ArticleCancer research2013
Tumor-immune dynamics regulated in the microenvironment inform the transient nature of immune-induced tumor dormancy.
Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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
31 citing papers in PubMed.
- GBP5 as a prognostic biomarker associated with immune cell infiltration, migration and invasion in clear cell renal cell carcinoma.Oncology letters · 2025Article
- Distinct evolutionary patterns of tumour-immune escape and elimination determined by extracellular matrix architectures.Journal of the Royal Society, Interface · 2025Article
- The NLRP3 inflammasome in urogenital cancers: structure, dual function, and therapeutic potential.Frontiers in oncology · 2025Review
- Practical parameter identifiability and handling of censored data with Bayesian inference in mathematical tumour models.NPJ systems biology and applications · 2024Article
- A vascularized breast cancer spheroid platform for the ranked evaluation of tumor microenvironment-targeted drugs by light sheet fluorescence microscopy.Nature communications · 2024Article
- Insights into the role of senescence in tumor dormancy: mechanisms and applications.Cancer metastasis reviews · 2023Review
- A practical guide for the generation of model-based virtual clinical trials.Frontiers in systems biology · 2023Article
- A reactive oxygen species-related signature to predict prognosis and aid immunotherapy in clear cell renal cell carcinoma.Frontiers in oncology · 2023Article
- Transition Therapy: Tackling the Ecology of Tumor Phenotypic Plasticity.Bulletin of mathematical biology · 2021Article
- Article
- Forecasting Individual Patient Response to Radiation Therapy in Head and Neck Cancer With a Dynamic Carrying Capacity Model.International journal of radiation oncology, biology, physics · 2021Article
- Dormant Tumor Cell Vaccination: A Mathematical Model of Immunological Dormancy in Triple-Negative Breast Cancer.Cancers · 2021Article
- Modeling Radioimmune Response-Current Status and Perspectives.Frontiers in oncology · 2021Review
- Cancer-induced immunosuppression can enable effectiveness of immunotherapy through bistability generation: A mathematical and computational examination.Journal of theoretical biology · 2020Article
- RCC Immune Microenvironment Subsequent to Targeted Therapy: A Friend or a Foe?Frontiers in oncology · 2020Review
- Cancer-educated mesenchymal stem cells promote the survival of cancer cells at primary and distant metastatic sites via the expansion of bone marrow-derived-PMN-MDSCs.Cell death & disease · 2019Article
- Anti-CD40 mAb enhanced efficacy of anti-PD1 against osteosarcoma.Journal of bone oncology · 2019Article
- Specific inhibition of PI3Kδ/γ enhances the efficacy of anti-PD1 against osteosarcoma cancer.Journal of bone oncology · 2019Article
- Illuminating the Numbers: Integrating Mathematical Models to Optimize Photomedicine Dosimetry and Combination Therapies.Frontiers in physics · 2019Article
- (-)-4-O-(4-O-β-D-glucopyranosylcaffeoyl) Quinic Acid Inhibits the Function of Myeloid-Derived Suppressor Cells to Enhance the Efficacy of Anti-PD1 against Colon Cancer.Pharmaceutical research · 2018Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Cancer in a host induces responses that increase the ability of the microenvironment to sustain the growing mass, for example, angiogenesis, but cancer cells can have varying sensitivities to these sustainability signals. Here, we show that these sensitivities are significant determinants of ultimate tumor fate, especially in response to treatments and immune interactions. We present a mathematical model of cancer-immune interactions that modifies generalized logistic growth with both immune-predation and immune-recruitment. The role of a growing environmental carrying capacity is discussed as a possible regulatory mechanism for tumor growth, and this regulation is shown to modify cancer-immune interactions and the possibility of achieving immune-induced tumor dormancy. This mathematical model qualitatively matches experimental observations of immune-induced tumor dormancy as it predicts dormancy as a transient period of growth that necessarily ends in either tumor elimination or tumor escape. As dormant tumors may exist asymptomatically and may be easier to treat with conventional therapy, an understanding of the mechanisms behind tumor dormancy may lead to new treatments aimed at prolonging the dormant state or converting an aggressive cancer to the dormant state.
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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.