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. 2021 Sep 20;12:5423. doi: 10.1038/s41467-021-25430-9

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — a A total of 134 cases (WXS: 112, WGS: 33) of childhood hepatoblastoma (HB) and hepatocellular carcinoma (HCC) were sorted by age at diagnosis. The bar graph at the top of the panel shows individual age at diagnosis (childhood HCC, n = 9; tween HB (age > 8), n = 6; child HB (age = 2–8), n = 38; infant HB (age < 2), n = 81). The middle of the panel shows the driver mutations detected in at least 3 cases in this cohort (missense mutation, dark green; in-frame deletion, light green; frame-shift deletion, purple; nonsense mutation, blue; mutation in splicing site, light blue; mutation in the promoter region, yellow) and the pathogenic germline variants (black). The image at the bottom of the panel shows clinical and pathological information. VLBW, very low birth weight (<1500 g); LBW, low birth weight (1500–2500 g); NBW, normal birth weight (2500–3500 g), HCC hepatocellular carcinoma, TLCT transitional liver cell tumor, Embry. embryonic, Macro macrotrabecular; BWS, Beckwith–Wiedemann Syndrome. b The number of somatic mutations per million base pairs of HCC (n = 269) and HB with VLBW (n = 15) and non-VLBW (n = 18) detected by WGS. Statistical significance was analyzed by Wilcoxon rank-sum test. c Correlations between the age at diagnosis and the number of somatic mutations of HB with VLBW (n = 15) and non-VLBW (n = 18). Statistical significance was analyzed by the Spearman correlation test. d Signatures of mutational processes extracted from the mutational catalog of 33 HBs with/without VLBW. e percentages of the contributing mutational signatures.