ArticleTheoretical biology & medical modelling2012
Immunoediting: evidence of the multifaceted role of the immune system in self-metastatic tumor growth.
Article in Theoretical biology & medical modelling, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 43 citations in OpenAlex.
- Spatially fractionated GRID radiation potentiates immune-mediated tumor control.Radiation oncology (London, England) · 2024Article
- Mathematical modeling of radiotherapy and its impact on tumor interactions with the immune system.Neoplasia (New York, N.Y.) · 2022Review
- Cancer systems immunology.eLife · 2020Review
- Illuminating the Numbers: Integrating Mathematical Models to Optimize Photomedicine Dosimetry and Combination Therapies.Frontiers in physics · 2019Article
- Multiscale Agent-Based and Hybrid Modeling of the Tumor Immune Microenvironment.Processes (Basel, Switzerland) · 2019Article
- Modeling triple-negative breast cancer heterogeneity: Effects of stromal macrophages, fibroblasts and tumor vasculature.Journal of theoretical biology · 2018Article
- A computational multiscale agent-based model for simulating spatio-temporal tumour immune response to PD1 and PDL1 inhibition.Journal of the Royal Society, Interface · 2017Article
- An agent-based model of triple-negative breast cancer: the interplay between chemokine receptor CCR5 expression, cancer stem cells, and hypoxia.BMC systems biology · 2017Article
- Modeling the Dichotomy of the Immune Response to Cancer: Cytotoxic Effects and Tumor-Promoting Inflammation.Bulletin of mathematical biology · 2017Article
- Agent-Based Modeling of Cancer Stem Cell Driven Solid Tumor Growth.Methods in molecular biology (Clifton, N.J.) · 2016Article
- Tumor-host signaling interaction reveals a systemic, age-dependent splenic immune influence on tumor development.Oncotarget · 2015Article
- A mathematical model of pre-diagnostic glioma growth.Journal of theoretical biology · 2015Article
- Relevance of tumor-infiltrating lymphocytes in breast cancer.BMC medicine · 2015Review
- NANOG signaling promotes metastatic capability of immunoedited tumor cells.Clinical & experimental metastasis · 2015Article
- Metastatic melanoma cells evade immune detection by silencing STAT1.International journal of molecular sciences · 2015Article
- An agent-based modeling framework linking inflammation and cancer using evolutionary principles: description of a generative hierarchy for the hallmarks of cancer and developing a bridge between mechanism and epidemiological data.Mathematical biosciences · 2015Article
- A journey to uncharted territory: new technical frontiers in studying tumor-stromal cell interactions.Integrative biology : quantitative biosciences from nano to macro · 2015Review
- Investigation of the essential role of platelet-tumor cell interactions in metastasis progression using an agent-based model.Theoretical biology & medical modelling · 2014Article
- Mathematical models of immune-induced cancer dormancy and the emergence of immune evasion.Interface focus · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe role of the immune system in tumor progression has been a subject for discussion for many decades. Numerous studies suggest that a low immune response might be beneficial, if not necessary, for tumor growth, and only a strong immune response can counter tumor growth and thus inhibit progression.
methodsWe implement a cellular automaton model previously described that captures the dynamical interactions between the cancer stem and non-stem cell populations of a tumor through a process of self-metastasis. By overlaying on this model the diffusion of immune reactants into the tumor from a peripheral source to target cells, we simulate the process of immune-system-induced cell kill on tumor progression.
resultsA low cytotoxic immune reaction continuously kills cancer cells and, although at a low rate, thereby causes the liberation of space-constrained cancer stem cells to drive self-metastatic progression and continued tumor growth. With increasing immune system strength, however, tumor growth peaks, and then eventually falls below the intrinsic tumor sizes observed without an immune response. With this increasing immune response the number and proportion of cancer stem cells monotonically increases, implicating an additional unexpected consequence, that of cancer stem cell selection, to the immune response.
conclusionsCancer stem cells and immune cytotoxicity alone are sufficient to explain the three-step "immunoediting" concept - the modulation of tumor growth through inhibition, selection and promotion.
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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.