Evidence map›Paper›PMID 26686751›Full record

ArticleIntegrative biology : quantitative biosciences from nano to macro2016

3-D individual cell based computational modeling of tumor cell-macrophage paracrine signaling mediated by EGF and CSF-1 gradients.

Hildur Knutsdottir, John S Condeelis, Eirikur Palsson

Open access · greenAbstract read
In one paragraph

Article in Integrative biology : quantitative biosciences from nano to macro, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

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  13. Modeling immune cell behavior across scales in cancer.Wiley interdisciplinary reviews. Systems biology and medicine · 2020
    Review
  14. Updates on mechanistic insights and targeting of tumour metastasis.Journal of cellular and molecular medicine · 2020
    Review
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  16. Article
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  19. Effect of Stromal Cells in Tumor Microenvironment on Metastasis Initiation.International journal of biological sciences · 2018
    Review
  20. Article
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

3 authors at 3 institutions in 3 countries.

Hildur KnutsdottirMathematics Department/Institute of Applied Mathematics, University of British Columbia, Vancouver, BC V6 T 1Z2, Canada.
John S Condeelis
Eirikur Palsson
Burnaby Hospital · CAIn-Q-Tel · USThe Bronx Defenders · US

Funding

Tumor Progression and MetastasisP01CA100324 · NCI · YESHIVA UNIVERSITY · PI CONDEELIS, JOHN S · 2003 to 2018
$30.0M
Signal transduction regulating tumor cell disseminationR01CA150344 · NCI · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI CONDEELIS, JOHN S · 2010 to 2020
$3.7M
NCI NIH HHS P01 CA100324NCI NIH HHS R01 CA150344
6 · The paper itself

Abstract

High density of macrophages in mammary tumors has been associated with a higher risk of metastasis and thus increased mortality in women. The EGF/CSF-1 paracrine signaling increases the number of invasive tumor cells by both recruiting tumor cells further away and manipulating the macrophages' innate ability to open up a passage into blood vessels thus promoting intravasation and finally metastasis. A 3-D individual-cell-based model is introduced, to better understand the tumor cell-macrophage interactions, and to explore how changing parameters of the paracrine signaling system affects the number of invasive tumor cells. The simulation data and videos of the cell movements correlated well with findings from both in vitro and in vivo experimental results. The model demonstrated how paracrine signaling is necessary to achieve co-migration of tumor cells and macrophages towards a specific signaling source. We showed how the paracrine signaling enhances the number of both invasive tumor cells and macrophages. The simulations revealed that for the in vitro experiments the imposed no-flux boundary condition might be affecting the results, and that changing the setup might lead to different experimental findings. In our simulations, the 3 : 1 tumor cell/macrophage ratio, observed in vivo, was robust for many parameters but sensitive to EGF signal strength and fraction of macrophages in the tumor. The model can be used to identify new agents for targeted therapy and we suggest that a successful strategy to prevent or limit invasion of tumor cells would be to block the tumor cell-macrophage paracrine signaling. This can be achieved by either blocking the EGF or CSF-1 receptors or supressing the EGF or CSF-1 signal.

Indexed as

Models, BiologicalParacrine CommunicationCell MovementComputer SimulationEpidermal Growth FactorHumansMacrophage Colony-Stimulating FactorMacrophagesNeoplasm InvasivenessNeoplasms, ExperimentalEpidermal Growth FactorMacrophage Colony-Stimulating Factor

Identifiers

PMID26686751
PMCPMC5013833
OpenAlexW2189919668

What OpenQuestion holds

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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.