Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (846 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A malignant neoplasm occurring in young children, primarily in the liver, composed of tissue resembling embryonal or fetal hepatic epithelium, or mixed epithelial and mesenchymal tissues. (Stedman, 25th ed)
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Hepatoblastomas.
Where it fits in the MeSH classification
- Broader topics
- Neoplasms, Complex and Mixed
Research landscape
PubMed indexes 2,377 records tagged with the MeSH heading “Hepatoblastoma” (counts retrieved 2026-10-29). 581 of them (24.4%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 727 records.
Reviews account for 294 records (12.4%) and meta-analyses for 11. Randomized controlled trials number 15 (0.6%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 373 |
| 2000-2009 | 696 |
| 2010-2019 | 727 |
| 2020 onward | 581 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 294 | 12.4% |
| Meta-analyses | 11 | 0.5% |
| Randomized controlled trials | 15 | 0.6% |
Method: PubMed query "Hepatoblastoma"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in cancer and oncology
Cancer research spans very different kinds of evidence. Laboratory studies in cell lines and animal models reveal mechanisms but often do not translate to patients. Early-phase trials mainly test safety and dosing, while phase 3 randomized trials and their meta-analyses are the usual basis for treatment conclusions. Outcomes also differ in meaning: tumour shrinkage, progression-free survival and overall survival are not interchangeable, and screening studies can be distorted by lead-time and overdiagnosis. When reading a result, check the cancer type and stage studied, the comparison treatment, and which outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| The N6-methyladenosine modification enhances ferroptosis resistance through inhibiting SLC7A11 mRNA deadenylation in hepatoblastoma | 2022 | Research article Design not recorded in structured metadata | 143 | cc by PMID 35522946 · DOI · PMC9076012 |
| Incidence trends and survival prediction of hepatoblastoma in children: a population-based study | 2019 | Research article Design not recorded in structured metadata | 119 | cc by PMID 31651371 · DOI · PMC6813130 |
| Genetic and epigenetic basis of hepatoblastoma diversity | 2021 | Research article Design not recorded in structured metadata | 101 | cc by PMID 34538872 · DOI · PMC8450290 |
| Effective therapeutic targeting of CTNNB1-mutant hepatoblastoma with WNTinib | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 41359441 · DOI · PMC13060634 |
The N6-methyladenosine modification enhances ferroptosis resistance through inhibiting SLC7A11 mRNA deadenylation in hepatoblastoma [1]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundSolute carrier family 7 member 11 (SLC7A11) is overexpressed in multiple human tumours and functions as a transporter importing cystine for glutathione biosynthesis.
- Closing excerpt
- Our study highlights a critical role of the m6A modification in SLC7A11-mediated ferroptosis, providing a potential strategy for HB therapy through blockade of the m6A-SLC7A11 axis.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (283 words)
BackgroundSolute carrier family 7 member 11 (SLC7A11) is overexpressed in multiple human tumours and functions as a transporter importing cystine for glutathione biosynthesis. It promotes tumour development in part by suppressing ferroptosis, a newly identified form of cell death that plays a pivotal role in the suppression of tumorigenesis. However, the role and underlying mechanisms of SLC7A11-mediated ferroptosis in hepatoblastoma (HB) remain largely unknown.MethodsReverse transcription quantitative real-time PCR (RT-qPCR) and western blotting were used to measure SLC7A11 levels. Cell proliferation, colony formation, lipid reactive oxygen species (ROS), MDA concentration, 4-HNE, GSH/GSSG ratio and cell death assays as well as subcutaneous xenograft experiments were used to elucidate the effects of SLC7A11 in HB cell proliferation and ferroptosis. Furthermore, MeRIP-qPCR, dual luciferase reporter, RNA pulldown, RNA immunoprecipitation (RIP) and RACE-PAT assays were performed to elucidate the underlying mechanism through which SLC7A11 was regulated by the m6A modification in HB.ResultsSLC7A11 expression was highly upregulated in HB. SLC7A11 upregulation promoted HB cell proliferation in vitro and in vivo, inhibiting HB cell ferroptosis. Mechanistically, SLC7A11 mRNA exhibited abnormal METTL3-mediated m6A modification, which enhanced its stability and expression. IGF2 mRNA-binding protein 1 (IGF2BP1) was identified as the m6A reader of SLC7A11, enhancing SLC7A11 mRNA stability and expression by inhibiting SLC7A11 mRNA deadenylation in an m6A-dependent manner. Moreover, IGF2BP1 was found to block BTG2/CCR4-NOT complex recruitment via competitively binding to PABPC1, thereby suppressing SLC7A11 mRNA deadenylation.ConclusionsOur findings demonstrated that the METTL3-mediated SLC7A11 m6A modification enhances HB ferroptosis resistance. The METTL3/IGF2BP1/m6A modification promotes SLC7A11 mRNA stability and upregulates its expression by inhibiting the deadenylation process. Our study highlights a critical role of the m6A modification in SLC7A11-mediated ferroptosis, providing a potential strategy for HB therapy through blockade of the m6A-SLC7A11 axis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 35522946 · DOI · PMC9076012
Incidence trends and survival prediction of hepatoblastoma in children: a population-based study [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundHepatoblastoma is a rare disease that nevertheless accounts for the majority of liver malignancies in children.
