ArticleNature communications2021
Melanoma subpopulations that rapidly escape MAPK pathway inhibition incur DNA damage and rely on stress signalling.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.
- MicroRNAs and Cellular Senescence in Melanoma: An Underexplored Link to Tumor Progression-A Systematic Review with Bioinformatics Analyses.International journal of molecular sciences · 2026Pooled it
- MAPK Inhibitor-Tolerant Persister Cells in Melanoma: Mechanisms and Therapeutic Vulnerabilities.Cancer science · 2026Review
- Article
- Dynamic Time-Resolved Remodeling of the Immune Microenvironment After Resistance to BRAF/MEK Inhibitors in Melanoma: Mechanisms, Biomarkers, and Emerging Therapeutic Strategies.International journal of molecular sciences · 2026Review
- Heterogeneous, population-level drug-tolerant persisters exhibit ion-channel remodeling and ferroptosis susceptibility.bioRxiv : the preprint server for biology · 2026Article
- mTOR inhibition enhances the antitumor efficacy of pan-RAF-MEK blockade by inhibiting the ATF4-MTHFD2 pathway.Cell death & disease · 2026Article
- The integrated stress response in cancer: mechanisms of tumor adaptation and therapeutic targeting.Biochemical Society transactions · 2026Review
- Plasticity, signaling, and metabolic rewiring in melanoma persister cells.Communications biology · 2026Review
- Chemotherapy Supports Cancer Cell Dissemination in a Melanoma Preclinical Model.Asian Pacific journal of cancer prevention : APJCP · 2026Article
- Clonal dynamics shaped by diverse drug-tolerant persister states in melanoma resistance.Molecular cancer · 2026Article
- Focal Adhesion and Cancer Cell Cycle-Associated Resistance.ACS omega · 2026Review
- DNA fragmentation factor B suppresses interferon to enable cancer persister cell regrowth.Nature cell biology · 2025Article
- Clonal dynamics shaped by diverse drug-tolerant persister states in melanoma resistance.bioRxiv : the preprint server for biology · 2025Article
- MAPK and mTORC1 signaling converge to drive cyclin D1 protein production to enable cell cycle reentry in melanoma persister cells.Science signaling · 2025Article
- How cancer arises: Genetics releases, plasticity creates, genetics stabilizes.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Exploring the Single-Cell Dynamics of FOXM1 Under Cell Cycle Perturbations.Cell proliferation · 2025Article
- Cx43 enhances response to BRAF/MEK inhibitors by reducing DNA repair capacity.Nature communications · 2025Article
- Molecular mechanisms altering cell identity in cancer.Oncogene · 2025Review
- Deciphering the history of ERK activity from fixed-cell immunofluorescence measurements.Nature communications · 2025Article
- CHOIR improves significance-based detection of cell types and states from single-cell data.Nature genetics · 2025Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Despite the increasing number of effective anti-cancer therapies, successful treatment is limited by the development of drug resistance. While the contribution of genetic factors to drug resistance is undeniable, little is known about how drug-sensitive cells first evade drug action to proliferate in drug. Here we track the responses of thousands of single melanoma cells to BRAF inhibitors and show that a subset of cells escapes drug via non-genetic mechanisms within the first three days of treatment. Cells that escape drug rely on ATF4 stress signalling to cycle periodically in drug, experience DNA replication defects leading to DNA damage, and yet out-proliferate other cells over extended treatment. Together, our work reveals just how rapidly melanoma cells can adapt to drug treatment, generating a mutagenesis-prone subpopulation that expands over time.
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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.