Evidence map›Paper›PMID 27388901›Full record

ArticlePloS one2016

Characterization of Breast Cancer Preclinical Models Reveals a Specific Pattern of Macrophage Polarization.

David Vallerand, Gérald Massonnet, Fatima Kébir, David Gentien, Zofia Maciorowski, Pierre De la Grange, Brigitte Sigal-Zafrani, Marion Richardson, Sandrine Humbert, Aurélie Thuleau and 9 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Overexpression of Nucleolin and Associated Genes in Prostate Cancer.International journal of molecular sciences · 2022
    Article
  5. Article
  6. Review
  7. 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

19 authors.

David VallerandTranslational Research Department, Laboratory of Preclinical Investigation, Institut Curie, PSL University, Paris, France.
Gérald MassonnetTranslational Research Department, Laboratory of Preclinical Investigation, Institut Curie, PSL University, Paris, France.
Fatima KébirDepartment of Pathology, Institut Curie, Paris, France.
David GentienPlatform of Molecular Biology Facilities, Institut Curie, PSL University, Paris, France.
Zofia MaciorowskiFlow Cytometry Core Facility, Institut Curie, PSL University, Paris, France.
Pierre De la GrangeGenoSplice Technology, Institut Universitaire d'Hématologie, Paris, France.
Brigitte Sigal-ZafraniDepartment of Pathology, Institut Curie, Paris, France.
Marion RichardsonDepartment of Pathology, Institut Curie, Paris, France.
Sandrine HumbertCNRS UMR3306, INSERM U1005, Institut Curie, PSL University, Orsay, France.
Aurélie ThuleauTranslational Research Department, Laboratory of Preclinical Investigation, Institut Curie, PSL University, Paris, France.
Franck AssayagTranslational Research Department, Laboratory of Preclinical Investigation, Institut Curie, PSL University, Paris, France.
Ludmilla de PlaterTranslational Research Department, Laboratory of Preclinical Investigation, Institut Curie, PSL University, Paris, France.
André NicolasDepartment of Pathology, Institut Curie, Paris, France.
Suzy SchollDepartment of Medical Oncology, Institut Curie, Institut Curie, Paris, France.
Elisabetta MarangoniTranslational Research Department, Laboratory of Preclinical Investigation, Institut Curie, PSL University, Paris, France.
Stefan WeigandRoche Diagnostics GmbH, Penzberg, Germany.
Sergio Roman-RomanTranslational Research Department, Institut Curie, PSL University, Paris, France.
Ariel SavinaInstitut Roche, Boulogne-Billancourt, France.
Didier DecaudinTranslational Research Department, Laboratory of Preclinical Investigation, Institut Curie, PSL University, Paris, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Drug discovery efforts have focused on the tumor microenvironment in recent years. However, few studies have characterized the stroma component in patient-derived xenografts (PDXs) and genetically engineered mouse models (GEMs). In this study, we characterized the stroma in various models of breast cancer tumors in mice. We performed transcriptomic and flow cytometry analyses on murine populations for a series of 25 PDXs and the two most commonly used GEMs (MMTV-PyMT and MMTV-erBb2). We sorted macrophages from five models. We then profiled gene expression in these cells, which were also subjected to flow cytometry for phenotypic characterization. Hematopoietic cell composition, mostly macrophages and granulocytes, differed between tumors. Macrophages had a specific polarization phenotype related to their M1/M2 classification and associated with the expression of genes involved in the recruitment, invasion and metastasis processes. The heterogeneity of the stroma component of the models studied suggests that tumor cells modify their microenvironment to satisfy their needs. Our observations suggest that such models are of relevance for preclinical studies.

Indexed as

AnimalsBreast NeoplasmsCell SeparationDisease Models, AnimalErb-b2 Receptor Tyrosine KinasesFemaleFlow CytometryGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMacrophagesMammary Neoplasms, AnimalMiceMice, TransgenicNeoplasm MetastasisPhenotypeERBB2 protein, humanErb-b2 Receptor Tyrosine Kinases

Identifiers

PMID27388901
PMCPMC4936680

What OpenQuestion holds

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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.