- Closing excerpt
- It provides accurate prognostic prediction for children with hepatoblastoma.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (176 words)
BackgroundHepatoblastoma is a rare disease that nevertheless accounts for the majority of liver malignancies in children. Due to limited epidemiological data, therapy for hepatoblastoma tends to be individualized. This study aimed to evaluate incidence trends of hepatoblastoma and to develop a nomogram to predict the survival of children with newly diagnosed hepatoblastoma on a population-based level.MethodsIndividuals up to 18 years of age with hepatoblastoma recorded in 18 registries of the Surveillance, Epidemiology, and End Results (SEER) database between 2004 and 2015 were examined. Joinpoint regression analyses were applied to assess incidence trends in annual percentage change (APC). Multivariable Cox regression was used to identify factors associated with overall survival (OS). A nomogram was constructed to predict OS in individual cases based on independent predictors. Concordance index (C-index) and calibration curves were used to evaluate predictive performance.ResultsBetween 2004 and 2015, hepatoblastoma incidence increased significantly (APC, 2.2%; 95% confidence interval [CI] 0.5% to 3.8%, P ConclusionsWe constructed a nomogram that integrates common factors associated with survival for hepatoblastoma patients. It provides accurate prognostic prediction for children with hepatoblastoma.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31651371 · DOI · PMC6813130
Genetic and epigenetic basis of hepatoblastoma diversity [3]
Abstract reading summary — source excerpts
- Opening excerpt
- 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.
- Closing excerpt
- Systematic molecular profiling of HB is a promising approach for understanding the epigenetic drivers of hepatoblast carcinogenesis and deriving clues for risk stratification.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (182 words)
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.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34538872 · DOI · PMC8450290
Effective therapeutic targeting of CTNNB1-mutant hepatoblastoma with WNTinib [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Hepatoblastoma (HB), the most frequent pediatric liver cancer (2.
