Evidence map›Paper›PMID 24332913›Full record

ArticleCell2013

Collective invasion in breast cancer requires a conserved basal epithelial program.

Kevin J Cheung, Edward Gabrielson, Zena Werb, Andrew J Ewald

Abstract read
In one paragraph

Article in Cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 531 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
531citing papers in PubMed, 2 pooled it
–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

531 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Article
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  5. A custom two-in-one HIST and line-scanning confocal excitation module.bioRxiv : the preprint server for biology · 2026
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471 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

4 authors.

Kevin J CheungDepartments of Cell Biology and Oncology, Center for Cell Dynamics, School of Medicine, Johns Hopkins University, Baltimore, MD 21205, USA.
Edward GabrielsonDepartment of Pathology, School of Medicine, Johns Hopkins University, Baltimore, MD 21205, USA.
Zena WerbDepartment of Anatomy, University of California, San Francisco, San Francisco, CA 94143, USA.
Andrew J EwaldDepartments of Cell Biology and Oncology, Center for Cell Dynamics, School of Medicine, Johns Hopkins University, Baltimore, MD 21205, USA. Electronic address: aewald2@jhmi.edu.

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
VACCINES--A NEW PARADIGM FOR BREAST CANCERP50CA088843 · NCI · JOHNS HOPKINS UNIVERSITY · PI DAVIDSON, NANCY ELLEN · 2000 to 2010
$27.8M
Theranostic Imaging of Metastatic Prostate CancerP50CA103175 · NCI · JOHNS HOPKINS UNIVERSITY · PI BARKER, PETER B · 2003 to 2015
$17.9M
ONCOLOGY: CHEMOTHERAPY, IMMUNOLOGY, BIOLOGYT32CA009071 · NCI · JOHNS HOPKINS UNIVERSITY · PI Mary Y Armanios, Nilofer S. Azad · 1985 to 2026
$12.8M
Role of Metalloproteinases in Mammary Gland RemodelingR01CA057621 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WERB, ZENA · 1993 to 2017
$9.0M
Environmental Effect on the Mammary Gland across the LifespanU01ES019458 · NIEHS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WERB, ZENA · 2010 to 2014
$2.5M
Analysis of the Signaling and Mechanical Cues Promoting Invasion in MelanomaU01CA155758 · NCI · YALE UNIVERSITY · PI LAUFFENBURGER, DOUGLAS A, LEVCHENKO, ANDRE · 2011 to 2015
$1.8M
Request for Zeiss LSM 510 MP Multiphoton Imaging SystemS10RR024550 · NCRR · JOHNS HOPKINS UNIVERSITY · PI KUO, SCOT CHARLES · 2008 to 2008
$500k
NCI NIH HHS P30 CA006973NCI NIH HHS P50 CA088843NCI NIH HHS P50 CA103175NCI NIH HHS P50 CA88843NCI NIH HHS R01 CA057621NCI NIH HHS T32 CA009071NCI NIH HHS U01 CA155758NCRR NIH HHS S10 RR024550NCRR NIH HHS S10RR024550NIEHS NIH HHS U01 ES019458
6 · The paper itself

Abstract

Carcinomas typically invade as a cohesive multicellular unit, a process termed collective invasion. It remains unclear how different subpopulations of cancer cells contribute to this process. We developed three-dimensional (3D) organoid assays to identify the most invasive cancer cells in primary breast tumors. Collective invasion was led by specialized cancer cells that were defined by their expression of basal epithelial genes, such as cytokeratin-14 (K14) and p63. Furthermore, K14+ cells led collective invasion in the major human breast cancer subtypes. Importantly, luminal cancer cells were observed to convert phenotypically to invasive leaders following induction of basal epithelial genes. Although only a minority of cells within luminal tumors expressed basal epithelial genes, knockdown of either K14 or p63 was sufficient to block collective invasion. Our data reveal that heterotypic interactions between epithelial subpopulations are critical to collective invasion. We suggest that targeting the basal invasive program could limit metastatic progression.

Indexed as

Neoplasm InvasivenessAnimalsBreast NeoplasmsCell Culture TechniquesCells, CulturedDisease Models, AnimalEpithelial CellsHumansKeratin-14Lung NeoplasmsMiceOrganoidsTranscription FactorsTumor Suppressor ProteinsKeratin-14TP63 protein, humanTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID24332913
PMCPMC3941206

What OpenQuestion holds

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Read underepoch 390

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.