ArticleNature biotechnology2016
High-throughput identification of genotype-specific cancer vulnerabilities in mixtures of barcoded tumor cell lines.
Article in Nature biotechnology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 230 papers, 1 of them a synthesis that pooled it.
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Who cites it
230 citing papers in PubMed, 1 synthesis or guideline pooled it, 378 citations in OpenAlex.
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- A stress-adaptive lipid kinase axis defines metabolic vulnerabilities in neuroendocrine prostate cancer.Cancer cell · 2026Article
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- A Stress-Adaptive Lipid Kinase Axis Defines Metabolic Vulnerabilities in Neuroendocrine Prostate Cancer.bioRxiv : the preprint server for biology · 2026Article
- Cancer Susceptibility to Stapled Oncolytic Peptides Is Dictated by Membrane Cholesterol and Inflammatory Signaling.Cancer research · 2026Article
- Deep Learning for Anticancer Drug Discovery Targeting Non-Apoptotic Regulated Cell Death Mechanisms.Pharmaceuticals (Basel, Switzerland) · 2026Review
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- Proximity-Induced Rewiring of Oncogenic Kinase Triggers Apoptosis.ACS central science · 2026Article
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- AMDRP: adaptive drug feature fusion and multihead bidirectional cross-attention network for drug-cancer cell response prediction.Molecular diversity · 2026Article
170 more citing papers are in PubMed but not listed here.
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Authors and funding
21 authors at 2 institutions in 1 country.
Funding
Abstract
Hundreds of genetically characterized cell lines are available for the discovery of genotype-specific cancer vulnerabilities. However, screening large numbers of compounds against large numbers of cell lines is currently impractical, and such experiments are often difficult to control. Here we report a method called PRISM that allows pooled screening of mixtures of cancer cell lines by labeling each cell line with 24-nucleotide barcodes. PRISM revealed the expected patterns of cell killing seen in conventional (unpooled) assays. In a screen of 102 cell lines across 8,400 compounds, PRISM led to the identification of BRD-7880 as a potent and highly specific inhibitor of aurora kinases B and C. Cell line pools also efficiently formed tumors as xenografts, and PRISM recapitulated the expected pattern of erlotinib sensitivity in vivo.
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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.