ArticleNature genetics2021
Genetic screening for single-cell variability modulators driving therapy resistance.
Article in Nature genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
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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
50 citing papers in PubMed, 77 citations in OpenAlex.
- Mechanistic modeling reveals a configurable AP-1 network governing cell-state heterogeneity and adaptive plasticity in melanoma cells.Cell reports · 2026Article
- PredictedInternational journal of molecular sciences · 2026Article
- Systematic multivariate analysis of chromatin complex dependencies reveals Set1C/COMPASS as a melanoma-enriched epigenetic vulnerability.PLoS computational biology · 2026Article
- Varying susceptibility of subpopulations along the epithelial-mesenchymal spectrum to undergo EMT.The FEBS journal · 2026Article
- Dissecting autonomous enzymatic variability in single cells.Nature communications · 2026Article
- Spatial transcriptomics reveals influence of microenvironment on intrinsic fates in melanoma therapy resistance.Genome biology · 2026Article
- AP-1 mediates cellular adaptation and memory formation.Nature communications · 2026Article
- Systematic multivariate analysis of chromatin complex dependencies reveals Set1C/COMPASS as a melanoma-enriched epigenetic vulnerability.bioRxiv : the preprint server for biology · 2026Article
- An expanded role for single-cell chemical genomics profiling in drug discovery.The Biochemical journal · 2026Review
- What makes genes burst.Trends in cell biology · 2026Review
- A memory-driven reinforcement learning model of phenotypic adaptation for anticipating therapeutic resistance in prostate cancer.bioRxiv : the preprint server for biology · 2025Article
- Clonal dynamics shaped by diverse drug-tolerant persister states in melanoma resistance.bioRxiv : the preprint server for biology · 2025Article
- Intercellular signaling reinforces single-cell level phenotypic transitions and facilitates robust re-equilibrium of heterogeneous cancer cell populations.Cell communication and signaling : CCS · 2025Article
- Heterogeneous therapy-resistant cancer cells have distinct and exploitable drug sensitivity profiles.bioRxiv : the preprint server for biology · 2025Article
- PKN2 Is a Dependency of the Mesenchymal-like Cancer Cell State.Cancer discovery · 2025Article
- Predicting cell properties with AI from 3D imaging flow cytometer data.Scientific reports · 2025Article
- Prevalence of and gene regulatory constraints on transcriptional adaptation in single cells.Genome biology · 2024Article
- AP-1 Mediates Cellular Adaptation and Memory Formation During Therapy Resistance.bioRxiv : the preprint server for biology · 2024Article
- Single-cell decoding of drug induced transcriptomic reprogramming in triple negative breast cancers.Genome biology · 2024Article
- Spatial transcriptomics reveals influence of microenvironment on intrinsic fates in melanoma therapy resistance.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Cellular plasticity describes the ability of cells to transition from one set of phenotypes to another. In melanoma, transient fluctuations in the molecular state of tumor cells mark the formation of rare cells primed to survive BRAF inhibition and reprogram into a stably drug-resistant fate. However, the biological processes governing cellular priming remain unknown. We used CRISPR-Cas9 genetic screens to identify genes that affect cell fate decisions by altering cellular plasticity. We found that many factors can independently affect cellular priming and fate decisions. We discovered a new plasticity-based mode of increasing resistance to BRAF inhibition that pushes cells towards a more differentiated state. Manipulating cellular plasticity through inhibition of DOT1L before the addition of the BRAF inhibitor resulted in more therapy resistance than concurrent administration. Our results indicate that modulating cellular plasticity can alter cell fate decisions and may prove useful for treating drug resistance in other cancers.
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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.