- Closing excerpt
- WNTinib delays tumor progression and increases survival in CTNNB1-mutated HB models, providing rationale to explore its use in human HB.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (205 words)
Hepatoblastoma (HB), the most frequent pediatric liver cancer (2.16 cases/million), has surgery and perioperative chemotherapy as primary treatment, with severe lifelong side effects. This study evaluates the efficacy of the Wnt/CTNNB1 inhibitor WNTinib as a potential HB treatment, since CTNNB1 mutations occur in 70-90% of HBs. WNTinib's efficacy was assessed in three animal models (n = 48): (a) patient-derived xenograft (PDX) HB tumors (n = 5 CTNNB1-mutant, n = 1 CTNNB1 wild-type) implanted in NSG mice; (b) PDX-derived TT001- and (c) HepG2-HB cells subcutaneously implanted in Fox1nu mice; and in two patient-derived organoids from CTNNB1-mutant HBs. WNTinib delayed tumor growth in n = 4/5 CTNNB1-mutant PDX models and significantly improved survival versus controls (P = 0.03), with no effect in the wild-type model. Further, in the TT001 and HepG2 models, WNTinib reduced tumor growth (P < 0.05 and P = 0.002) and extended survival (P = 0.03 and P = 0.008), respectively. In HB organoids, WNTinib demonstrated greater efficacy than standard-of-care cisplatin (P = 0.009, org-1), and its antitumor effect was further enhanced when combined with chemotherapy (P = 0.01, org-1; P = 0.007, org-22). WNTinib delays tumor progression and increases survival in CTNNB1-mutated HB models, providing rationale to explore its use in human HB.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41359441 · DOI · PMC13060634
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article The epidemiology of hepatoblastoma [5]
- Research article Towards an international pediatric liver tumor consensus classification: proceedings of the Los Angeles COG liver tumors symposium [6]
- Research article Hepatoblastoma state of the art: pathology, genetics, risk stratification, and chemotherapy [7]
- Research article 2017 PRETEXT: radiologic staging system for primary hepatic malignancies of childhood revised for the Paediatric Hepatic International Tumour Trial (PHITT) [8]
- Research article Liver transplantation for hepatoblastoma: results from the International Society of Pediatric Oncology (SIOP) study SIOPEL-1 and review of the world experience [9]
- Research article Evaluation of the pediatric patient for liver transplantation: 2014 practice guideline by the American Association for the Study of Liver Diseases, American Society of Transplantation and the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition [10]
References
- Liu L, He J, Sun G, Huang N, Bian Z, Xu C, et al.. The N6-methyladenosine modification enhances ferroptosis resistance through inhibiting SLC7A11 mRNA deadenylation in hepatoblastoma. . 2022. PMID 35522946 · DOI · PMC9076012
- Feng J, Polychronidis G, Heger U, Frongia G, Mehrabi A, Hoffmann K. Incidence trends and survival prediction of hepatoblastoma in children: a population-based study. . 2019. PMID 31651371 · DOI · PMC6813130
- Nagae G, Yamamoto S, Fujita M, Fujita T, Nonaka A, Umeda T, et al.. Genetic and epigenetic basis of hepatoblastoma diversity. . 2021. PMID 34538872 · DOI · PMC8450290
- Balaseviciute U, Huguet-Pradell J, Abril-Fornaguera J, Gris-Oliver A, Rialdi A, Fernández-Martínez E, et al.. Effective therapeutic targeting of CTNNB1-mutant hepatoblastoma with WNTinib. . 2026. PMID 41359441 · DOI · PMC13060634
- Spector LG, Birch J. The epidemiology of hepatoblastoma. Pediatr Blood Cancer. 2012. PMID 22692949 · DOI
- López-Terrada D, Alaggio R, de Dávila MT, Czauderna P, Hiyama E, Katzenstein H, et al.. Towards an international pediatric liver tumor consensus classification: proceedings of the Los Angeles COG liver tumors symposium. Mod Pathol. 2014. PMID 24008558 · DOI
- Czauderna P, Lopez-Terrada D, Hiyama E, Häberle B, Malogolowkin MH, Meyers RL. Hepatoblastoma state of the art: pathology, genetics, risk stratification, and chemotherapy. Curr Opin Pediatr. 2014. PMID 24322718 · DOI
- Towbin AJ, Meyers RL, Woodley H, Miyazaki O, Weldon CB, Morland B, et al.. 2017 PRETEXT: radiologic staging system for primary hepatic malignancies of childhood revised for the Paediatric Hepatic International Tumour Trial (PHITT). Pediatr Radiol. 2018. PMID 29427028 · DOI
- Otte JB, Pritchard J, Aronson DC, Brown J, Czauderna P, Maibach R, et al.. Liver transplantation for hepatoblastoma: results from the International Society of Pediatric Oncology (SIOP) study SIOPEL-1 and review of the world experience. Pediatr Blood Cancer. 2004. PMID 14752798 · DOI
- Squires RH, Ng V, Romero R, Ekong U, Hardikar W, Emre S, et al.. Evaluation of the pediatric patient for liver transplantation: 2014 practice guideline by the American Association for the Study of Liver Diseases, American Society of Transplantation and the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition. Hepatology. 2014. PMID 24782219 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
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