TY - JOUR
T1 - Hepatocellular Carcinoma Risk Stratification by Genetic Profiling in Patients with Cirrhosis
AU - Fujiwara, Naoto
AU - Hoshida, Yujin
N1 - Funding Information:
This work is supported by Uehara Memorial Foundation (to N.F.) and U.S. NIH/NIDDK R01 DK099558, European Union ERC-2014-AdG-671231 HEPCIR, Irma T. Hirschl Trust, U.S. Department of Defense W81XWH-16–1-0363, and Cancer Prevention and Research Institute of Texas RR180016 (to Y.H.).
Publisher Copyright:
© 2019 by Thieme Medical Publishers, Inc.
PY - 2019
Y1 - 2019
N2 - Prediction of future hepatocellular carcinoma (HCC) risk in the sizable chronic liver disease population is an urgent unmet need to enable regular HCC screening for early detection. Germline deoxyribonucleic acid polymorphisms likely represent etiology-specific host factors that determine HCC susceptibility, including single nucleotide polymorphisms in EGF, IFNL3, MICA, and TLL1 in hepatitis C with or without active viral infection, and PNPLA3, TM6SF2, and MBOAT7 in metabolic liver diseases. Transcriptome-based prognostic liver signature in diseased liver tissue has been associated with long-term HCC risk in viral and metabolic etiologies. Transcriptomic signatures of hepatic injury and specific cell type such as aggregated lymphocytes also predict HCC development. Circulating factors such as proteins and their chemical modification, nucleotides, and metabolites may serve for less-invasive assessment of short-or long-term HCC risk. These biomarkers will enable individual HCC risk-based personalized clinical management for cost-effective early HCC detection and improvement of patient survival.
AB - Prediction of future hepatocellular carcinoma (HCC) risk in the sizable chronic liver disease population is an urgent unmet need to enable regular HCC screening for early detection. Germline deoxyribonucleic acid polymorphisms likely represent etiology-specific host factors that determine HCC susceptibility, including single nucleotide polymorphisms in EGF, IFNL3, MICA, and TLL1 in hepatitis C with or without active viral infection, and PNPLA3, TM6SF2, and MBOAT7 in metabolic liver diseases. Transcriptome-based prognostic liver signature in diseased liver tissue has been associated with long-term HCC risk in viral and metabolic etiologies. Transcriptomic signatures of hepatic injury and specific cell type such as aggregated lymphocytes also predict HCC development. Circulating factors such as proteins and their chemical modification, nucleotides, and metabolites may serve for less-invasive assessment of short-or long-term HCC risk. These biomarkers will enable individual HCC risk-based personalized clinical management for cost-effective early HCC detection and improvement of patient survival.
KW - Risk prediction
KW - cirrhosis
KW - hepatocellular carcinoma
KW - precision medicine
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U2 - 10.1055/s-0039-1681031
DO - 10.1055/s-0039-1681031
M3 - Article
C2 - 30912093
AN - SCOPUS:85065206286
SN - 0272-8087
VL - 39
SP - 153
EP - 162
JO - Seminars in Liver Disease
JF - Seminars in Liver Disease
IS - 2
ER -