Evidence map›Paper›PMID 24739973›Full record

ArticleNature2014

Oncogene-like induction of cellular invasion from centrosome amplification.

Susana A Godinho, Remigio Picone, Mithila Burute, Regina Dagher, Ying Su, Cheuk T Leung, Kornelia Polyak, Joan S Brugge, Manuel Théry, David Pellman

Abstract read
In one paragraph

Article in Nature, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 273 papers.

0numbers the graph read from it
0cells of the map it votes in
273citing papers in PubMed
19.0field-weighted citation impact, top 1% 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

273 citing papers in PubMed, 420 citations in OpenAlex.

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213 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

10 authors at 4 institutions in 3 countries.

Susana A Godinho1] Howard Hughes Medical Institute, Department of Pediatric Oncology, Dana-Farber Cancer Institute and Pediatric Hematology/Oncology, Children's Hospital, Boston, Massachusetts 02115, USA [2] Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA [3] Barts Cancer Institute, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK (S.A.G.); Department of Pharmacology, University of Minnesota, Minneapolis, Minnesota 55455, USA (C.T.L.).
Remigio Picone1] Howard Hughes Medical Institute, Department of Pediatric Oncology, Dana-Farber Cancer Institute and Pediatric Hematology/Oncology, Children's Hospital, Boston, Massachusetts 02115, USA [2] Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA.
Mithila Burute1] Institut de Recherche en Technologie et Science pour le Vivant, UMR5168 CEA/UJF/INRA/CNRS, Grenoble, France [2] Hôpital Saint Louis, Institut Universitaire d'Hematologie, U1160 INSERM/AP-HP/Université Paris Diderot, Paris 75010, France [3] CYTOO SA, Grenoble 38054, France.
Regina Dagher1] Howard Hughes Medical Institute, Department of Pediatric Oncology, Dana-Farber Cancer Institute and Pediatric Hematology/Oncology, Children's Hospital, Boston, Massachusetts 02115, USA [2] Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA.
Ying SuDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.
Cheuk T Leung1] Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA [2] Barts Cancer Institute, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK (S.A.G.); Department of Pharmacology, University of Minnesota, Minneapolis, Minnesota 55455, USA (C.T.L.).
Kornelia PolyakDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.
Joan S BruggeDepartment of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA.
Manuel Théry1] Institut de Recherche en Technologie et Science pour le Vivant, UMR5168 CEA/UJF/INRA/CNRS, Grenoble, France [2] Hôpital Saint Louis, Institut Universitaire d'Hematologie, U1160 INSERM/AP-HP/Université Paris Diderot, Paris 75010, France.
David Pellman1] Howard Hughes Medical Institute, Department of Pediatric Oncology, Dana-Farber Cancer Institute and Pediatric Hematology/Oncology, Children's Hospital, Boston, Massachusetts 02115, USA [2] Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA.
Harvard University · USHoward Hughes Medical Institute · USUniversité Grenoble Alpes · FRUniversité Joseph Fourier · FR

Funding

Polyploidy, aneuploidy and genome stabilityR01GM083299 · NIGMS · DANA-FARBER CANCER INST · PI PELLMAN, DAVID S · 2007 to 2015
$2.9M
European Research Council 310472Howard Hughes Medical InstituteNIGMS NIH HHS GM083299-1NIGMS NIH HHS R01 GM083299
6 · The paper itself

Abstract

Centrosome amplification has long been recognized as a feature of human tumours; however, its role in tumorigenesis remains unclear. Centrosome amplification is poorly tolerated by non-transformed cells and, in the absence of selection, extra centrosomes are spontaneously lost. Thus, the high frequency of centrosome amplification, particularly in more aggressive tumours, raises the possibility that extra centrosomes could, in some contexts, confer advantageous characteristics that promote tumour progression. Using a three-dimensional model system and other approaches to culture human mammary epithelial cells, we find that centrosome amplification triggers cell invasion. This invasive behaviour is similar to that induced by overexpression of the breast cancer oncogene ERBB2 (ref. 4) and indeed enhances invasiveness triggered by ERBB2. Our data indicate that, through increased centrosomal microtubule nucleation, centrosome amplification increases Rac1 activity, which disrupts normal cell-cell adhesion and promotes invasion. These findings demonstrate that centrosome amplification, a structural alteration of the cytoskeleton, can promote features of malignant transformation.

Indexed as

Genes, erbB-2AneuploidyBreastBreast NeoplasmsCell AdhesionCell LineCell Transformation, NeoplasticCentrosomeDisease ProgressionEnzyme ActivationEpithelial CellsErb-b2 Receptor Tyrosine KinasesHumansMicrotubulesNeoplasm Invasivenessrac1 GTP-Binding ProteinErb-b2 Receptor Tyrosine Kinasesrac1 GTP-Binding ProteinRAC1 protein, human

Identifiers

PMID24739973
PMCPMC4061398
OpenAlexW2036747263

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.