ArticlePloS one2026
Which evolutionary game-theoretic model best captures NSCLC dynamics?
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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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Who cites it
2 citing papers in PubMed.
- Can evolutionary therapy be applied in non-small cell lung cancer?Scientific reports · 2026Article
- Migrastatic therapy as a potential game-changer in adaptive cancer treatment.Scientific reports · 2026Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Understanding and predicting the eco-evolutionary dynamics of cancer requires identifying mathematical models that best capture tumor growth and treatment response. In this study, we fit a family of two-population models to in-vitro data from non-small cell lung cancer (NSCLC), tracking drug-sensitive and drug-resistant cells under varying environmental conditions. The dataset, originally presented by Kaznatcheev et al., includes conditions with and without the drug Alectinib and cancer-associated fibroblasts (CAFs). We compare combinations of growth models (logistic, Gompertz, and von Bertalanffy) and drug efficacy terms (Norton-Simon, linear, and ratio-dependent) to identify which best explains the observed dynamics. Our models incorporate density dependence, frequency-dependent competition, and drug response, enabling mechanistic interpretation of tumor cell interactions. The logistic model with ratio-dependent drug efficacy best fits monoculture data. Using growth parameters from monocultures, we estimate inter-type competition coefficients in co-cultures. We find that growth rate and carrying capacity are stable across CAF conditions, while competition and drug efficacy parameters shift, altering interaction dynamics. Notably, CAFs promote coexistence between resistant and sensitive cells, whereas Alectinib results in competitive exclusion. Our results underscore the need to evaluate both model fit and biological plausibility to guide therapeutic modeling of cancer.
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