Evidence map›Paper›PMID 24958746›Full record

ArticleToxicologic pathology2015

Gene expression of mesothelioma in vinylidene chloride-exposed F344/N rats reveal immune dysfunction, tissue damage, and inflammation pathways.

Pamela E Blackshear, Arun R Pandiri, Hiroaki Nagai, Sachin Bhusari, Hue-Hua Hong, Thai-Vu T Ton, Natasha P Clayton, Michael Wyde, Keith R Shockley, Shyamal D Peddada and 3 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Toxicologic pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.5field-weighted citation impact, top 29% 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

0 citing papers in PubMed, 10 citations in OpenAlex.

No citing paper in PubMed yet.

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

13 authors at 4 institutions in 1 country.

Pamela E BlackshearCellular and Molecular Pathology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA Integrated Laboratory Systems, Inc., Research Triangle Park, North Carolina, USA.
Arun R PandiriCellular and Molecular Pathology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA Experimental Pathology Laboratories, Inc., Research Triangle Park, North Carolina, USA.
Hiroaki NagaiCellular and Molecular Pathology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA.
Sachin BhusariCellular and Molecular Pathology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA.
Hue-Hua HongCellular and Molecular Pathology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA.
Thai-Vu T TonCellular and Molecular Pathology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA.
Natasha P ClaytonCellular and Molecular Pathology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA.
Michael WydeExperimental Toxicology Group, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA.
Keith R ShockleyBiostatistics Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA.
Shyamal D PeddadaBiostatistics Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA.
Kevin E GerrishLaboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA.
Robert C SillsCellular and Molecular Pathology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA.
Mark J HoenerhoffCellular and Molecular Pathology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA hoenerho@med.umich.edu.
National Institute of Environmental Health Sciences · USNational Institutes of Health · USExperimental Pathology Laboratories · USResearch Triangle Park Foundation · US

Funding

Gene Expression and MicroarraysZICES102445 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI GERRISH, KEVIN · 2009 to 2025
$31.6M
DNA Microarray Data AnalysisZIAES103166 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI SHOCKLEY, KEITH · 2013 to 2025
$1.3M
Collaborative research in environmental health sciencesZIAES103066 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI PEDDADA, SHYAMAL · 2012 to 2017
$732k
Research and testing activities for the National Toxicology Program (NTP)ZIAES103227 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI TICE, RAYMOND · 2014 to 2014
$514k
Intramural NIH HHS Z99 ES999999
6 · The paper itself

Abstract

A majority (∼80%) of human malignant mesotheliomas are asbestos-related. However, non-asbestos risk factors (radiation, chemicals, and genetic factors) account for up to 30% of cases. A recent 2-year National Toxicology Program carcinogenicity bioassay showed that male F344/N rats exposed to the industrial toxicant vinylidene chloride (VDC) resulted in a marked increase in malignant mesothelioma. Global gene expression profiles of these tumors were compared to spontaneous mesotheliomas and the F344/N rat mesothelial cell line (Fred-PE) in order to characterize the molecular features and chemical-specific profiles of mesothelioma in VDC-exposed rats. As expected, mesotheliomas from control and VDC-exposed rats shared pathways associated with tumorigenesis, including cellular and tissue development, organismal injury, embryonic development, inflammatory response, cell cycle regulation, and cellular growth and proliferation, while mesotheliomas from VDC-exposed rats alone showed overrepresentation of pathways associated with pro-inflammatory pathways and immune dysfunction such as the nuclear factor kappa-light-chain-enhancer of activated B cells signaling pathway, interleukin (IL)-8 and IL-12 signaling, interleukin responses, Fc receptor signaling, and natural killer and dendritic cells signaling, as well as overrepresentation of DNA damage and repair. These data suggest that a chronic, pro-inflammatory environment associated with VDC exposure may exacerbate disturbances in oncogene, growth factor, and cell cycle regulation, resulting in an increased incidence of mesothelioma.

Indexed as

AnimalsCell Line, TumorDichloroethylenesDNA DamageFemaleGene Expression Regulation, NeoplasticGenes, cdcImmune System DiseasesInflammationLung NeoplasmsMaleMesotheliomaMesothelioma, MalignantMicroarray AnalysisPeritoneal NeoplasmsRatsDichloroethylenesRNA, Neoplasmvinylidene chlorideF344/N ratFred-PE cellsgene expressionmesothelial cellmesotheliomamicroarrayNational Toxicology Programvinylidene chloride

Identifiers

PMID24958746
PMCPMC4275413
OpenAlexW2133063088

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.