Evidence map›Paper›PMID 28484924›Full record

ArticleBreast cancer research and treatment2017

Development of mammary hyperplasia, dysplasia, and invasive ductal carcinoma in transgenic mice expressing the 8p11 amplicon oncogene NSD3.

Brittany Turner-Ivey, Ericka L Smith, Alex C Rutkovsky, Laura S Spruill, Jamie N Mills, Stephen P Ethier

Abstract read
In one paragraph

Article in Breast cancer research and treatment, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

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  5. PROTACs Targeting Epigenetic Proteins.Acta materia medica · 2023
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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

6 authors at 1 institution in 1 country.

Brittany Turner-IveyDepartment of Pathology and Laboratory Medicine, Hollings Cancer Center, Medical University of South Carolina, 68 President St, Charleston, SC, 29425, USA.
Ericka L SmithDepartment of Pathology and Laboratory Medicine, Hollings Cancer Center, Medical University of South Carolina, 68 President St, Charleston, SC, 29425, USA.
Alex C RutkovskyDepartment of Pathology and Laboratory Medicine, Hollings Cancer Center, Medical University of South Carolina, 68 President St, Charleston, SC, 29425, USA.
Laura S SpruillDepartment of Pathology and Laboratory Medicine, Hollings Cancer Center, Medical University of South Carolina, 68 President St, Charleston, SC, 29425, USA.
Jamie N MillsDepartment of Pathology and Laboratory Medicine, Hollings Cancer Center, Medical University of South Carolina, 68 President St, Charleston, SC, 29425, USA.
Stephen P EthierDepartment of Pathology and Laboratory Medicine, Hollings Cancer Center, Medical University of South Carolina, 68 President St, Charleston, SC, 29425, USA. ethier@musc.edu.ORCID http://orcid.org/0000-0003-4420-8594
Medical University of South Carolina · US

Funding

Translational Science Laboratory Shared ResourceP30CA138313 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI RAYMOND N. DUBOIS · 2009 to 2026
$42.7M
Breast cancer oncogenes on the 8p11 amplicon.R01CA100724 · NCI · WAYNE STATE UNIVERSITY · PI ETHIER, STEPHEN P. · 2003 to 2014
$3.5M
NCI NIH HHS P30 CA138313NCI NIH HHS R01 CA100724
6 · The paper itself

Abstract

purposeNSD3 has been implicated as a candidate driver oncogene from the 8p11-p12 locus, and we have previously published evidence for its amplification and overexpression in human breast cancer. This aim of this study was to further characterize the transforming function of NSD3 in vivo.

methodsWe generated a transgenic mouse model in which NSD3 gene expression was driven by the MMTV promoter and expressed in mammary epithelium of FVB mice. Mammary glands were fixed and whole mounts were stained with carmine to visualize gland structure. Mammary tumors were formalin-fixed, and paraffin embedded (FFPE) tumors were stained with hematoxylin and eosin.

resultsPups born to transgenic females were significantly underdeveloped compared to pups born to WT females due to a lactation defect in transgenic female mice. Whole mount analysis of the mammary glands of transgenic female mice revealed a profound defect in functional differentiation of mammary gland alveoli that resulted in the lactation defect. We followed parous and virgin NSD3 transgenic and control mice to 50 weeks of age and observed that several NSD3 parous females developed mammary tumors. Whole mount analysis of the mammary glands of tumor-bearing mice revealed numerous areas of mammary hyperplasia and ductal dysplasia. Histological analysis showed that mammary tumors were high-grade ductal carcinomas, and lesions present in other mammary glands exhibited features of alveolar hyperplasia, ductal dysplasia, and carcinoma in situ.

conclusionsOur results are consistent with our previous studies and demonstrate that NSD3 is a transforming breast cancer oncogene.

Indexed as

AnimalsCarcinoma, Ductal, BreastCell Transformation, NeoplasticFemaleHistone-Lysine N-MethyltransferaseHumansHyperplasiaLactationMammary Neoplasms, ExperimentalMiceMice, TransgenicNeoplasm GradingNuclear ProteinsPromoter Regions, GeneticHistone-Lysine N-MethyltransferaseNSD3 protein, humanNuclear ProteinsAmpliconBreast cancerER positiveNSD3OncogeneTransgenic mouse modelWHSC1L1

Identifiers

PMID28484924
PMCPMC5928774
OpenAlexW2612638446

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Registered trials

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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.