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. 2020 Jul 7;4:20. doi: 10.1038/s41698-020-0125-y

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© The Author(s) 2020

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. 6 — All hepatoblastoma cells are commonly derived from immature hepatocytes with aberrant activation of the Wnt signaling pathway, whereas heterogeneity among cases arises from the diversity of the differentiation stage of the origins. Clusters E1/E2 are derived from liver progenitor cells at an earlier differentiation stage and consequently harbor hypermethylation of HNF4A/CEBPA-binding regions that leads to expression profiles mimicking fetal liver, which explain the poorly differentiated pathology and aggressive cell proliferation. In addition, clusters E1/E2 highly express NQO1 due to promoter hypomethylation, which induces chemoresistance. Cluster F arises from hepatoblasts at a relatively mature stage, harbors genetic features that are opposite of those observed in clusters E1/E2, and represents good prognosis.