Evidence map›Paper›PMID 31905933›Full record

ArticleInternational journal of molecular sciences2019

Overexpression of Hepatocyte Chemerin-156 Lowers Tumor Burden in a Murine Model of Diethylnitrosamine-Induced Hepatocellular Carcinoma.

Elisabeth M Haberl, Rebekka Pohl, Lisa Rein-Fischboeck, Susanne Feder, Christopher J Sinal, Astrid Bruckmann, Marcus Hoering, Sabrina Krautbauer, Gerhard Liebisch, Christa Buechler

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Chemerin-156 is the Active Isoform in Human Hepatic Stellate Cells.International journal of molecular sciences · 2020
    Article
  8. Article
  9. Article
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

10 authors at 3 institutions in 2 countries.

Elisabeth M HaberlDepartment of Internal Medicine I, Regensburg University Hospital, 93053 Regensburg, Germany.
Rebekka PohlDepartment of Internal Medicine I, Regensburg University Hospital, 93053 Regensburg, Germany.
Lisa Rein-FischboeckDepartment of Internal Medicine I, Regensburg University Hospital, 93053 Regensburg, Germany.
Susanne FederDepartment of Internal Medicine I, Regensburg University Hospital, 93053 Regensburg, Germany.
Christopher J SinalDepartment of Pharmacology, Dalhousie University, Halifax, NS B3H 4R2, Canada.
Astrid BruckmannBiochemistry Center Regensburg (BZR), Laboratory for RNA Biology, University of Regensburg, 93042 Regensburg, Germany.
Marcus HoeringInstitute of Clinical Chemistry and Laboratory Medicine, Regensburg University Hospital, 93053 Regensburg, Germany.
Sabrina KrautbauerInstitute of Clinical Chemistry and Laboratory Medicine, Regensburg University Hospital, 93053 Regensburg, Germany.
Gerhard LiebischInstitute of Clinical Chemistry and Laboratory Medicine, Regensburg University Hospital, 93053 Regensburg, Germany.
Christa BuechlerDepartment of Internal Medicine I, Regensburg University Hospital, 93053 Regensburg, Germany.ORCID 0000-0002-5635-3994
University Hospital Regensburg · DEDalhousie University · CAUniversity of Regensburg · DE

Funding

CIHR CJSDeutsche Forschungsgemeinschaft BU 1141/13-1
6 · The paper itself

Abstract

The tumor inhibitory potential of the highly active chemerin-156 isoform was described in orthotopic models of hepatocellular carcinoma (HCC). The majority of HCC arises in the fibrotic liver, which was not reproduced in these studies. Here, a potential therapeutic activity of chemerin-156 was evaluated in diethylnitrosamine (DEN)-induced liver cancer, which mimics fibrosis-associated HCC. Mice were infected with adeno-associated virus (AAV) six months after DEN injection to overexpress chemerin-156 in the liver, and animals injected with non-recombinant-AAV served as controls. Three months later, the animals were killed. Both groups were comparable with regard to liver steatosis and fibrosis. Of note, the number of very small tumors was reduced by chemerin-156. Anyhow, the expression of inflammatory and profibrotic genes was similar in larger tumors of control and chemerin-156-AAV-infected animals. Although genes with a role in lipid metabolism, like

Indexed as

AnimalsCarcinoma, HepatocellularChemokinesCholesterolDiethylnitrosamineDiglyceridesDisease Models, AnimalGene Expression Regulation, NeoplasticHepatocytesIntercellular Signaling Peptides and ProteinsLipid MetabolismLiverLiver NeoplasmsLiver Neoplasms, ExperimentalMaleMicechemerin protein, mouseChemokinesCholesterolCMKLR1 protein, mouseDiethylnitrosamineDiglyceridesIntercellular Signaling Peptides and ProteinsProtein IsoformsReceptors, ChemokineTriglyceridesadenoassociated viruschemerin activitychemokine-like receptor 1liverTriglycerides

Identifiers

PMID31905933
PMCPMC6982125
OpenAlexW2998386519

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.