Evidence map›Paper›PMID 24633177›Full record

ArticlePloS one2014

Xmrk, kras and myc transgenic zebrafish liver cancer models share molecular signatures with subsets of human hepatocellular carcinoma.

Weiling Zheng, Zhen Li, Anh Tuan Nguyen, Caixia Li, Alexander Emelyanov, Zhiyuan Gong

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

45 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
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  6. Transcriptional background effects on a tumor driver gene in different pigment cell types of medaka.Journal of experimental zoology. Part B, Molecular and developmental evolution · 2024
    Article
  7. Methods to Study Liver Disease Using Zebrafish Larvae.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  8. Article
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  10. eLife · 2023
    Article
  11. Zebrafish Models of Paediatric Brain Tumours.International journal of molecular sciences · 2022
    Review
  12. Article
  13. Article
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  15. Article
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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 2 institutions in 1 country.

Weiling ZhengDepartment of Biological Sciences, National University of Singapore, Singapore, Singapore.
Zhen LiDepartment of Biological Sciences, National University of Singapore, Singapore, Singapore.
Anh Tuan NguyenDepartment of Biological Sciences, National University of Singapore, Singapore, Singapore.
Caixia LiDepartment of Biological Sciences, National University of Singapore, Singapore, Singapore.
Alexander EmelyanovInstitute of Cell and Molecular Biology, Singapore, Singapore.
Zhiyuan GongDepartment of Biological Sciences, National University of Singapore, Singapore, Singapore.
National University of Singapore · SGInstitute of Molecular and Cell Biology · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previously three oncogene transgenic zebrafish lines with inducible expression of xmrk, kras or Myc in the liver have been generated and these transgenic lines develop oncogene-addicted liver tumors upon chemical induction. In the current study, comparative transcriptomic approaches were used to examine the correlation of the three induced transgenic liver cancers with human liver cancers. RNA profiles from the three zebrafish tumors indicated relatively small overlaps of significantly deregulated genes and biological pathways. Nevertheless, the three transgenic tumor signatures all showed significant correlation with advanced or very advanced human hepatocellular carcinoma (HCC). Interestingly, molecular signature from each oncogene-induced zebrafish liver tumor correlated with only a small subset of human HCC samples (24-29%) and there were conserved up-regulated pathways between the zebrafish and correlated human HCC subgroup. The three zebrafish liver cancer models together represented nearly half (47.2%) of human HCCs while some human HCCs showed significant correlation with more than one signature defined from the three oncogene-addicted zebrafish tumors. In contrast, commonly deregulated genes (21 up and 16 down) in the three zebrafish tumor models generally showed accordant deregulation in the majority of human HCCs, suggesting that these genes might be more consistently deregulated in a broad range of human HCCs with different molecular mechanisms and thus serve as common diagnosis markers and therapeutic targets. Thus, these transgenic zebrafish models with well-defined oncogene-induced tumors are valuable tools for molecular classification of human HCCs and for understanding of molecular drivers in hepatocarcinogenesis in each human HCC subgroup.

Indexed as

AnimalsAnimals, Genetically ModifiedCarcinoma, HepatocellularGene Expression Regulation, NeoplasticGenes, rasHumansLiver NeoplasmsLiver Neoplasms, ExperimentalProto-Oncogene Proteins c-mycReceptor Protein-Tyrosine KinasesZebrafishProto-Oncogene Proteins c-mycReceptor Protein-Tyrosine Kinases

Identifiers

PMID24633177
PMCPMC3954698
OpenAlexW2051882187

What OpenQuestion holds

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LicenceCC BY
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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.