ArticlePloS one2018
Competition and niche construction in a model of cancer metastasis.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Fisher Information Limits on Genetic Stability, Diversity, and Regulation.Bulletin of mathematical biology · 2026Article
- Premetastatic niche mechanics and organotropism in breast cancer.npj biological physics and mechanics · 2025Review
- Colorectal cancer and dormant metastases: Put to sleep or destroy?World journal of gastrointestinal oncology · 2024Article
- Molecular perspectives on systemic priming and concomitant immunity in colorectal carcinoma.Journal of the Egyptian National Cancer Institute · 2024Review
- The role of evolutionary game theory in spatial and non-spatial models of the survival of cooperation in cancer: a review.Journal of the Royal Society, Interface · 2022Review
- Tumors Are Evolutionary Island-Like Ecosystems.Genome biology and evolution · 2021Article
- Emerging insights into the biology of metastasis: A review article.Iranian journal of basic medical sciences · 2019Review
- [Research Advances of Ang-2 in Non-small Cell Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2018Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Niche construction theory states that not only does the environment act on populations to generate Darwinian selection, but organisms reciprocally modify the environment and the sources of natural selection. Cancer cells participate in niche construction as they alter their microenvironments and create pre-metastatic niches; in fact, metastasis is a product of niche construction. Here, we present a mathematical model of niche construction and metastasis. Our model contains producers, which pay a cost to contribute to niche construction that benefits all tumor cells, and cheaters, which reap the benefits without paying the cost. We derive expressions for the conditions necessary for metastasis, showing that the establishment of a mutant lineage that promotes metastasis depends on niche construction specificity and strength of interclonal competition. We identify a tension between the arrival and invasion of metastasis-promoting mutants, where tumors composed only of cheaters remain small but are susceptible to invasion whereas larger tumors containing producers may be unable to facilitate metastasis depending on the level of niche construction specificity. Our results indicate that even if metastatic subclones arise through mutation, metastasis may be hindered by interclonal competition, providing a potential explanation for recent surprising findings that most metastases are derived from early mutants in primary tumors.
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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.