorKhor, Chiea Chuen
dc.contributor.authorKoh, Woon Puay
dc.contributor.authorRisch, Harvey
dc.contributor.authorWang, Xin Wei
dc.contributor.authorYu, Herbert
dc.date.accessioned2021-12-07T19:50:14Z
dc.date.available2021-12-07T19:50:14Z
dc.date.issued2021-11-27
dc.identifier.urihttp://hdl.handle.net/10713/17313
dc.description.abstractBackground 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.en_US
dc.description.urihttps://doi.org/10.1002/jgh3.12682en_US
dc.language.isoenen_US
dc.publisherWiley-Blackwellen_US
dc.relation.ispartofJGH Openen_US
dc.subjectgenome-wide association studyen_US
dc.subjectliver canceren_US
dc.subjectnonalcoholic fatty liver diseaseen_US
dc.subjectPNPLA3en_US
dc.subjectSAMM50en_US
dc.titleGenetic susceptibility to hepatocellular carcinoma in chromosome 22q13.31, findings of a genome-wide association studyen_US
dc.typeArticleen_US
dc.identifier.doi10.1002/jgh3.12682


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