Evidence map›Paper›PMID 33134907›Full record

ReviewJHEP reports : innovation in hepatology2020

Epigenetics in hepatocellular carcinoma development and therapy: The tip of the iceberg.

Maite G Fernández-Barrena, María Arechederra, Leticia Colyn, Carmen Berasain, Matias A Avila

Abstract readReview
In one paragraph

Review in JHEP reports : innovation in hepatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing 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

78 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Crosstalk BetweenCancers · 2026
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

18 more citing papers are in PubMed but not listed here.

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

5 authors.

Maite G Fernández-BarrenaHepatology Program CIMA, University of Navarra, Pamplona, Spain.
María ArechederraHepatology Program CIMA, University of Navarra, Pamplona, Spain.
Leticia ColynHepatology Program CIMA, University of Navarra, Pamplona, Spain.
Carmen BerasainHepatology Program CIMA, University of Navarra, Pamplona, Spain.
Matias A AvilaHepatology Program CIMA, University of Navarra, Pamplona, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is a deadly tumour whose causative agents are generally well known, but whose pathogenesis remains poorly understood. Nevertheless, key genetic alterations are emerging from a heterogeneous molecular landscape, providing information on the tumorigenic process from initiation to progression. Among these molecular alterations, those that affect epigenetic processes are increasingly recognised as contributing to carcinogenesis from preneoplastic stages. The epigenetic machinery regulates gene expression through intertwined and partially characterised circuits involving chromatin remodelers, covalent DNA and histone modifications, and dedicated proteins reading these modifications. In this review, we summarise recent findings on HCC epigenetics, focusing mainly on changes in DNA and histone modifications and their carcinogenic implications. We also discuss the potential drugs that target epigenetic mechanisms for HCC treatment, either alone or in combination with current therapies, including immunotherapies.

Indexed as

5acC, 5-acetylcytosine5fC, 5-formylcytosine5hmC, 5-hydoxymethyl cytosine5mC, 5-methylcytosineAcetyl-CoA, acetyl coenzyme ABER, base excision repairBRD, bromodomainCDA, cytidine deaminaseCGI, CpG islandCIMP, CGI methylator phenotypeCTLA-4, cytotoxic T-lymphocyte-associated protein 4DNMT, DNA methyltransferaseDNMTi, DNMT inhibitorEpigeneticsFAD, flavin adenine dinucleotideHAT, histone acetyltransferasesHCC, hepatocellular carcinomaHDAC, histone deacetylaseHDACi, HDAC inhibitorHDM, histone demethylaseHepatocellular carcinomaHMT, histone methyltransferaseKMT, lysine methyltransferaseLSD/KDM, lysine specific demethylasesNAFLD, non-alcoholic fatty liver diseasencRNAs, non-coding RNAsNK, natural killerNPC, nasopharyngeal carcinomaPD1, programmed cell death protein 1PD-L1, programmed cell death ligand-1PHD, plant homeodomainPTM, post-translational modificationSAM, S-adenosyl-L-methionineTDG, thymidine-DNA-glycosylaseTERT, telomerase reverse transcriptaseTET, ten-eleven translocationTherapyTME, tumour microenvironmentTSG, tumour suppressor geneUHRF1, ubiquitin like with PHD and ring finger domains 1VEGF, vascular endothelial growth factorα-KG, α-ketoglutarate

Identifiers

PMID33134907
PMCPMC7585149

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.