Evidence map›Paper›PMID 21076615›Full record

ArticleNeoplasia (New York, N.Y.)2010

Loss of STAT1 from mouse mammary epithelium results in an increased Neu-induced tumor burden.

Peter J Klover, William J Muller, Gertraud W Robinson, Ruth M Pfeiffer, Daisuke Yamaji, Lothar Hennighausen

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

80 citing papers in PubMed, 104 citations in OpenAlex.

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  11. Analysis of intestinal epithelial cell responses tobioRxiv : the preprint server for biology · 2023
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20 more citing papers are in PubMed but not listed here.

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 4 institutions in 2 countries.

Peter J KloverLaboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA. peter_klover@yahoo.com
William J Muller
Gertraud W Robinson
Ruth M Pfeiffer
Daisuke Yamaji
Lothar Hennighausen
National Institute of Diabetes and Digestive and Kidney Diseases · USMcGill University Health Centre · CANational Cancer Institute · USNational Institutes of Health · US

Funding

Genetic Approaches To Understanding Organ Development and FunctionZIADK061000 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HENNIGHAUSEN, LOTHAR · 2009 to 2025
$24.7M
6 · The paper itself

Abstract

Type I and type II classes of interferons (IFNs) signal through the JAK/STAT1 pathway and are known to be important in adaptive and innate immune responses and in protection against tumors. Although STAT1 is widely considered a tumor suppressor, it remains unclear, however, if this function occurs in tumor cells (cell autonomous) or if STAT1 acts primarily through immune cells. Here, the question of whether STAT1 has a cell autonomous role in mammary tumor formation was addressed in a mouse model of ERBB2/neu-induced breast cancer in the absence and presence of STAT1. For this purpose, mice that carry floxed Stat1 alleles, which permit cell-specific removal of STAT1, were generated. To induce tumors only in mammary cells lacking STAT1, Stat1 floxed mice were crossed with transgenic mice that express cre recombinase and the neu oncogene under the mouse mammary tumor virus LTR (Stat1fl/fl NIC). Stat1 was effectively deleted in mammary epithelium of virgin Stat1fl/fl NIC females. Time-to-tumor onset was significantly shorter in Stat1fl/fl NIC females than in WT NIC (Wilcoxon rank sum test, P = .02). The median time-to-tumor onset in the Stat1fl/fl NIC mice was 49.4 weeks, whereas it was 62.4 weeks in the WT NIC mice. These results suggest that STAT1 in mammary epithelial cells may play a role in suppressing tumorigenesis. The Stat1 floxed allele described in this study is also a unique resource to determine the cellular targets of IFNs and STAT1 action, which should aid our understanding and appreciation of these pathways.

Indexed as

AnimalsBlotting, WesternCell NucleusCells, CulturedEmbryo, MammalianEpitheliumErb-b2 Receptor Tyrosine KinasesFemaleFibroblastsKaplan-Meier EstimateMaleMammary Glands, AnimalMammary Neoplasms, AnimalMiceMice, 129 StrainMice, KnockoutErb-b2 Receptor Tyrosine KinasesStat1 protein, mouseSTAT1 Transcription Factor

Identifiers

PMID21076615
PMCPMC2978912
OpenAlexW1608112211

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.