Evidence map›Paper›PMID 35327538›Full record

ArticleBiomolecules2022

Population Dynamics of Epithelial-Mesenchymal Heterogeneity in Cancer Cells.

Paras Jain, Sugandha Bhatia, Erik W Thompson, Mohit Kumar Jolly

Open access · goldAbstract read
In one paragraph

Article in Biomolecules, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

10 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
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  3. How cancer arises: Genetics releases, plasticity creates, genetics stabilizes.Proceedings of the National Academy of Sciences of the United States of America · 2025
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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 at 2 institutions in 2 countries.

Paras JainCentre for BioSystems Science and Engineering, Indian Institute of Science, Bangalore 560012, India.
Sugandha BhatiaSchool of Biomedical Sciences, Faculty of Health, Queensland University of Technology, Brisbane 4000, Australia.ORCID 0000-0003-3092-8283
Erik W ThompsonSchool of Biomedical Sciences, Faculty of Health, Queensland University of Technology, Brisbane 4000, Australia.ORCID 0000-0002-9723-4924
Mohit Kumar JollyCentre for BioSystems Science and Engineering, Indian Institute of Science, Bangalore 560012, India.ORCID 0000-0002-6631-2109
Indian Institute of Science Bangalore · INTranslational Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phenotypic heterogeneity is a hallmark of aggressive cancer behaviour and a clinical challenge. Despite much characterisation of this heterogeneity at a multi-omics level in many cancers, we have a limited understanding of how this heterogeneity emerges spontaneously in an isogenic cell population. Some longitudinal observations of dynamics in epithelial-mesenchymal heterogeneity, a canonical example of phenotypic heterogeneity, have offered us opportunities to quantify the rates of phenotypic switching that may drive such heterogeneity. Here, we offer a mathematical modeling framework that explains the salient features of population dynamics noted in PMC42-LA cells: (a) predominance of EpCAM

Indexed as

Epithelial-Mesenchymal TransitionNeoplasmsEpithelial Cell Adhesion MoleculeHumansPopulation DynamicsTranscription FactorsEpithelial Cell Adhesion MoleculeTranscription Factorsasymmetric cell divisionepithelial-mesenchymal heterogeneityepithelial-mesenchymal plasticitypopulation dynamics

Identifiers

PMID35327538
PMCPMC8945776
OpenAlexW4220677394

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.