Table 1.

Prevalence of main genetic alterations involved in hepatocarcinogenesis

Gene	Type of genetic alteration	Function	Prevalence	Reference (year)
TERT (telomerase reverse-transcriptase)	Mutation (nucleotide substitutions) HBV-DNA insertions	Increased telomerase expression	60–90 (%)	Nault (2013) [3] Bruix (2015) [4] Nault (2015) [5]
CTNNB1 (cadherin-associated protein β1)	Exon 3 deletion Missense mutations HBV-DNA insertions	Activation of β-catenin Associated with IL6/JAK/STAT activation and inflammation	25–62 (%)	Huang (2012) [6] Guichard (2012) [7] Kan (2013) [8] Tian (2015) [9] Nault (2017) [10]
TP53 (tumor Protein 53)	Mutation codon 249	Loss of function as tumor suppressor gene Gain of function as oncogene Loss of regulation of the immune response	13–48 (%)	Guichard (2012) [7] Takai (2014) [11] Schulze (2015) [12] Yamamoto (2018) [13] Long (2019) [14]
CDKN2A (cyclin-dependent kinase inhibitor 2A)	Homozygous deletions/mutations or epigenetic silencing	Loss of function as tumor suppressor gene	2–12	Guichard (2012) [7] Totoki (2014) [15] Schulze (2015) [16] Tian (2015) [9]
VEGFA (vascular endothelial growth factor A)	Gene amplification	Promotion of angiogenesis Stimulation of HGF production	7–11%	Zucman (2015) [1] Chiang ‘(2008) [17] Llovelet (2016) [18] Oh (2019) [19] Horwitz (2014) [20]
FGF19 (fibroblast growth factor 19)	Gene amplification	Proliferative signaling Anti-apoptosis	6.5%	Raja (2019) [21] [22]
AXIN1-2, ARID2, ARID1A, TSC1/TSC2, KEAP1, MLL2 RPS6KA3	Multiple mechanisms	WNT/β-catenin pathway SWI/SNF chromatin remodeling complexes Activation of the AKT/MTOR signaling Control of histone methylation	Low frequency	Zucman (2015) [1] Nault (2017) [10]