Evidence map›Paper›PMID 19285513›Full record

ArticleJournal of theoretical biology2009

Evolution of cell motility in an individual-based model of tumour growth.

P Gerlee, A R A Anderson

Open access · greenAbstract read
In one paragraph

Article in Journal of theoretical biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Article
  3. Metastasis and the evolution of dispersal.Proceedings. Biological sciences · 2019
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Integrated PK-PD and agent-based modeling in oncology.Journal of pharmacokinetics and pharmacodynamics · 2015
    Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Multiscale models of breast cancer progression.Annals of biomedical engineering · 2012
    Review
  18. Article
  19. Review
  20. Multiscale cancer modeling.Annual review of biomedical engineering · 2011
    Review
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

2 authors at 2 institutions in 2 countries.

P GerleeNiels Bohr Institute, Center for Models of Life, Copenhagen Ø, Denmark. gerlee@nbi.uk
A R A Anderson
Moffitt Cancer Center · USNiels Brock · DK

Funding

TrainingU54CA113007 · NCI · VANDERBILT UNIVERSITY · PI ESTRADA-RODGERS, LOURDES · 2004 to 2014
$19.2M
NCI NIH HHS U54 CA 113007NCI NIH HHS U54 CA113007
6 · The paper itself

Abstract

Tumour invasion is driven by proliferation and importantly migration into the surrounding tissue. Cancer cell motility is also critical in the formation of metastases and is therefore a fundamental issue in cancer research. In this paper we investigate the emergence of cancer cell motility in an evolving tumour population using an individual-based modelling approach. In this model of tumour growth each cell is equipped with a micro-environment response network that determines the behaviour or phenotype of the cell based on the local environment. The response network is modelled using a feed-forward neural network, which is subject to mutations when the cells divide. With this model we have investigated the impact of the micro-environment on the emergence of a motile invasive phenotype. The results show that when a motile phenotype emerges the dynamics of the model are radically changed and we observe faster growing tumours exhibiting diffuse morphologies. Further we observe that the emergence of a motile subclone can occur in a wide range of micro-environmental growth conditions. Iterated simulations showed that in identical growth conditions the evolutionary dynamics either converge to a proliferating or migratory phenotype, which suggests that the introduction of cell motility into the model changes the shape of fitness landscape on which the cancer cell population evolves and that it now contains several local maxima. This could have important implications for cancer treatments which focus on the gene level, as our results show that several distinct genotypes and critically distinct phenotypes can emerge and become dominant in the same micro-environment.

Indexed as

Neural Networks, ComputerCell MovementExtracellular MatrixHumansNeoplasm InvasivenessNeoplasmsNeoplasm SeedingNeoplastic Stem CellsNeovascularization, PathologicPhenotype

Identifiers

PMID19285513
PMCPMC2706369
OpenAlexW2042332837

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.