Evidence map›Paper›PMID 31277602›Full record

ArticleBMC cancer2019

The role of clonal communication and heterogeneity in breast cancer.

Ana Martín-Pardillos, Ángeles Valls Chiva, Gemma Bande Vargas, Pablo Hurtado Blanco, Roberto Piñeiro Cid, Pedro J Guijarro, Stefan Hümmer, Eva Bejar Serrano, Aitor Rodriguez-Casanova, Ángel Diaz-Lagares and 9 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

36 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Article
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  5. Tumor-Tissue Boundaries as Instructive Interfaces in Breast Cancer Cell Invasion.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  6. Article
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  8. Article
  9. Article
  10. Article
  11. Omics Technologies Improving Breast Cancer Research and Diagnostics.International journal of molecular sciences · 2023
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Cell Fate of Retinal Progenitor Cells: In Ovo UbC-StarTrack Analysis.International journal of molecular sciences · 2022
    Article
  19. Article
  20. 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 at 8 institutions in 1 country.

Ana Martín-PardillosTranslational Molecular Pathology Group, Vall d'Hebron Research Institute, Barcelona, Spain. ana.martin@vhir.org.ORCID http://orcid.org/0000-0003-1717-8465
Ángeles Valls ChivaTranslational Molecular Pathology Group, Vall d'Hebron Research Institute, Barcelona, Spain.
Gemma Bande VargasTranslational Molecular Pathology Group, Vall d'Hebron Research Institute, Barcelona, Spain.
Pablo Hurtado BlancoCancer Modelling Lab, Roche-CHUS Joint Unit, Santiago de Compostela, Spain.
Roberto Piñeiro CidCIBERONC (Centro de Investigación Biomédica en Red de Cáncer), Madrid, Spain.
Pedro J GuijarroTranslational Molecular Pathology Group, Vall d'Hebron Research Institute, Barcelona, Spain.
Stefan HümmerTranslational Molecular Pathology Group, Vall d'Hebron Research Institute, Barcelona, Spain.
Eva Bejar SerranoTranslational Molecular Pathology Group, Vall d'Hebron Research Institute, Barcelona, Spain.
Aitor Rodriguez-CasanovaCancer Epigenomics, Translational Medical Oncology (Oncomet), Health Research Institute of Santiago (IDIS), University Clinical Hospital of Santiago (CHUS), Santiago de Compostela, Spain.
Ángel Diaz-LagaresCIBERONC (Centro de Investigación Biomédica en Red de Cáncer), Madrid, Spain.
Josep CastellviHospital Vall d'Hebron, Anatomía Patológica, Barcelona, Spain.
Samuel Miravet-VerdeEMBL/CRG Systems Biology Research Unit, Centre for Genomic Regulation (CRG), The Institute of Science and Technology, Barcelona, Spain.
Luis SerranoEMBL/CRG Systems Biology Research Unit, Centre for Genomic Regulation (CRG), The Institute of Science and Technology, Barcelona, Spain.
María Lluch-SenarEMBL/CRG Systems Biology Research Unit, Centre for Genomic Regulation (CRG), The Institute of Science and Technology, Barcelona, Spain.
Víctor SebastianDepartment of Chemical Engineering, Aragon Institute of Nanoscience (INA), University of Zaragoza, Zaragoza, Spain.
Ana BribianDepartment of Molecular, Cellular and Developmental Neurobiology, Instituto Cajal-CSIC, Madrid, Spain.
Laura López-MascaraqueDepartment of Molecular, Cellular and Developmental Neurobiology, Instituto Cajal-CSIC, Madrid, Spain.
Rafael López-LópezCancer Epigenomics, Translational Medical Oncology (Oncomet), Health Research Institute of Santiago (IDIS), University Clinical Hospital of Santiago (CHUS), Santiago de Compostela, Spain.
Santiago Ramón Y CajalTranslational Molecular Pathology Group, Vall d'Hebron Research Institute, Barcelona, Spain. sramon@vhebron.net.
Vall d'Hebron Institut de Recerca · ESInstituto de Investigación Sanitaria de Santiago · ESCentre for Genomic Regulation · ESInstituto Cajal · ESRoche (Spain) · ESInstitució Catalana de Recerca i Estudis Avançats · ESUniversidad de Zaragoza · ESVall d'Hebron Hospital Universitari · ES

Funding

Centro de Investigación Biomédica en Red de Cáncer CIBERONC; CB16/12/00363Fondo de Investigaciones Sanitarias PI17/02247 and PI14/01320FP7 People: Marie-Curie Actions (COFUND) 267128Generalitat de Catalunya AGAUR; 2017 SGR 1799 and 2014 SGR 1131ISCIII JR17/00016
6 · The paper itself

Abstract

backgroundCancer is a rapidly evolving, multifactorial disease that accumulates numerous genetic and epigenetic alterations. This results in molecular and phenotypic heterogeneity within the tumor, the complexity of which is further amplified through specific interactions between cancer cells. We aimed to dissect the molecular mechanisms underlying the cooperation between different clones.

methodsWe produced clonal cell lines derived from the MDA-MB-231 breast cancer cell line, using the UbC-StarTrack system, which allowed tracking of multiple clones by color: GFP C3, mKO E10 and Sapphire D7. Characterization of these clones was performed by growth rate, cell metabolic activity, wound healing, invasion assays and genetic and epigenetic arrays. Tumorigenicity was tested by orthotopic and intravenous injections. Clonal cooperation was evaluated by medium complementation, co-culture and co-injection assays.

resultsCharacterization of these clones in vitro revealed clear genetic and epigenetic differences that affected growth rate, cell metabolic activity, morphology and cytokine expression among cell lines. In vivo, all clonal cell lines were able to form tumors; however, injection of an equal mix of the different clones led to tumors with very few mKO E10 cells. Additionally, the mKO E10 clonal cell line showed a significant inability to form lung metastases. These results confirm that even in stable cell lines heterogeneity is present. In vitro, the complementation of growth medium with medium or exosomes from parental or clonal cell lines increased the growth rate of the other clones. Complementation assays, co-growth and co-injection of mKO E10 and GFP C3 clonal cell lines increased the efficiency of invasion and migration.

conclusionsThese findings support a model where interplay between clones confers aggressiveness, and which may allow identification of the factors involved in cellular communication that could play a role in clonal cooperation and thus represent new targets for preventing tumor progression.

Indexed as

Genetic HeterogeneityAnimalsApoptosisBreast NeoplasmsCell CommunicationCell Line, TumorCell MovementCell SurvivalClone CellsCoculture TechniquesCytokinesDNA Transposable ElementsFemaleGene ExpressionHeterograftsHumansCytokinesDNA Transposable ElementsBreastCancerCloneCommunicationCooperationHeterogeneityMDA-MB-231MetastasisTumor

Identifiers

PMID31277602
PMCPMC6612119
OpenAlexW2954287039

What OpenQuestion holds

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LicenceCC BY
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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.