ArticleCell proliferation2011
Mathematical model of the role of intercellular signalling in intercellular cooperation during tumorigenesis.
Article in Cell proliferation, 2011. 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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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.
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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.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Tumor microenvironment governs the prognostic landscape of immunotherapy for head and neck squamous cell carcinoma: A computational model-guided analysis.PLoS computational biology · 2025Article
- Mathematical models of intercellular signaling in breast cancer.Seminars in cancer biology · 2025Review
- Non-cell-autonomous effects yield lower clonal diversity in expanding tumors.Scientific reports · 2017Article
- Magnetic assembly of 3D cell clusters: visualizing the formation of an engineered tissue.Cell proliferation · 2016Article
- First principles of Hamiltonian medicine.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014Article
- Mathematical model of the effect of intercellular cooperative interactions in cancer during drug therapy.Annual ORNL Biomedical Science and Engineering Center Conference. ORNL Biomedical Science and Engineering Center Conference · 2013Article
- Inter-cellular signaling network reveals a mechanistic transition in tumor microenvironment.Integrative biology : quantitative biosciences from nano to macro · 2012Article
- Mathematical model of heterogeneous cancer growth with an autocrine signalling pathway.Cell proliferation · 2012Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesIntercellular cooperation has been hypothesized to enhance cell proliferation during cancer metastasis through autocrine signalling cascades and mathematical models can provide valuable insights into underlying mechanisms of metastatic tumorigenesis. Here, we present a model that incorporates signal-stimulated cell proliferation, and investigate influences of diffusion-driven heterogeneity in signal concentration on proliferation dynamics. MATERIALS AND
methodsOur model incorporates signal production through both autocrine and paracrine pathways, and signal diffusion and loss for a metastasizing cell population at a host site. We use the signalling pathway of IL-6 for illustration where this signalling species forms an intermediate complex with its receptor IL-6R. This in turn forms a heterodimeric complex with transmembrane protein gp130, ultimately resulting in production of downstream signals. Cell population dynamics are taken to follow a modified logistic equation for which the rate term is dependent on local IL-6 concentration. RESULTS AND
conclusionsOur spatiotemporal model agrees closely with experimental results. The model is also able to predict two phenomena typical of metastatic tumorigenesis - host tissue preference and long periods of proliferation dormancy. It confirms that diffusivity of the signalling species in a host tissue plays a significant role during the process. Our results show that the proliferation-apoptosis balance is tipped in favour of the former for host sites that have relatively smaller signal diffusivities.
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Registered trials
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.