Evidence map›Paper›PMID 33364589›Full record

ArticleiScience2021

Selection-driven tumor evolution with public goods leads to patterns of clonal expansion consistent with neutral growth.

Jack Edwards, Andriy Marusyk, David Basanta

Abstract read
In one paragraph

Article in iScience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Review
  2. A modelling framework for cancer ecology and evolution.Journal of the Royal Society, Interface · 2024
    Article
  3. Article
  4. Onco-Breastomics: An Eco-Evo-Devo Holistic Approach.International journal of molecular sciences · 2024
    Review
  5. Review
  6. Article
  7. Modeling colorectal cancer evolution.Journal of human genetics · 2021
    Review
  8. 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.

Jack EdwardsIntegrated Mathematical Oncology Department, H. Lee Moffitt Cancer Center & Research Institute, 12902 USF Magnolia Drive, Tampa, FL 33612, USA.
Andriy MarusykCancer Physiology Department, H. Lee Moffitt Cancer Center & Research Institute, 12902 Magnolia Drive, SRB 4 Rm 24000H, Tampa, Florida 33612, USA.
David BasantaIntegrated Mathematical Oncology Department, H. Lee Moffitt Cancer Center & Research Institute, 12902 USF Magnolia Drive, Tampa, FL 33612, USA.

Funding

Multiscale Modeling of Bone Environment Responses to Metastatic Prostate CancerU01CA202958 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI BASANTA GUTIERREZ, DAVID, LYNCH, CONOR C · 2016 to 2020
$3.3M
Defining bone ecosystem effects on metastatic prostate cancer evolution and treatment response using an integrated mathematical modeling approachU01CA244101 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI BASANTA GUTIERREZ, DAVID, LYNCH, CONOR C · 2020 to 2024
$2.3M
NCI NIH HHS U01 CA202958NCI NIH HHS U01 CA244101
6 · The paper itself

Abstract

Cancers are the result of eco-evolutionary processes fueled by heritable phenotypic diversification and driven by environmentally dependent selection. Space represents a key growth-limiting ecological resource, the ability to explore this resource is likely under strong selection. Using agent-based modeling, we explored the interplay between phenotypic strategies centered on gaining access to new space through cell-extrinsic degradation of extracellular matrix barriers and the exploitation of this resource through maximizing cell proliferation. While cell proliferation is a cell-intrinsic property, newly accessed space represents a public good, which can benefit both producers and non-producers. We found that this interplay results in ecological succession, enabling emergence of large, heterogeneous, and highly proliferative populations. Even though in our simulations both remodeling and proliferation strategies were under strong positive selection, their interplay led to sub-clonal architecture that could be interpreted as evidence for neutral evolution, warranting cautious interpretation of inferences from sequencing of cancer genomes.

Indexed as

CancerCancer Systems BiologyEvolutionary Theories

Identifiers

PMID33364589
PMCPMC7753957

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.