Evidence map›Paper›PMID 27867514›Full record

ArticleClinical & translational immunology2016

Hepatitis C virus drives the pathogenesis of hepatocellular carcinoma: from immune evasion to carcinogenesis.

Miriam Canavese, Danushka Wijesundara, Guy J Maddern, Branka Grubor-Bauk, Ehud Hauben

Open access · goldAbstract read
In one paragraph

Article in Clinical & translational immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.5field-weighted citation impact, top 39% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

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  8. SNP rs2240688 inTranslational cancer research · 2020
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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

5 authors at 3 institutions in 1 country.

Miriam CanaveseLiver Metastasis Research Group, Discipline of Surgery, The Basil Hetzel Institute for Translational Health Research, The Queen Elizabeth Hospital, University of Adelaide , Adelaide, South Australia, Australia.
Danushka WijesundaraVirology Laboratory, Discipline of Surgery, The Basil Hetzel Institute for Translational Health Research, The Queen Elizabeth Hospital, University of Adelaide , Adelaide, South Australia, Australia.
Guy J MaddernLiver Metastasis Research Group, Discipline of Surgery, The Basil Hetzel Institute for Translational Health Research, The Queen Elizabeth Hospital, University of Adelaide , Adelaide, South Australia, Australia.
Branka Grubor-BaukVirology Laboratory, Discipline of Surgery, The Basil Hetzel Institute for Translational Health Research, The Queen Elizabeth Hospital, University of Adelaide , Adelaide, South Australia, Australia.
Ehud HaubenLiver Metastasis Research Group, Discipline of Surgery, The Basil Hetzel Institute for Translational Health Research, The Queen Elizabeth Hospital, University of Adelaide , Adelaide, South Australia, Australia.
Basil Hetzel Institute · AUUniversity of Adelaide · AUQueen Elizabeth Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Persistent hepatitis C virus (HCV) infection is associated with high incidence of hepatocellular carcinoma (HCC), the most common primary malignancy of the liver with over half a million new cases diagnosed annually worldwide. The aryl hydrocarbon receptor (AhR) is a ubiquitously expressed transcription factor and its activation by environmental chemicals and by its endogenous ligand kynurenine (Kyn) has been implicated in a variety of tumour-promoting processes such as transformation, tumorigenesis and in immunosuppression that enables tumour survival and growth. Kyn is generated constitutively by human tumour cells via tryptophan (Trp)-2,3-dioxygenase (TDO), a Trp-degrading enzyme expressed in liver, brain and cancer cells. Notably, it has been shown that TDO-derived Kyn suppresses anti-tumour immune responses, thus promoting tumour-cell survival through activation of the AhR pathway. In the context of HCV infection-associated HCC, it was shown that AhR signalling is increased in HCV-infected hepatocytes, and that modifications in the expression of AhR pathway-specific genes are associated with the progression of HCV infection into HCC. Based on these observations, we present and discuss here the hypothesis that HCV infection promotes HCC by modulation of the TDO-Kyn-AhR pathway, resulting in tumorigenesis as well as in suppression of both anti-HCV and anti-tumour immune responses.

Identifiers

PMID27867514
PMCPMC5099426
OpenAlexW2528166303

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.