ArticleNature communications2017
Common and cell-type specific responses to anti-cancer drugs revealed by high throughput transcript profiling.
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 56 papers, 1 of them a synthesis that pooled it.
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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
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 108 citations in OpenAlex.
- Genomic meta-analysis of the interplay between 3D chromatin organization and gene expression programs under basal and stress conditions.Epigenetics & chromatin · 2018Pooled it
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- A renaissance in targeting the PI3K/AKT/mTOR pathway.Nature reviews. Drug discovery · 2026Review
- A Ponatinib-Associated Transcriptomic Signature: Implications for Cardiovascular Toxicity.International journal of molecular sciences · 2026Article
- ROR1-PI3K/AKT signaling drives adaptive resistance to cell cycle blockade in TP53 mutated ovarian cancer.Cell death & disease · 2026Article
- Pharmacogenomic Synthetic Lethal Screens Reveal Hidden Vulnerabilities and New Therapeutic Approaches for Treatment of NF1-Associated Tumors.Molecular cancer therapeutics · 2026Article
- Microenvironmental signals combine to induce non-additive molecular and phenotypic responses in mammary epithelial cells.iScience · 2025Article
- Utility of Multicellular Spheroids for Investigating Mechanisms of Chemoresistance in Triple-Negative Breast Cancer.International journal of molecular sciences · 2025Review
- A multiplex single-cell RNA-Seq pharmacotranscriptomics pipeline for drug discovery.Nature chemical biology · 2025Article
- Integrating pharmacogenomics and cheminformatics with diverse disease phenotypes for cell type-guided drug discovery.Genome medicine · 2025Article
- Article
- Tracing back primed resistance in cancer via sister cells.Nature communications · 2024Article
- DendroX: multi-level multi-cluster selection in dendrograms.BMC genomics · 2024Article
- AutoTransOP: translating omics signatures without orthologue requirements using deep learning.NPJ systems biology and applications · 2024Article
- TTD: Therapeutic Target Database describing target druggability information.Nucleic acids research · 2024Article
- MDTR: a knowledge-guided interpretable representation for quantifying liver toxicity at transcriptomic level.Frontiers in pharmacology · 2024Article
- Cholesterol mediated ferroptosis suppression reveals essential roles of Coenzyme Q and squalene.Communications biology · 2023Article
- Lysin (K)-specific demethylase 1 inhibition enhances proteasome inhibitor response and overcomes drug resistance in multiple myeloma.Experimental hematology & oncology · 2023Article
- Article
- Gene expression prediction based on neighbour connection neural network utilizing gene interaction graphs.PloS one · 2023Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
More effective use of targeted anti-cancer drugs depends on elucidating the connection between the molecular states induced by drug treatment and the cellular phenotypes controlled by these states, such as cytostasis and death. This is particularly true when mutation of a single gene is inadequate as a predictor of drug response. The current paper describes a data set of ~600 drug cell line pairs collected as part of the NIH LINCS Program ( http://www.lincsproject.org/ ) in which molecular data (reduced dimensionality transcript L1000 profiles) were recorded across dose and time in parallel with phenotypic data on cellular cytostasis and cytotoxicity. We report that transcriptional and phenotypic responses correlate with each other in general, but whereas inhibitors of chaperones and cell cycle kinases induce similar transcriptional changes across cell lines, changes induced by drugs that inhibit intra-cellular signaling kinases are cell-type specific. In some drug/cell line pairs significant changes in transcription are observed without a change in cell growth or survival; analysis of such pairs identifies drug equivalence classes and, in one case, synergistic drug interactions. In this case, synergy involves cell-type specific suppression of an adaptive drug response.
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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.