ArticleNature communications2017
Spatial competition constrains resistance to targeted cancer therapy.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 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.
The trial behind it
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
68 citing papers in PubMed, 132 citations in OpenAlex.
- A microbial therapy-mimicry assay shows how spatial resource dynamics control resistance escape.Nature ecology & evolution · 2026Article
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- In silico models in oncology, neurology, and epidemiology: systems-level and multiscale perspectives.NPJ systems biology and applications · 2026Review
- Single-threshold-guided adaptive cancer therapy with partial-cycle treatment: A mechanistic and reinforcement learning analysis.PLoS computational biology · 2026Article
- Developing virtual physiology of human tumor tissue for malignancy assessment.NPJ precision oncology · 2026Article
- Chronic and non-canonical cGAS-STING activation: implications for health, disease, cancer, and emerging therapeutic opportunities.Apoptosis : an international journal on programmed cell death · 2026Review
- Delaying cancer progression by integrating toxicity constraints in a model of adaptive therapy.NPJ systems biology and applications · 2026Article
- A Systematic Review of Evidence for the Cost of Therapeutic Resistance in Cancer.bioRxiv : the preprint server for biology · 2025Article
- Impacts of competition and phenotypic plasticity on the viability of adaptive therapy.Mathematical biosciences · 2025Article
- Adaptive Therapy Exploits Fitness Deficits in Chemotherapy-Resistant Ovarian Cancer to Achieve Long-Term Tumor Control.Cancer research · 2025Article
- Deriving Optimal Treatment Timing for Adaptive Therapy: Matching the Model to the Tumor Dynamics.Bulletin of mathematical biology · 2025Article
- Article
- Systems biology successes and areas for opportunity in prostate cancer.Endocrine-related cancer · 2025Review
- Using spatial statistics to infer game-theoretic interactions in an agent-based model of cancer cells.bioRxiv : the preprint server for biology · 2025Article
- Validation of polymorphic Gompertzian model of cancer through in vitro and in vivo data.PloS one · 2025Article
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- An expanded view of cell competition.Development (Cambridge, England) · 2024Review
- Communication between cancer cell subtypes by exosomes contributes to nasopharyngeal carcinoma metastasis and poor prognosis.Precision clinical medicine · 2024Article
- Impact of stroma remodeling on forces experienced by cancer cells and stromal cells within a pancreatic tumor tissue.Biomedical engineering online · 2024Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adaptive therapy (AT) aims to control tumour burden by maintaining therapy-sensitive cells to exploit their competition with resistant cells. This relies on the assumption that resistant cells have impaired cellular fitness. Here, using a model of resistance to a pharmacological cyclin-dependent kinase inhibitor (CDKi), we show that this assumption is valid when competition between cells is spatially structured. We generate CDKi-resistant cancer cells and find that they have reduced proliferative fitness and stably rewired cell cycle control pathways. Low-dose CDKi outperforms high-dose CDKi in controlling tumour burden and resistance in tumour spheroids, but not in monolayer culture. Mathematical modelling indicates that tumour spatial structure amplifies the fitness penalty of resistant cells, and identifies their relative fitness as a critical determinant of the clinical benefit of AT. Our results justify further investigation of AT with kinase inhibitors.
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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.