Evidence map›Paper›PMID 15084239›Full record

ArticleBreast cancer research : BCR2004

Molecular analysis of metastasis in a polyomavirus middle T mouse model: the role of osteopontin.

Katayoun Alavi Jessen, Stephenie Y Liu, Clifford G Tepper, Juliana Karrim, Erik T McGoldrick, Andrea Rosner, Robert J Munn, Lawrence J T Young, Alexander D Borowsky, Robert D Cardiff and 1 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in Breast cancer research : BCR, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.3field-weighted citation impact, top 10% 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

33 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
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  5. A Syngeneic ErbB2 Mammary Cancer Model for Preclinical Immunotherapy Trials.Journal of mammary gland biology and neoplasia · 2019
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  11. Role of TGF-β signaling in generation of CD39+CD73+ myeloid cells in tumors.Journal of immunology (Baltimore, Md. : 1950) · 2014
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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

11 authors at 2 institutions in 1 country.

Katayoun Alavi JessenDepartment of Pathology, University of California, Davis, School of Medicine, Sacramento, California, USA.
Stephenie Y Liu
Clifford G Tepper
Juliana Karrim
Erik T McGoldrick
Andrea Rosner
Robert J Munn
Lawrence J T Young
Alexander D Borowsky
Robert D Cardiff
Jeffrey P Gregg
University of California, Davis · USUniversity of California Davis Medical Center · US

Funding

UCD MUTANT MOUSE REGIONAL RESOURCE CENTER: GENSAT PROJECTU42RR014905 · NCRR · UNIVERSITY OF CALIFORNIA DAVIS · PI LLOYD, KC KENT · 1999 to 2011
$20.5M
BIOLOGY OF NEOPLASTIC TRANSFORMATION IN BREAST CANCERR01CA089140 · NCI · UNIVERSITY OF CALIFORNIA DAVIS · PI CARDIFF, ROBERT D · 2001 to 2005
$1.6M
NCI NIH HHS R01 CA089140NCI NIH HHS R01-CA89140-01NCRR NIH HHS U42 RR014905NCRR NIH HHS U42RR14905
6 · The paper itself

Abstract

introductionIn order to study metastatic disease, we employed the use of two related polyomavirus middle T transgenic mouse tumor transplant models of mammary carcinoma (termed Met and Db) that display significant differences in metastatic potential.

methodsThrough suppression subtractive hybridization coupled to the microarray, we found osteopontin (OPN) to be a highly expressed gene in the tumors of the metastatic mouse model, and a lowly expressed gene in the tumors of the lowly metastatic mouse model. We further analyzed the role of OPN in this model by examining sense and antisense constructs using in vitro and in vivo methods.

resultsWith in vivo metastasis assays, the antisense Met cells showed no metastatic tumor formation to the lungs of recipient mice, while wild-type Met cells, with higher levels of OPN, showed significant amounts of metastasis. The Db cells showed a significantly reduced metastasis rate in the in vivo metastasis assay as compared with the Met cells. Db cells with enforced overexpression of OPN showed elevated levels of OPN but did not demonstrate an increase in the rate of metastasis compared with the wild-type Db cells.

conclusionsWe conclude that OPN is an essential regulator of the metastatic phenotype seen in polyomavirus middle T-induced mammary tumors. Yet OPN expression alone is not sufficient to cause metastasis. These data suggest a link between metastasis and phosphatidylinositol-3-kinase-mediated transcriptional upregulation of OPN, but additional phosphatidylinositol-3-kinase-regulated genes may be essential in precipitating the metastasis phenotype in the polyomavirus middle T model.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsAntigens, Polyomavirus TransformingCell Transformation, NeoplasticCell Transformation, ViralFemaleGene Expression ProfilingGene LibraryLung NeoplasmsMammary Neoplasms, ExperimentalMiceNeoplasm ProteinsNeoplasm TransplantationOligodeoxyribonucleotides, AntisenseOsteopontinPhosphatidylinositol 3-KinasesAntigens, Polyomavirus TransformingNeoplasm ProteinsOligodeoxyribonucleotides, AntisenseOsteopontinPhosphatidylinositol 3-KinasesRecombinant Fusion ProteinsRNA, ComplementarySialoglycoproteinsSpp1 protein, mouse

Identifiers

PMID15084239
PMCPMC400667
OpenAlexW1538123806

What OpenQuestion holds

Textmetadata
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.