ArticlePLoS computational biology2019
Phenotypic heterogeneity and evolution of melanoma cells associated with targeted therapy resistance.
Article in PLoS computational biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 57 citations in OpenAlex.
- Trial
- Signalling Entropy Across Measurement Scales: A Compositional Dilution Lemma and Cross-Modality Invariance for Information-Theoretic Analysis of Cancer Transcriptomes.Entropy (Basel, Switzerland) · 2026Article
- Sequential transcriptional waves and NF-κB-driven chromatin remodeling direct drug-induced dedifferentiation in cancer.Nature communications · 2026Article
- Melanoma treatment in the era of nanotechnology and precision medicine.Journal of nanobiotechnology · 2025Review
- A TGF-βR/IL-2R immunomodulatory fusion protein transforms immunosuppression into T cell activation to enhance adoptive T cell therapy.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Deep learning identifies heterogeneous subpopulations in breast cancer cell lines.npj biomedical innovations · 2025Article
- Signaling and transcriptional dynamics underlying early adaptation to oncogenic BRAF inhibition.Cell systems · 2025Article
- Recent Developments in Single-Cell Metabolomics by Mass Spectrometry─A Perspective.Journal of proteome research · 2025Review
- Mannose metabolism reshapes T cell differentiation to enhance anti-tumor immunity.Cancer cell · 2025Article
- Mutually exclusive teams-like patterns of gene regulation characterize phenotypic heterogeneity along the noradrenergic-mesenchymal axis in neuroblastoma.Cancer biology & therapy · 2024Article
- Kinetic Trajectories of Glucose Uptake in Single Cancer Cells Reveal a Drug-Induced Cell-State Change Within Hours of Drug Treatment.The journal of physical chemistry. B · 2024Article
- Mechanisms of Melanoma Progression and Treatment Resistance: Role of Cancer Stem-like Cells.Cancers · 2024Review
- Systematic analysis and optimization of early warning signals for critical transitions using distribution data.iScience · 2023Article
- Toward a systems-level probing of tumor clonality.iScience · 2023Review
- Phenotype Switching and the Melanoma Microenvironment; Impact on Immunotherapy and Drug Resistance.International journal of molecular sciences · 2023Review
- Pterostilbene-Mediated Inhibition of Cell Proliferation and Cell Death Induction in Amelanotic and Melanotic Melanoma.International journal of molecular sciences · 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
- Archetype tasks link intratumoral heterogeneity to plasticity and cancer hallmarks in small cell lung cancer.Cell systems · 2022Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Phenotypic plasticity is associated with non-genetic drug tolerance in several cancers. Such plasticity can arise from chromatin remodeling, transcriptomic reprogramming, and/or protein signaling rewiring, and is characterized as a cell state transition in response to molecular or physical perturbations. This, in turn, can confound interpretations of drug responses and resistance development. Using BRAF-mutant melanoma cell lines as the prototype, we report on a joint theoretical and experimental investigation of the cell-state transition dynamics associated with BRAF inhibitor drug tolerance. Thermodynamically motivated surprisal analysis of transcriptome data was used to treat the cell population as an entropy maximizing system under the influence of time-dependent constraints. This permits the extraction of an epigenetic potential landscape for drug-induced phenotypic evolution. Single-cell flow cytometry data of the same system were modeled with a modified Fokker-Planck-type kinetic model. The two approaches yield a consistent picture that accounts for the phenotypic heterogeneity observed over the course of drug tolerance development. The results reveal that, in certain plastic cancers, the population heterogeneity and evolution of cell phenotypes may be understood by accounting for the competing interactions of the epigenetic potential landscape and state-dependent cell proliferation. Accounting for such competition permits accurate, experimentally verifiable predictions that can potentially guide the design of effective treatment strategies.
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What OpenQuestion holds
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.