Evidence map›Paper›PMID 26258068›Full record

ReviewFrontiers in oncology2015

Implications of the Hybrid Epithelial/Mesenchymal Phenotype in Metastasis.

Mohit Kumar Jolly, Marcelo Boareto, Bin Huang, Dongya Jia, Mingyang Lu, Eshel Ben-Jacob, José N Onuchic, Herbert Levine

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 443 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
443citing papers in PubMed, 1 pooled it
26.7field-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

443 citing papers in PubMed, 1 synthesis or guideline pooled it, 688 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Cell plasticity in cancer and therapy resistance.Experimental & molecular medicine · 2026
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383 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

8 authors at 1 institution in 1 country.

Mohit Kumar JollyCenter for Theoretical Biological Physics, Rice University , Houston, TX , USA ; Department of Bioengineering, Rice University , Houston, TX , USA.
Marcelo BoaretoCenter for Theoretical Biological Physics, Rice University , Houston, TX , USA ; Institute of Physics, University of São Paulo , São Paulo , Brazil.
Bin HuangCenter for Theoretical Biological Physics, Rice University , Houston, TX , USA ; Department of Chemistry, Rice University , Houston, TX , USA.
Dongya JiaCenter for Theoretical Biological Physics, Rice University , Houston, TX , USA ; Graduate Program in Systems, Synthetic and Physical Biology, Rice University , Houston, TX , USA.
Mingyang LuCenter for Theoretical Biological Physics, Rice University , Houston, TX , USA.
Eshel Ben-JacobCenter for Theoretical Biological Physics, Rice University , Houston, TX , USA ; School of Physics and Astronomy, and The Sagol School of Neuroscience, Tel-Aviv University , Tel-Aviv , Israel ; Department of Biosciences, Rice University , Houston, TX , USA.
José N OnuchicCenter for Theoretical Biological Physics, Rice University , Houston, TX , USA ; Department of Chemistry, Rice University , Houston, TX , USA ; Department of Physics and Astronomy, Rice University , Houston, TX , USA ; Department of Biosciences, Rice University , Houston, TX , USA.
Herbert LevineCenter for Theoretical Biological Physics, Rice University , Houston, TX , USA ; Department of Bioengineering, Rice University , Houston, TX , USA ; Department of Physics and Astronomy, Rice University , Houston, TX , USA ; Department of Biosciences, Rice University , Houston, TX , USA.
Rice University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transitions between epithelial and mesenchymal phenotypes - the epithelial to -mesenchymal transition (EMT) and its reverse the mesenchymal to epithelial transition (MET) - are hallmarks of cancer metastasis. While transitioning between the epithelial and mesenchymal phenotypes, cells can also attain a hybrid epithelial/mesenchymal (E/M) (i.e., partial or intermediate EMT) phenotype. Cells in this phenotype have mixed epithelial (e.g., adhesion) and mesenchymal (e.g., migration) properties, thereby allowing them to move collectively as clusters. If these clusters reach the bloodstream intact, they can give rise to clusters of circulating tumor cells (CTCs), as have often been seen experimentally. Here, we review the operating principles of the core regulatory network for EMT/MET that acts as a "three-way" switch giving rise to three distinct phenotypes - E, M and hybrid E/M - and present a theoretical framework that can elucidate the role of many other players in regulating epithelial plasticity. Furthermore, we highlight recent studies on partial EMT and its association with drug resistance and tumor-initiating potential; and discuss how cell-cell communication between cells in a partial EMT phenotype can enable the formation of clusters of CTCs. These clusters can be more apoptosis-resistant and have more tumor-initiating potential than singly moving CTCs with a wholly mesenchymal (complete EMT) phenotype. Also, more such clusters can be formed under inflammatory conditions that are often generated by various therapies. Finally, we discuss the multiple advantages that the partial EMT or hybrid E/M phenotype have as compared to a complete EMT phenotype and argue that these collectively migrating cells are the primary "bad actors" of metastasis.

Indexed as

cancer stem cellscancer systems biologycell-fate decisionsintermediate EMTpartial EMT

Identifiers

PMID26258068
PMCPMC4507461
OpenAlexW1689351220

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.