Evidence map›Paper›PMID 39596558›Full record

ReviewGenes2024

Metabolic and Epigenetic Mechanisms in Hepatoblastoma: Insights into Tumor Biology and Therapeutic Targets.

Yuanji Fu, Raquel Francés, Claudia Monge, Christophe Desterke, Agnès Marchio, Pascal Pineau, Yunhua Chang-Marchand, Jorge Mata-Garrido

Abstract readReview
In one paragraph

Review in Genes, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
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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

8 authors.

Yuanji FuCNRS, INSERM, Institut Necker Enfants Malades, Université Paris Cité, 75015 Paris, France.ORCID 0000-0002-2226-8230
Raquel FrancésEnergy & Memory, Brain Plasticity Unit, CNRS, ESPCI Paris, PSL Research University, 75006 Paris, France.ORCID 0000-0003-1428-4852
Claudia MongeINSERM U993, Unité Organisation Nucléaire et Oncogenèse, Institut Pasteur, Université Paris Cité, 75006 Paris, France.ORCID 0000-0002-1215-5857
Christophe DesterkeFaculté de Médecine du Kremlin Bicêtre, Université Paris-Sud, Université Paris-Saclay, 94270 Le Kremlin-Bicêtre, France.ORCID 0000-0001-7679-2524
Agnès MarchioINSERM U993, Unité Organisation Nucléaire et Oncogenèse, Institut Pasteur, Université Paris Cité, 75006 Paris, France.
Pascal PineauINSERM U993, Unité Organisation Nucléaire et Oncogenèse, Institut Pasteur, Université Paris Cité, 75006 Paris, France.ORCID 0000-0002-9407-1592
Yunhua Chang-MarchandCNRS, INSERM, Institut Necker Enfants Malades, Université Paris Cité, 75015 Paris, France.
Jorge Mata-GarridoINSERM U993, Unité Organisation Nucléaire et Oncogenèse, Institut Pasteur, Université Paris Cité, 75006 Paris, France.ORCID 0009-0004-5726-8814

Funding

Filière Santé Maladie Rare du Foie de l'Adulte et de l'Enfant S-AC23007MEAE AMBASS FRANCE AU PEROU FSPI S-AC23007
6 · The paper itself

Abstract

backgroundHepatoblastoma, the most common pediatric liver malignancy, is characterized by significant molecular heterogeneity and poor prognosis in advanced stages. Recent studies highlight the importance of metabolic reprogramming and epigenetic dysregulation in hepatoblastoma pathogenesis. This review aims to explore the metabolic alterations and epigenetic mechanisms involved in hepatoblastoma and how these processes contribute to tumor progression and survival.

methodsRelevant literature on metabolic reprogramming, including enhanced glycolysis, mitochondrial dysfunction, and shifts in lipid and amino acid metabolism, as well as epigenetic mechanisms like DNA methylation, histone modifications, and non-coding RNAs, was reviewed. The interplay between these pathways and their potential as therapeutic targets were examined.

resultsHepatoblastoma exhibits metabolic shifts that support tumor growth and survival, alongside epigenetic changes that regulate gene expression and promote tumor progression. These pathways are interconnected, with metabolic changes influencing the epigenetic landscape and vice versa.

conclusionsThe dynamic interplay between metabolism and epigenetics in hepatoblastoma offers promising avenues for therapeutic intervention. Future research should focus on integrating metabolic and epigenetic therapies to improve patient outcomes, addressing current gaps in knowledge to develop more effective treatments.

Indexed as

DNA MethylationEpigenesis, GeneticHepatoblastomaLiver NeoplasmsGene Expression Regulation, NeoplasticHumanscancer metabolismepigeneticshepatoblastomatherapeutic targetstumor biology

Identifiers

PMID39596558
PMCPMC11593527

What OpenQuestion holds

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Registered trials

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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.