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• W2468596757 abstract "// Je-Gun Joung 1, * , Sang Yun Ha 5, * , Joon Seol Bae 1 , Jae-Yong Nam 1, 2 , Geum-Youn Gwak 6 , Hae-Ock Lee 1, 4 , Dae-Soon Son 1, 3 , Cheol-Keun Park 5 , Woong-Yang Park 1, 2, 4 1 Samsung Genome Institute, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea 2 Samsung Advanced Institute for Health Sciences and Technology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea 3 Samsung Biomedical Research Institute, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea 4 Departments of Molecular Cell Biology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea 5 Departments of Pathology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea 6 Departments of Internal Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea * These authors have contributed equally to this work Correspondence to: Cheol-Keun Park, email: ckpark@skku.edu Woong-Yang Park, email: woongyang.park@samsung.com Keywords: hepatocellular carcinoma, dysplastic nodules, whole-exome sequencing, single nucleotide variation, copy number variation Received: October 24, 2015     Accepted: May 17, 2016     Published: July 09, 2016 ABSTRACT Dysplastic nodules are premalignant neoplastic nodules found in explanted livers with cirrhosis. Genetic signatures of premalignant dysplastic nodules (DNs) with concurrent hepatocellular carcinoma (HCC) may provide an insight in the molecular evolution of hepatocellular carcinogenesis. We analyzed four patients with multifocal nodular lesions and cirrhotic background by whole-exome sequencing (WES). The genomic profiles of somatic single nucleotide variations (SNV) and copy number variations (CNV) in DNs were compared to those of HCCs. The number and variant allele frequency of somatic SNVs of DNs and HCCs in each patient was identical along the progression of pathological grade. The somatic SNVs in DNs showed little conservation in HCC. Additionally, CNVs showed no conservation. Phylogenetic analysis based on SNVs and copy number profiles indicated a nonlinear segregation pattern, implying independent development of DNs and HCC in each patient. Thus, somatic mutations in DNs may be developed separately from other malignant nodules in the same liver, suggesting a nonlinear model for hepatocarcinogenesis from DNs to HCC." @default.
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• W2468596757 date "2016-07-09" @default.
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• W2468596757 title "Nonlinear tumor evolution from dysplastic nodules to hepatocellular carcinoma" @default.
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• W2468596757 doi "https://doi.org/10.18632/oncotarget.10502" @default.
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