Evidence map›Paper›PMID 21571946›Full record

ArticleToxicologic pathology2011

Global gene profiling of spontaneous hepatocellular carcinoma in B6C3F1 mice: similarities in the molecular landscape with human liver cancer.

Mark J Hoenerhoff, Arun R Pandiri, Stephanie A Lahousse, Hu-Hua Hong, Tai-Vu Ton, Tiwanda Masinde, Scott S Auerbach, Kevin Gerrish, Pierre R Bushel, Keith R Shockley and 2 more

Open access · greenAbstract read
In one paragraph

Article in Toxicologic pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 45 citations in OpenAlex.

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  15. Molecular mechanisms of fibrosis-associated promotion of liver carcinogenesis.Toxicological sciences : an official journal of the Society of Toxicology · 2013
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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

12 authors at 2 institutions in 1 country.

Mark J HoenerhoffCellular and Molecular Pathology Branch, National Institute of Environmental Health Science, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA. hoenerhm@niehs.nih.gov
Arun R Pandiri
Stephanie A Lahousse
Hu-Hua Hong
Tai-Vu Ton
Tiwanda Masinde
Scott S Auerbach
Kevin Gerrish
Pierre R Bushel
Keith R Shockley
Shyamal D Peddada
Robert C Sills
National Institute of Environmental Health Sciences · USNational Institutes of Health · US

Funding

Gene Expression and MicroarraysZICES102445 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI GERRISH, KEVIN · 2009 to 2025
$31.6M
Microarray and Genome InformaticsZIAES102345 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI BUSHEL, ROBERT · 2009 to 2021
$10.8M
Genetic Alterations In Rodent CancerZIAES021219 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI SILLS, ROBERT · 2009 to 2013
$6.0M
NIEHS Statistical Consulting ServiceZIAES045005 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI PEDDADA, SHYAMAL · 2009 to 2011
$2.8M
Collaborative research in environmental health sciencesZIAES103066 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI PEDDADA, SHYAMAL · 2012 to 2017
$732k
Intramural NIH HHS Z99 ES999999
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is an important cause of morbidity and mortality worldwide. Although the risk factors of human HCC are well known, the molecular pathogenesis of this disease is complex, and in general, treatment options remain poor. The use of rodent models to study human cancer has been extensively pursued, both through genetically engineered rodents and rodent models used in carcinogenicity and toxicology studies. In particular, the B6C3F1 mouse used in the National Toxicology Program (NTP) two-year bioassay has been used to evaluate the carcinogenic effects of environmental and occupational chemicals, and other compounds. The high incidence of spontaneous HCC in the B6C3F1 mouse has challenged its use as a model for chemically induced HCC in terms of relevance to the human disease. Using global gene expression profiling, we identify the dysregulation of several mediators similarly altered in human HCC, including re-expression of fetal oncogenes, upregulation of protooncogenes, downregulation of tumor suppressor genes, and abnormal expression of cell cycle mediators, growth factors, apoptosis regulators, and angiogenesis and extracellular matrix remodeling factors. Although major differences in etiology and pathogenesis remain between human and mouse HCC, there are important similarities in global gene expression and molecular pathways dysregulated in mouse and human HCC. These data provide further support for the use of this model in hazard identification of compounds with potential human carcinogenicity risk, and may help in better understanding the mechanisms of tumorigenesis resulting from chemical exposure in the NTP two-year carcinogenicity bioassay.

Indexed as

AnimalsApoptosisBlotting, WesternCarcinogenicity TestsCarcinogensCarcinoma, HepatocellularCell CycleComputational BiologyDatabases, GeneticDisease Models, AnimalDown-RegulationFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticGenes, Tumor SuppressorGenetic Association StudiesCarcinogensTranscription Factors

Identifiers

PMID21571946
PMCPMC4955670
OpenAlexW2142869689

What OpenQuestion holds

Textmetadata
LicenceTDM
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.