Evidence map›Paper›PMID 35239640›Full record

ArticlePLoS computational biology2022

Autocrine signaling can explain the emergence of Allee effects in cancer cell populations.

Philip Gerlee, Philipp M Altrock, Adam Malik, Cecilia Krona, Sven Nelander

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.7field-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

21 citing papers in PubMed, 21 citations in OpenAlex.

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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

5 authors at 3 institutions in 3 countries.

Philip GerleeMathematical Sciences, Chalmers University of Technology, Gothenburg, Sweden.ORCID 0000-0001-8503-0177
Philipp M AltrockDepartment of Integrated Mathematical Oncology, Moffitt Cancer Center, Tampa, Florida, United States of America.ORCID 0000-0001-7731-3345
Adam MalikDepartment of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.ORCID 0000-0003-1356-9039
Cecilia KronaDepartment of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.ORCID 0000-0001-6458-1949
Sven NelanderDepartment of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.ORCID 0000-0003-1758-1262
Uppsala University · SEChalmers University of Technology · SEMoffitt Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In many human cancers, the rate of cell growth depends crucially on the size of the tumor cell population. Low, zero, or negative growth at low population densities is known as the Allee effect; this effect has been studied extensively in ecology, but so far lacks a good explanation in the cancer setting. Here, we formulate and analyze an individual-based model of cancer, in which cell division rates are increased by the local concentration of an autocrine growth factor produced by the cancer cells themselves. We show, analytically and by simulation, that autocrine signaling suffices to cause both strong and weak Allee effects. Whether low cell densities lead to negative (strong effect) or reduced (weak effect) growth rate depends directly on the ratio of cell death to proliferation, and indirectly on cellular dispersal. Our model is consistent with experimental observations from three patient-derived brain tumor cell lines grown at different densities. We propose that further studying and quantifying population-wide feedback, impacting cell growth, will be central for advancing our understanding of cancer dynamics and treatment, potentially exploiting Allee effects for therapy.

Indexed as

Autocrine CommunicationNeoplasmsEcologyFeedbackHumansModels, BiologicalPopulation DensityPopulation Dynamics

Identifiers

PMID35239640
PMCPMC8923455
OpenAlexW4214836883

What OpenQuestion holds

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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.