Evidence map›Paper›PMID 30177788›Full record

ArticleScientific reports2018

Activation of hepatic stem cells compartment during hepatocarcinogenesis in a HBsAg HBV-transgenic mouse model.

Beatrice Anfuso, Korri E El-Khobar, Susan I Ie, Claudio Avellini, Oriano Radillo, Alan Raseni, Claudio Tiribelli, Caecilia H C Sukowati

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 24% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. State of the art treatment of hepatitis B virus hepatocellular carcinoma and the role of hepatitis B surface antigen post-liver transplantation and resection.Liver international : official journal of the International Association for the Study of the Liver · 2022
    Review
  7. Article
  8. Article
  9. Article
  10. 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

8 authors at 4 institutions in 2 countries.

Beatrice AnfusoFondazione Italiana Fegato, AREA Science Park Basovizza, SS14 km 163.5, 34149, Trieste, Italy.ORCID 0000-0001-7819-6830
Korri E El-KhobarEijkman Institute for Molecular Biology, Jl. Diponegoro 69, 10430, Jakarta, Indonesia.
Susan I IeEijkman Institute for Molecular Biology, Jl. Diponegoro 69, 10430, Jakarta, Indonesia.
Claudio AvelliniDepartment of Medical and Biological Sciences, University Hospital, Piazzale Santa Maria della Misericordia 15, 33100, Udine, Italy.
Oriano RadilloLaboratory of Clinical Analysis, Children Hospital Burlo Garofolo IRCCS, Via dell'Istria, 65, 34137, Trieste, Italy.
Alan RaseniLaboratory of Clinical Analysis, Children Hospital Burlo Garofolo IRCCS, Via dell'Istria, 65, 34137, Trieste, Italy.
Claudio TiribelliFondazione Italiana Fegato, AREA Science Park Basovizza, SS14 km 163.5, 34149, Trieste, Italy.ORCID 0000-0001-6596-7595
Caecilia H C SukowatiFondazione Italiana Fegato, AREA Science Park Basovizza, SS14 km 163.5, 34149, Trieste, Italy. caecilia.sukowati@fegato.it.ORCID 0000-0001-9699-7578
Fondazione Italiana Fegato · ITEijkman Institute for Molecular Biology · IDIRCCS Materno Infantile Burlo Garofolo · ITOspedale Santa Maria della Misericordia di Udine · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic infection of Hepatitis B Virus (HBV) is one of the highest risk factors of hepatocellular carcinoma (HCC). The accumulation of HBV surface antigen (HBsAg) into hepatocytes induces inflammation and oxidative stress, impairing their replicative ability and allowing the activation of the hepatic stem cells (SC) compartment. This study aimed to understand the involvement of SC during hepatocarcinogenesis in HBsAg-related liver damage, from early injury until HCC. HBsAg-transgenic (TG) and wild type (WT) mouse were followed at several stages of the liver damage: inflammation, early hepatocytes damage, dysplasia, and HCC. Serum transaminases, liver histology, and diagnostic data were collected. The expressions of SC and cancer stem cells (CSC) markers was analyzed by RT-qPCR, immunohistochemistry and Western blot. Starting from 3 months, TG animals showed a progressive liver damage characterized by transaminases increase. The up-regulations of SCs markers Cd34 and Sca-1 started from the beginning of the inflammatory stage while progressive increase of Krt19 and Sox9 and CSCs markers Epcam and Cd133 from early hepatic injury. The expressions of Cd133, Cd34, and Afp were significantly higher in HCC compared to paired non-HCC tissue, in contrast to Epcam and Krt19. Western blot and IHC confirmed the positivity of Cd34 and Cd133 in small cells subpopulation.

Indexed as

AC133 AntigenAnimalsAntigens, CD34Antigens, LyBiomarkers, TumorCarcinogenesisCarcinoma, HepatocellularDisease Models, AnimalEpithelial Cell Adhesion MoleculeGene ExpressionHepatitis B, ChronicHepatitis B Surface AntigensHepatitis B virusHepatocytesHumansKeratin-19AC133 Antigenalpha-fetoprotein receptor, mouseAntigens, CD34Antigens, LyBiomarkers, TumorEpithelial Cell Adhesion MoleculeHepatitis B Surface AntigensKeratin-19Ly6a protein, mouseMembrane ProteinsProm1 protein, mouseReceptors, PeptideSox9 protein, mouseSOX9 Transcription FactorTransaminases

Identifiers

PMID30177788
PMCPMC6120871
OpenAlexW2889194305

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.