Evidence map›Paper›PMID 26819517›Full record

ReviewWorld journal of gastroenterology2016

Significance of hepatitis virus infection in the oncogenic initiation of hepatocellular carcinoma.

Caecilia H C Sukowati, Korri E El-Khobar, Susan I Ie, Beatrice Anfuso, David H Muljono, Claudio Tiribelli

Open access · bronzeAbstract readReview
In one paragraph

Review in World journal of gastroenterology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
7.9field-weighted citation impact, top 2% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.

  1. Pooled it
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  19. Virome and bacteriome: two sides of the same coin.Current opinion in virology · 2019
    Review
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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

6 authors at 1 institution in 3 countries.

Caecilia H C SukowatiCaecilia HC Sukowati, Beatrice Anfuso, Claudio Tiribelli, Fondazione Italiana Fegato ONLUS, AREA Science Park Basovizza, 34149 Trieste, Italy.
Korri E El-KhobarCaecilia HC Sukowati, Beatrice Anfuso, Claudio Tiribelli, Fondazione Italiana Fegato ONLUS, AREA Science Park Basovizza, 34149 Trieste, Italy.
Susan I IeCaecilia HC Sukowati, Beatrice Anfuso, Claudio Tiribelli, Fondazione Italiana Fegato ONLUS, AREA Science Park Basovizza, 34149 Trieste, Italy.
Beatrice AnfusoCaecilia HC Sukowati, Beatrice Anfuso, Claudio Tiribelli, Fondazione Italiana Fegato ONLUS, AREA Science Park Basovizza, 34149 Trieste, Italy.
David H MuljonoCaecilia HC Sukowati, Beatrice Anfuso, Claudio Tiribelli, Fondazione Italiana Fegato ONLUS, AREA Science Park Basovizza, 34149 Trieste, Italy.
Claudio TiribelliCaecilia HC Sukowati, Beatrice Anfuso, Claudio Tiribelli, Fondazione Italiana Fegato ONLUS, AREA Science Park Basovizza, 34149 Trieste, Italy.
The University of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is one of the most common causes of cancer-related death worldwide. Chronic infection of hepatitis B virus (HBV) and/or hepatitis C virus (HCV) is a major risk factor in the development of the HCC, independently from excessive alcohol abuse and metabolic disease. Since the biology of HBV and HCV is different, their oncogenic effect may go through different mechanisms, direct and/or indirect. Viral hepatitis infection is associated with cellular inflammation, oxidative stress, and DNA damage, that may lead to subsequent hepatic injuries such as chronic hepatitis, fibrosis, cirrhosis, and finally HCC. Direct oncogenic properties of these viruses are related with their genotypic characteristics and the ability of viral proteins to interact with host proteins, thus altering the molecular pathways balance of the cells. In addition, the integration of HBV DNA, especially the gene S and X, in a particular site of the host genome can disrupt chromosomal stability and may activate various oncogenic mechanisms, including those in hematopoietic cells. Recently, several studies also had demonstrated that viral hepatitis could trigger the population of hepatic cancer stem cells. This review summarize available pre-clinical and clinical data in literature regarding oncogenic properties of HBV and HCV in the early initiation of HCC.

Indexed as

Cell Transformation, ViralOncogenesAnimalsCarcinoma, HepatocellularGene Expression Regulation, NeoplasticGene Expression Regulation, ViralGenotypeHepacivirusHepatitis B, ChronicHepatitis B virusHepatitis C, ChronicHost-Pathogen InteractionsHumansLiver NeoplasmsNeoplastic Stem CellsRisk FactorsHepatitis B virusHepatitis C virusHepatocellular carcinomaOncogenicityViral pathogenicity

Identifiers

PMID26819517
PMCPMC4721983
OpenAlexW2406411725

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.