Evidence map›Paper›PMID 25206269›Full record

ReviewWorld journal of gastroenterology2014

Molecular mechanism of hepatitis B virus-induced hepatocarcinogenesis.

Mirko Tarocchi, Simone Polvani, Giada Marroncini, Andrea Galli

Open access · hybridAbstract readReview
In one paragraph

Review in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed, 1 pooled it
11.6field-weighted citation impact, top 1% 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

114 citing papers in PubMed, 1 synthesis or guideline pooled it, 187 citations in OpenAlex.

  1. Pooled it
  2. Article
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  4. Review
  5. Article
  6. Article
  7. Review
  8. Narra J · 2025
    Article
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  18. Article
  19. Role of p53 suppression in the pathogenesis of hepatocellular carcinoma.World journal of gastrointestinal pathophysiology · 2023
    Review
  20. Hepatitis B virus-induced hepatocellular carcinoma: a persistent global problem.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2023
    Review

54 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

4 authors at 1 institution in 1 country.

Mirko TarocchiMirko Tarocchi, Simone Polvani, Andrea Galli, Department of Experimental and Clinical Biomedical Sciences, University of Florence, 50139 Florence, Italy.
Simone PolvaniMirko Tarocchi, Simone Polvani, Andrea Galli, Department of Experimental and Clinical Biomedical Sciences, University of Florence, 50139 Florence, Italy.
Giada MarronciniMirko Tarocchi, Simone Polvani, Andrea Galli, Department of Experimental and Clinical Biomedical Sciences, University of Florence, 50139 Florence, Italy.
Andrea GalliMirko Tarocchi, Simone Polvani, Andrea Galli, Department of Experimental and Clinical Biomedical Sciences, University of Florence, 50139 Florence, Italy.
University of Florence · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis B virus (HBV) infection is a global public health problem with approximately 2 billion people that have been exposed to the virus. HBV is a member of a family of small, enveloped DNA viruses called hepadnaviruses, and has a preferential tropism for hepatocytes of mammals and birds. Epidemiological studies have proved a strong correlation between chronic hepatitis B virus infection and the development of hepatocellular carcinoma (HCC). HCC is the fifth most common malignancy with about 700000 new cases each year, and more than 50% of them arise in HBV carriers. A large number of studies describe the way in which HBV can contribute to HCC development. Multiple mechanisms have been proposed, including the accumulation of genetic damage due to immune-mediated hepatic inflammation and the induction of oxidative stress. There is evidence of the direct effects of the viral proteins HBx and HBs on the cell biology. Integration of HBV-DNA into the human genome is considered an early event in the carcinogenic process and can induce, through insertional mutagenesis, the alteration of gene expression and chromosomal instability. HBV has also epigenetic effects through the modification of the genomic methylation status. Furthermore, the virus plays an important role in the regulation of microRNA expression. This review will summarize the many mechanisms involved in HBV-related liver carcinogenesis.

Indexed as

Cell Transformation, ViralAnimalsAntiviral AgentsCarcinoma, HepatocellularHepatitis BHepatitis B virusHumansLiver NeoplasmsAntiviral AgentsCell biologyChronic hepatitis B infectionHepatitis B VirusHepatocarcinogenesisHepatocellular carcinoma

Identifiers

PMID25206269
PMCPMC4155355
OpenAlexW2064364170

What OpenQuestion holds

Textmetadata
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.