Evidence map›Paper›PMID 33764483›Full record

ArticleSeminars in liver disease2021

Molecular Mechanisms of Hepatoblastoma.

Yi Zhang, Antonio Solinas, Stefano Cairo, Matthias Evert, Xin Chen, Diego F Calvisi

Open access · greenAbstract read
In one paragraph

Article in Seminars in liver disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.2field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

37 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Article
  3. Trefoil Factor-3 Is a Hypoxia-Triggered Pro-Tumorigenic Factor in Hepatoblastoma.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. The Role of IR in Pediatric Liver Cancer.Seminars in interventional radiology · 2025
    Review
  16. Article
  17. Gas1-Mediated Suppression of Hepatoblastoma Tumorigenesis.The American journal of pathology · 2025
    Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 5 institutions in 4 countries.

Yi ZhangKey Laboratory of Biorheological Science and Technology, Ministry of Education, College of Bioengineering, Chongqing University, Chongqing, China.
Antonio SolinasDepartment of Biomedical Sciences, University of Sassari, Sassari, Italy.
Stefano CairoXenTech, Evry, France.
Matthias EvertInstitute of Pathology, University of Regensburg, Regensburg, Germany.
Xin ChenDepartment of Bioengineering and Therapeutic Sciences and Liver Center, University of California, San Francisco, California.
Diego F CalvisiInstitute of Pathology, University of Regensburg, Regensburg, Germany.
University of Regensburg · DEChongqing University · CNCittà della Speranza Foundation · ITUniversity of California, San Francisco · USUniversity of Sassari · IT

Funding

UCSF Liver Core CenterP30DK026743 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Holger Willenbring · 1986 to 2026
$30.7M
Yap and beta-catenin interactions in liver: Implications in PathophysiologyR01CA204586 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHEN, XIN, MONGA, SATDARSHAN SINGH · 2016 to 2020
$2.1M
201806050132 China Scholarship CouncilNCI NIH HHS R01 CA204586NIDDK NIH HHS P30 DK026743P30DK026743 UCSF Liver CenterR01CA204586 NIH
6 · The paper itself

Abstract

Hepatoblastoma (HB) is the predominant primary liver tumor in children. While the prognosis is favorable when the tumor can be resected, the outcome is dismal for patients with progressed HB. Therefore, a better understanding of the molecular mechanisms responsible for HB is imperative for early detection and effective treatment. Sequencing analysis of human HB specimens unraveled the pivotal role of Wnt/β-catenin pathway activation in this disease. Nonetheless, β-catenin activation alone does not suffice to induce HB, implying the need for additional alterations. Perturbations of several pathways, including Hippo, Hedgehog, NRF2/KEAP1, HGF/c-Met, NK-1R/SP, and PI3K/AKT/mTOR cascades and aberrant activation of c-MYC, n-MYC, and EZH2 proto-oncogenes, have been identified in HB, although their role requires additional investigation. Here, we summarize the current knowledge on HB molecular pathogenesis, the relevance of the preclinical findings for the human disease, and the innovative therapeutic strategies that could be beneficial for the treatment of HB patients.

Indexed as

HepatoblastomaLiver NeoplasmsChildHumansKelch-Like ECH-Associated Protein 1NF-E2-Related Factor 2Phosphatidylinositol 3-KinasesKelch-Like ECH-Associated Protein 1NF-E2-Related Factor 2Phosphatidylinositol 3-Kinases

Identifiers

PMID33764483
PMCPMC8524782
OpenAlexW3122244534

What OpenQuestion holds

Textmetadata
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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.