Evidence map›Paper›PMID 25601208›Full record

ArticleStem cell reports2015

Disequilibrium of BMP2 levels in the breast stem cell niche launches epithelial transformation by overamplifying BMPR1B cell response.

Marion Chapellier, Elodie Bachelard-Cascales, Xenia Schmidt, Flora Clément, Isabelle Treilleux, Emmanuel Delay, Alexandre Jammot, Christine Ménétrier-Caux, Gaëtan Pochon, Roger Besançon and 6 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2015. 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
3.7field-weighted citation impact, top 5% 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, 67 citations in OpenAlex.

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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

16 authors at 7 institutions in 1 country.

Marion ChapellierCNRS UMR5286, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Inserm U1052, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Université de Lyon, 69000 Lyon, France; Department of Immunity, Virus, and Microenvironment, 69000 Lyon, France; Université de Lyon 1, ISPB, 69000 Lyon, France.
Elodie Bachelard-CascalesInserm U916, Institut Bergonié, University of Bordeaux, 33076 Bordeaux, France.
Xenia SchmidtCNRS UMR5286, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Inserm U1052, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Université de Lyon, 69000 Lyon, France; Department of Immunity, Virus, and Microenvironment, 69000 Lyon, France; Université de Lyon 1, ISPB, 69000 Lyon, France.
Flora ClémentCNRS UMR5286, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Inserm U1052, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Université de Lyon, 69000 Lyon, France; Department of Immunity, Virus, and Microenvironment, 69000 Lyon, France; Université de Lyon 1, ISPB, 69000 Lyon, France.
Isabelle TreilleuxCNRS UMR5286, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Inserm U1052, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Université de Lyon, 69000 Lyon, France; Department of Immunity, Virus, and Microenvironment, 69000 Lyon, France; Université de Lyon 1, ISPB, 69000 Lyon, France; Centre Léon Bérard, 69000 Lyon, France.
Emmanuel DelayCNRS UMR5286, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Inserm U1052, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Université de Lyon, 69000 Lyon, France; Department of Immunity, Virus, and Microenvironment, 69000 Lyon, France; Université de Lyon 1, ISPB, 69000 Lyon, France; Centre Léon Bérard, 69000 Lyon, France.
Alexandre JammotCNRS UMR5286, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Inserm U1052, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Université de Lyon, 69000 Lyon, France; Department of Immunity, Virus, and Microenvironment, 69000 Lyon, France; Université de Lyon 1, ISPB, 69000 Lyon, France.
Christine Ménétrier-CauxCNRS UMR5286, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Inserm U1052, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Université de Lyon, 69000 Lyon, France; Department of Immunity, Virus, and Microenvironment, 69000 Lyon, France; Université de Lyon 1, ISPB, 69000 Lyon, France; Centre Léon Bérard, 69000 Lyon, France.
Gaëtan PochonCNRS UMR5286, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Inserm U1052, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Université de Lyon, 69000 Lyon, France; Department of Immunity, Virus, and Microenvironment, 69000 Lyon, France; Université de Lyon 1, ISPB, 69000 Lyon, France.
Roger BesançonCNRS UMR5286, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Inserm U1052, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Université de Lyon, 69000 Lyon, France; Department of Immunity, Virus, and Microenvironment, 69000 Lyon, France; Université de Lyon 1, ISPB, 69000 Lyon, France.
Thibault VoeltzelCNRS UMR5286, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Inserm U1052, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Université de Lyon, 69000 Lyon, France; Department of Immunity, Virus, and Microenvironment, 69000 Lyon, France; Université de Lyon 1, ISPB, 69000 Lyon, France.
Claude Caron de FromentelCNRS UMR5286, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Inserm U1052, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Université de Lyon, 69000 Lyon, France; Department of Immunity, Virus, and Microenvironment, 69000 Lyon, France; Université de Lyon 1, ISPB, 69000 Lyon, France.
Christophe CauxCNRS UMR5286, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Inserm U1052, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Université de Lyon, 69000 Lyon, France; Department of Immunity, Virus, and Microenvironment, 69000 Lyon, France; Université de Lyon 1, ISPB, 69000 Lyon, France; Centre Léon Bérard, 69000 Lyon, France.
Jean-Yves BlayCNRS UMR5286, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Inserm U1052, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Université de Lyon, 69000 Lyon, France; Department of Immunity, Virus, and Microenvironment, 69000 Lyon, France; Université de Lyon 1, ISPB, 69000 Lyon, France; Centre Léon Bérard, 69000 Lyon, France.
Richard IggoInserm U916, Institut Bergonié, University of Bordeaux, 33076 Bordeaux, France.
Véronique Maguer-SattaCNRS UMR5286, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Inserm U1052, Centre de Recherche en Cancérologie de Lyon, 69000 Lyon, France; Université de Lyon, 69000 Lyon, France; Department of Immunity, Virus, and Microenvironment, 69000 Lyon, France; Université de Lyon 1, ISPB, 69000 Lyon, France. Electronic address: veronique.maguer-satta@lyon.unicancer.fr.
Centre National de la Recherche Scientifique · FRInserm · FRCentre de Recherche en Cancérologie de Lyon · FRUniversité Claude Bernard Lyon 1 · FRCentre Léon Bérard · FRImmunité et Cancer · FRUniversité de Bordeaux · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Understanding the mechanisms of cancer initiation will help to prevent and manage the disease. At present, the role of the breast microenvironment in transformation remains unknown. As BMP2 and BMP4 are important regulators of stem cells and their niches in many tissues, we investigated their function in early phases of breast cancer. BMP2 production by tumor microenvironment appeared to be specifically upregulated in luminal tumors. Chronic exposure of immature human mammary epithelial cells to high BMP2 levels initiated transformation toward a luminal tumor-like phenotype, mediated by the receptor BMPR1B. Under physiological conditions, BMP2 controlled the maintenance and differentiation of early luminal progenitors, while BMP4 acted on stem cells/myoepithelial progenitors. Our data also suggest that microenvironment-induced overexpression of BMP2 may result from carcinogenic exposure. We reveal a role for BMP2 and the breast microenvironment in the initiation of stem cell transformation, thus providing insight into the etiology of luminal breast cancer.

Indexed as

Gene AmplificationBone Morphogenetic Protein 2Bone Morphogenetic Protein Receptors, Type IBone Morphogenetic ProteinsBreast NeoplasmsCarcinogensCell Line, TumorCell Transformation, NeoplasticEpithelial CellsFemaleGene Expression Regulation, NeoplasticHumansImmunohistochemistryNeoplastic Stem CellsSignal TransductionStem Cell NicheBone Morphogenetic Protein 2Bone Morphogenetic Protein Receptors, Type IBone Morphogenetic ProteinsCarcinogens

Identifiers

PMID25601208
PMCPMC4325271
OpenAlexW2088854061

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.