ArticleNature communications2021
Genetic and epigenetic basis of hepatoblastoma diversity.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 2 of them syntheses that pooled it.
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Who cites it
74 citing papers in PubMed, 2 syntheses or guidelines pooled it, 112 citations in OpenAlex.
- Multiancestry Transcriptome-Wide Association Study Identifies Candidate Genes Associated with Hepatoblastoma.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2025Pooled it
- The immunotherapy advancement targeting malignant blastomas in early childhood.Frontiers in oncology · 2023Pooled it
- Global landscape of liver disease burden in 1990-2021.iScience · 2026Article
- Developmental timing distinguishes pediatric and adult cancers through retention and rewiring mechanisms.Nature communications · 2026Review
- Differential Wnt/β-catenin signaling via TCF7L2/LEF1 binding specificity shapes cellular and tumor phenotypes.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Preclinical Drug-Response Profiling Identifies BMI1 Inhibition as a Therapeutic Option for Hepatoblastoma.International journal of molecular sciences · 2026Article
- Proteasome Targeting with Carfilzomib Induces Reactive Oxygen Species-Mediated Apoptosis in Hepatoblastoma.Cells · 2026Article
- Effective therapeutic targeting of CTNNB1-mutant hepatoblastoma with WNTinib.Molecular oncology · 2026Article
- Malignant Hepatocellular Neoplasm, Not Otherwise Specified, Displays Poorer Chemoresponsiveness and Postoperative Prognosis Than Hepatoblastoma.Cancer research and treatment · 2026Article
- Pediatric Hepatoblastoma: From Developmental Molecular Mechanisms to Innovative Therapeutic Strategies.Cancers · 2026Review
- Noncoding RNAs in Pediatric Solid Tumors: Advances in Understanding and Critical Knowledge Gaps.Cells · 2026Review
- Precision Oncology for Pediatric Solid Tumors Using In-Hospital Pediatric/AYA Malignancy-Specific Panel Sequencing.Cancer science · 2026Article
- ALKBH1 gene polymorphisms confer hepatoblastoma susceptibility in Chinese children.Scientific reports · 2026Article
- TCF3 activates super-enhancer-driven TRIB2 overexpression to suppress ferroptosis and promote hepatoblastoma proliferation.Journal of experimental & clinical cancer research : CR · 2025Article
- Review
- ASCL2 contributes to clinical assessments of breast cancer and mediates tumor progression via the interaction with CLDN3.Scientific reports · 2025Article
- Derivation of Genetically Defined Murine Hepatoblastoma Cell Lines with Angiogenic Potential.Cancers · 2025Article
- Identification of a Growth-Promoting Gene Cluster in the Region 2q24 as a Driver of Tumorigenesis in Childhood Hepatoblastoma.The American journal of pathology · 2025Article
- Novel CTNNB1 gene mutations reveal critical pathogenic mechanisms in pediatric hepatoblastoma.Pediatric surgery international · 2025Article
- From preneoplastic lesion to heterogenous tumor: recent insights into hepatoblastoma biology and therapeutic opportunities.Molecular cancer · 2025Review
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors at 11 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatoblastoma (HB) is the most common pediatric liver malignancy; however, hereditary predisposition and acquired molecular aberrations related to HB clinicopathological diversity are not well understood. Here, we perform an integrative genomic profiling of 163 pediatric liver tumors (154 HBs and nine hepatocellular carcinomas) based on the data acquired from a cohort study (JPLT-2). The total number of somatic mutations is precious low (0.52/Mb on exonic regions) but correlated with age at diagnosis. Telomerase reverse transcriptase (TERT) promoter mutations are prevalent in the tween HBs, selective in the transitional liver cell tumor (TLCT, > 8 years old). DNA methylation profiling reveals that classical HBs are characterized by the specific hypomethylated enhancers, which are enriched with binding sites for ASCL2, a regulatory transcription factor for definitive endoderm in Wnt-pathway. Prolonged upregulation of ASCL2, as well as fetal-liver-like methylation patterns of IGF2 promoters, suggests their "cell of origin" derived from the premature hepatoblast, similar to intestinal epithelial cells, which are highly proliferative. Systematic molecular profiling of HB is a promising approach for understanding the epigenetic drivers of hepatoblast carcinogenesis and deriving clues for risk stratification.
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