Tumour-immune dynamics models
Predator-prey style equations describe how immune cells hunt tumour cells, and they reproduce dormancy, escape and the delayed, sometimes explosive, responses seen with immunotherapy; they now help design combination and scheduling trials.
Overview
Kuznetsov and colleagues' 1994 model treated effector immune cells and tumour cells as interacting populations, reproducing dormancy, sneaking-through and oscillations. Later models added checkpoints, exhaustion, antigen presentation and cytokines, and have been used to explain pseudoprogression and hyperprogression under PD-1 blockade, to propose sequencing of radiotherapy and immunotherapy, and to simulate CAR-T expansion and cytokine release. Quantitative systems pharmacology models of checkpoint blockade are increasingly used by developers to choose doses and combinations.
How it works
Coupled ordinary differential equations for tumour and immune populations with recruitment, killing, exhaustion and suppression terms, whose equilibria correspond to dormancy, escape or elimination.
- Explains non-linear immunotherapy responses
- Guides sequencing with radiotherapy and chemotherapy
- Extends to CAR-T kinetics
- Immune parameters are poorly identifiable
- Spatial and antigen heterogeneity simplified
- Predictions rarely validated prospectively
Latest papers
topQuery for this technology: (TITLE:"Tumour-immune dynamics models" OR ABSTRACT:"Tumour-immune dynamics models") AND (cancer OR tumor OR tumour OR oncology OR carcinoma OR lymphoma OR leukemia OR leukaemia OR myeloma OR sarcoma OR melanoma OR glioma). Results are unfiltered search hits about Tumour-immune dynamics models, not a curated reading list.
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