ArticleBiophysical journal2018
A Nonquiescent "Idling" Population State in Drug-Treated, BRAF-Mutated Melanoma.
Article in Biophysical journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 41 citations in OpenAlex.
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- MAPK and mTORC1 signaling converge to drive cyclin D1 protein production to enable cell cycle reentry in melanoma persister cells.Science signaling · 2025Article
- Systems Biology of the Cancer Cell.Annual review of biomedical engineering · 2025Review
- Cancer drug-tolerant persister cells: from biological questions to clinical opportunities.Nature reviews. Cancer · 2024Review
- Purinergic CaCancers · 2024Article
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- Unified tumor growth mechanisms from multimodel inference and dataset integration.PLoS computational biology · 2023Article
- Metabolic Reprogramming in Colon Cancer Cells Persistently Infected with Newcastle Disease Virus.Cancers · 2023Article
- Quantifying cancer cell plasticity with gene regulatory networks and single-cell dynamics.Frontiers in network physiology · 2023Review
- Quantitative landscapes reveal trajectories of cell-state transitions associated with drug resistance in melanoma.iScience · 2022Article
- A mechanistic modeling framework reveals the key principles underlying tumor metabolism.PLoS computational biology · 2022Article
- Systems-level network modeling deciphers the master regulators of phenotypic plasticity and heterogeneity in melanoma.iScience · 2021Article
- An Integrative Analysis of The Micro-RNAs Contributing in Stemness, Metastasis and B-Raf Pathways in Malignant Melanoma and Melanoma Stem Cell.Cell journal · 2021Article
- An in vitro model of tumor heterogeneity resolves genetic, epigenetic, and stochastic sources of cell state variability.PLoS biology · 2021Article
- Receptor-Driven ERK Pulses Reconfigure MAPK Signaling and Enable Persistence of Drug-Adapted BRAF-Mutant Melanoma Cells.Cell systems · 2020Article
- An Integrative Gene Expression and Mathematical Flux Balance Analysis Identifies Targetable Redox Vulnerabilities in Melanoma Cells.Cancer research · 2020Article
- Drug-Tolerant Idling Melanoma Cells Exhibit Theory-Predicted Metabolic Low-Low Phenotype.Frontiers in oncology · 2020Article
- Modeling heterogeneous tumor growth dynamics and cell-cell interactions at single-cell and cell-population resolution.Current opinion in systems biology · 2019Article
- Modelling bistable tumour population dynamics to design effective treatment strategies.Journal of theoretical biology · 2019Article
- Emerging roles of H3K9me3, SETDB1 and SETDB2 in therapy-induced cellular reprogramming.Clinical epigenetics · 2019Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Targeted therapy is an effective standard of care in BRAF-mutated malignant melanoma. However, the duration of tumor remission varies unpredictably among patients, and relapse is almost inevitable. Here, we examine the responses of several BRAF-mutated melanoma cell lines (including isogenic subclones) to BRAF inhibitors. We observe complex response dynamics across cell lines, with short-term responses (<100 h) varying from cell line to cell line. In the long term, however, we observe equilibration of all drug-treated populations into a nonquiescent state characterized by a balanced rate of death and division, which we term the "idling" state, and to our knowledge, this state has not been previously reported. Using mathematical modeling, we propose that the observed population-level dynamics are the result of cells transitioning between basins of attraction within a drug-modified phenotypic landscape. Each basin is associated with a drug-induced proliferation rate, a recently introduced metric of an antiproliferative drug effect. The idling population state represents a new dynamic equilibrium in which cells are distributed across the landscape such that the population achieves zero net growth. By fitting our model to experimental drug-response data, we infer the phenotypic landscapes of all considered melanoma cell lines and provide a unifying view of how BRAF-mutated melanomas respond to BRAF inhibition. We hypothesize that the residual disease observed in patients after targeted therapy is composed of a significant number of idling cells. Thus, defining molecular determinants of the phenotypic landscape that idling populations occupy may lead to "targeted landscaping" therapies based on rational modification of the landscape to favor basins with greater drug susceptibility.
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