Evidence map›Paper›PMID 21244661›Full record

ArticleGenome biology2011

Network analysis of skin tumor progression identifies a rewired genetic architecture affecting inflammation and tumor susceptibility.

David A Quigley, Minh D To, Il Jin Kim, Kevin K Lin, Donna G Albertson, Jonas Sjolund, Jesús Pérez-Losada, Allan Balmain

Open access · goldAbstract read
In one paragraph

Article in Genome biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.2field-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

27 citing papers in PubMed, 49 citations in OpenAlex.

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  16. The developing story of Sprouty and cancer.Cancer metastasis reviews · 2014
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  19. A network perspective on unraveling the role of TRP channels in biology and disease.Pflugers Archiv : European journal of physiology · 2014
    Review
  20. 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

8 authors at 3 institutions in 2 countries.

David A QuigleyHelen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA 94158, USA.
Minh D To
Il Jin Kim
Kevin K Lin
Donna G Albertson
Jonas Sjolund
Jesús Pérez-Losada
Allan Balmain
University of California, San Francisco · USUCSF Helen Diller Family Comprehensive Cancer Center · USUniversidad de Salamanca · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGermline polymorphisms can influence gene expression networks in normal mammalian tissues and can affect disease susceptibility. We and others have shown that analysis of this genetic architecture can identify single genes and whole pathways that influence complex traits, including inflammation and cancer susceptibility. Whether germline variants affect gene expression in tumors that have undergone somatic alterations, and the extent to which these variants influence tumor progression, is unknown.

resultsUsing an integrated linkage and genomic analysis of a mouse model of skin cancer that produces both benign tumors and malignant carcinomas, we document major changes in germline control of gene expression during skin tumor development resulting from cell selection, somatic genetic events, and changes in the tumor microenvironment. The number of significant expression quantitative trait loci (eQTL) is progressively reduced in benign and malignant skin tumors when compared to normal skin. However, novel tumor-specific eQTL are detected for several genes associated with tumor susceptibility, including IL18 (Il18), Granzyme E (Gzme), Sprouty homolog 2 (Spry2), and Mitogen-activated protein kinase kinase 4 (Map2k4).

conclusionsWe conclude that the genetic architecture is substantially altered in tumors, and that eQTL analysis of tumors can identify host factors that influence the tumor microenvironment, mitogen-activated protein (MAP) kinase signaling, and cancer susceptibility.

Indexed as

Gene Regulatory NetworksGenetic Predisposition to DiseaseAnimalsBiomarkers, TumorCell Transformation, NeoplasticComparative Genomic HybridizationDisease ProgressionGene Expression Regulation, NeoplasticInflammationMiceMitogen-Activated Protein KinasesPolymorphism, GeneticQuantitative Trait LociSignal TransductionSkin NeoplasmsBiomarkers, TumorMitogen-Activated Protein Kinases

Identifiers

PMID21244661
PMCPMC3091303
OpenAlexW2098935079

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.