Evidence map›Paper›PMID 29920274›Full record

ArticleDevelopmental cell2018

EMT Subtype Influences Epithelial Plasticity and Mode of Cell Migration.

Nicole M Aiello, Ravikanth Maddipati, Robert J Norgard, David Balli, Jinyang Li, Salina Yuan, Taiji Yamazoe, Taylor Black, Amine Sahmoud, Emma E Furth and 2 more

Abstract read
In one paragraph

Article in Developmental cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 455 papers.

0numbers the graph read from it
0cells of the map it votes in
455citing 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

455 citing papers in PubMed.

  1. Article
  2. Article
  3. Cell plasticity in cancer and therapy resistance.Experimental & molecular medicine · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

395 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors.

Nicole M AielloDepartment of Medicine, Gastroenterology Division, Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, 421 Curie Blvd, 512 BRB II/III, Philadelphia, PA 19104, USA.
Ravikanth MaddipatiDepartment of Medicine, Gastroenterology Division, Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, 421 Curie Blvd, 512 BRB II/III, Philadelphia, PA 19104, USA.
Robert J NorgardDepartment of Medicine, Gastroenterology Division, Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, 421 Curie Blvd, 512 BRB II/III, Philadelphia, PA 19104, USA.
David BalliDepartment of Medicine, Gastroenterology Division, Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, 421 Curie Blvd, 512 BRB II/III, Philadelphia, PA 19104, USA.
Jinyang LiDepartment of Medicine, Gastroenterology Division, Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, 421 Curie Blvd, 512 BRB II/III, Philadelphia, PA 19104, USA.
Salina YuanDepartment of Medicine, Gastroenterology Division, Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, 421 Curie Blvd, 512 BRB II/III, Philadelphia, PA 19104, USA.
Taiji YamazoeDepartment of Medicine, Gastroenterology Division, Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, 421 Curie Blvd, 512 BRB II/III, Philadelphia, PA 19104, USA.
Taylor BlackDepartment of Medicine, Gastroenterology Division, Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, 421 Curie Blvd, 512 BRB II/III, Philadelphia, PA 19104, USA.
Amine SahmoudDepartment of Medicine, Gastroenterology Division, Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, 421 Curie Blvd, 512 BRB II/III, Philadelphia, PA 19104, USA.
Emma E FurthDepartment of Pathology and Laboratory Medicine, Hospital of the University of Pennsylvania, Philadelphia, PA 19104, USA.
Dafna Bar-SagiDepartment of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, NY 10016, USA.
Ben Z StangerDepartment of Medicine, Gastroenterology Division, Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, 421 Curie Blvd, 512 BRB II/III, Philadelphia, PA 19104, USA; Department of Cell and Developmental Biology, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA. Electronic address: bstanger@exchange.upenn.edu.

Funding

Vaccine FacilityP30CA016087 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ADRIANA HEGUY · 1985 to 2026
$83.1M
TRANSGENIC AND CHIMERIC MOUSE COREP30DK050306 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI Ken Hashigiwa Cadwell · 1997 to 2026
$32.5M
Physician Scientist Training in Clinical OncologyK12CA076931 · NCI · UNIVERSITY OF PENNSYLVANIA · PI STEPHEN Patrick HUNGER, LYNN M. SCHUCHTER · 1997 to 2026
$16.5M
Immunobiology and immunotherapy of pancreatic cancerR01CA169123 · NCI · UNIVERSITY OF PENNSYLVANIA · PI STANGER, BEN Z, VONDERHEIDE, ROBERT H · 2012 to 2016
$3.1M
The role of progenitor cells in pancreatic acinar renewal and pre-malignant progressionK08DK109492 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI MADDIPATI, RAVIKANTH · 2017 to 2020
$676k
Elucidating the role and regulation of epithelial plasticity in metastasisF31CA177163 · NCI · UNIVERSITY OF PENNSYLVANIA · PI AIELLO, NICOLE · 2014 to 2016
$87k
NCI NIH HHS F31 CA177163NCI NIH HHS K12 CA076931NCI NIH HHS P30 CA016087NCI NIH HHS R01 CA169123NIDDK NIH HHS K08 DK109492NIDDK NIH HHS P30 DK050306
6 · The paper itself

Abstract

Epithelial-mesenchymal transition (EMT) is strongly implicated in tumor cell invasion and metastasis. EMT is thought to be regulated primarily at the transcriptional level through the repressive activity of EMT transcription factors. However, these classical mechanisms have been parsed out almost exclusively in vitro, leaving questions about the programs driving EMT in physiological contexts. Here, using a lineage-labeled mouse model of pancreatic ductal adenocarcinoma to study EMT in vivo, we found that most tumors lose their epithelial phenotype through an alternative program involving protein internalization rather than transcriptional repression, resulting in a "partial EMT" phenotype. Carcinoma cells utilizing this program migrate as clusters, contrasting with the single-cell migration pattern associated with traditionally defined EMT mechanisms. Moreover, many breast and colorectal cancer cell lines utilize this alternative program to undergo EMT. Collectively, these results suggest that carcinoma cells have different ways of losing their epithelial program, resulting in distinct modes of invasion and dissemination.

Indexed as

AnimalsCadherinsCell Line, TumorCell MovementCell PlasticityEpithelial CellsEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansMiceNeoplasm InvasivenessPancreatic NeoplasmsSignal TransductionTranscription FactorsCadherinsCdh1 protein, mouseTranscription Factorscirculating tumor cellscollective migrationE-cadherinepithelial-mesenchymal transitionlineage tracingmetastasispancreatic cancerpartial EMTtumor cell clusters

Identifiers

PMID29920274
PMCPMC6014628

What OpenQuestion holds

Textmetadata
LicenceTDM
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.