Evidence map›Paper›PMID 37803056›Full record

ArticleNPJ systems biology and applications2023

Understanding and leveraging phenotypic plasticity during metastasis formation.

Saumil Shah, Lisa-Marie Philipp, Stefano Giaimo, Susanne Sebens, Arne Traulsen, Michael Raatz

Abstract read
In one paragraph

Article in NPJ systems biology and applications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Article
  2. RUNX2 cooperates with SREBP1 to rewire cancer metabolism and promote aggressiveness.Journal of experimental & clinical cancer research : CR · 2025
    Article
  3. Article
  4. Article
  5. Review
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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

6 authors.

Saumil ShahDepartment of Theoretical Biology, Max Planck Institute for Evolutionary Biology, August-Thienemann-Str. 2, 24306, Plön, Germany. shah@evolbio.mpg.de.ORCID http://orcid.org/0000-0003-1642-4687
Lisa-Marie PhilippInstitute for Experimental Cancer Research, Kiel University and University Hospital Schleswig-Holstein, Campus Kiel, Arnold-Heller-Str. 3, Building U30, Entrance 1, 24105, Kiel, Germany.
Stefano GiaimoDepartment of Theoretical Biology, Max Planck Institute for Evolutionary Biology, August-Thienemann-Str. 2, 24306, Plön, Germany.
Susanne SebensInstitute for Experimental Cancer Research, Kiel University and University Hospital Schleswig-Holstein, Campus Kiel, Arnold-Heller-Str. 3, Building U30, Entrance 1, 24105, Kiel, Germany.
Arne TraulsenDepartment of Theoretical Biology, Max Planck Institute for Evolutionary Biology, August-Thienemann-Str. 2, 24306, Plön, Germany.
Michael RaatzDepartment of Theoretical Biology, Max Planck Institute for Evolutionary Biology, August-Thienemann-Str. 2, 24306, Plön, Germany.ORCID http://orcid.org/0000-0002-6968-6560

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer metastasis is the process of detrimental systemic spread and the primary cause of cancer-related fatalities. Successful metastasis formation requires tumor cells to be proliferative and invasive; however, cells cannot be effective at both tasks simultaneously. Tumor cells compensate for this trade-off by changing their phenotype during metastasis formation through phenotypic plasticity. Given the changing selection pressures and competitive interactions that tumor cells face, it is poorly understood how plasticity shapes the process of metastasis formation. Here, we develop an ecology-inspired mathematical model with phenotypic plasticity and resource competition between phenotypes to address this knowledge gap. We find that phenotypically plastic tumor cell populations attain a stable phenotype equilibrium that maintains tumor cell heterogeneity. Considering treatment types inspired by chemo- and immunotherapy, we highlight that plasticity can protect tumors against interventions. Turning this strength into a weakness, we corroborate current clinical practices to use plasticity as a target for adjuvant therapy. We present a parsimonious view of tumor plasticity-driven metastasis that is quantitative and experimentally testable, and thus potentially improving the mechanistic understanding of metastasis at the cell population level, and its treatment consequences.

Indexed as

Biological EvolutionNeoplasmsAdaptation, PhysiologicalHumansModels, TheoreticalPhenotype

Identifiers

PMID37803056
PMCPMC10558468

What OpenQuestion holds

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LicenceCC BY
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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.