Discovering the anticancer potential of non-oncology drugs by systematic viability profiling
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Abstract
Anticancer uses of non-oncology drugs have occasionally been found, but such discoveries have been serendipitous. We sought to create a public resource containing the growth-inhibitory activity of 4,518 drugs tested across 578 human cancer cell lines. We used PRISM (profiling relative inhibition simultaneously in mixtures), a molecular barcoding method, to screen drugs against cell lines in pools. An unexpectedly large number of non-oncology drugs selectively inhibited subsets of cancer cell lines in a manner predictable from the molecular features of the cell lines. Our findings include compounds that killed by inducing phosphodiesterase 3A-Schlafen 12 complex formation, vanadium-containing compounds whose killing depended on the sulfate transporter SLC26A2, the alcohol dependence drug disulfiram, which killed cells with low expression of metallothioneins, and the anti-inflammatory drug tepoxalin, which killed via the multidrug resistance protein ATP-binding cassette subfamily B member 1 (ABCB1). The PRISM drug repurposing resource (https://depmap.org/repurposing) is a starting point to develop new oncology therapeutics, and more rarely, for potential direct clinical translation. Golub and colleagues tested thousands of drugs not originally developed for oncology across 578 human cancer cell lines, revealing growth-inhibitory effects and providing a resource to identify drugs with the potential to be repurposed for cancer.
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Mining correlations between cytotoxicity of 4,518 clinical and preclinical small molecules and E3 ligase expression across hundreds of cancer cell lines identified CR8, a CDK inhibitor, as a molecular glue degrader.
“Through systematic mining of databases for correlations between the cytotoxicity of 4,518 clinical and pre-clinical small molecules and E3 ligase expression levels across hundreds of human cancer cell lines,3–5 we identified CR8, a cyclin-dependent kinase (CDK) inhibitor,6 as a compound that acts as a molecular glue degrader.”
From The CDK inhibitor CR8 acts as a molecular glue degrader that depletes cyclin K (2020) · cites this paper as [4]
The Abstract (page unavailable) describes a resource measuring the growth-inhibitory activity of 4,518 drugs across 578 human cancer cell lines, and Results, ‘Predictive models of killing activity’ (page unavailable), reports that mRNA expression predicted drug response. The cited passages do not establish the more specific correlation with E3 ligase expression. Citations 3–5 attach to the database-mining clause; the sentence presents CR8’s identification as the citing authors’ own finding, not this source’s. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThe AUC formulation used places AUC values on a scale between 0 and 1, where lower AUC values indicate increased sensitivity to treatment.
“This formulation puts AUC values on a scale between 0 and 1, where lower AUC values indicate increased sensitivity to treatment (43).”
From Mechanisms of Resistance to Oncogenic KRAS Inhibition in Pancreatic Cancer (2024) · cites this paper as [43]
The Methods section (“Dose-response analysis”) says lower AUC indicates greater treatment sensitivity and that the normalized formulation places AUC between 0 and 1. It limits that range to curves whose lower asymptotes are less than 1, a condition the citing sentence omits. (LLM, conf=0.86)
Experimental — accuracy not yet measuredCancer cell-line collections are deeply annotated, offering mutational, gene expression, protein abundance, and epigenetic profiles.
“Cancer cell-line collections are deeply annotated, offering a wealth of data to the “cell” branch of the input, including mutational, gene expression, protein abundance, and epigenetic profiles, among others.187,188”
From Advancing Targeted Protein Degradation via Multiomics Profiling and Artificial Intelligence (2023) · cites this paper as [188]
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Xie, Q., Du, Y., Ghosh, S., Rajendran, S., Cohen-Gadol, A. A., Baizabal, J.-M., Nephew, K. P., Han, L., & Shen, J. (2025) · NPJ Precision Oncology · doi:10.1038/s41698-025-00829-5 · Cited by 10 · see citing works
The EFFECT benchmark suite: measuring cancer sensitivity prediction performance - without the bias
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- Authors
- Corsello, S. M., Nagari, R. T., Spangler, R. D., Rossen, J., Kocak, M., Bryan, J. G., Humeidi, R., Peck, D., Wu, X., Tang, A. A., Wang, V. M., Bender, S. A., Lemire, E., Narayan, R., Montgomery, P., Ben-David, U., Garvie, C. W., Chen, Y., Rees, M. G., Lyons, N. J., McFarland, J. M., Wong, B. T., Wang, L., Dumont, N., O’Hearn, P. J., Stefan, E., Doench, J. G., Harrington, C. N., Greulich, H., Meyerson, M., Vazquez, F., Subramanian, A., Roth, J. A., Bittker, J. A., Boehm, J. S., Mader, C. C., Tsherniak, A., & Golub, T. R.
- Affiliations
- Broad Institute (US)
- Corresponding author
- Golub, Todd R.
- ORCID
- Corsello, Steven M.
- Nagari, Rohith T.
- Rossen, Jordan
- Kocak, Mustafa
- Bryan, Jordan G.
- Wu, Xiaoyun
- Lemire, Evan
- Montgomery, Philip
- Ben-David, Uri
- Garvie, Colin W.
- Rees, Matthew G.
- McFarland, James M.
- Wang, Li
- Dumont, Nancy
- O’Hearn, Patrick J.
- Doench, John G.
- Harrington, Caitlin N.
- Greulich, Heidi
- Meyerson, Matthew
- Subramanian, Aravind
- Roth, Jennifer A.
- Bittker, Joshua A.
- Boehm, Jesse S.
- Tsherniak, Aviad
- Golub, Todd R.
- Venue
- Nature Cancer
- Published
- 2020-01-20
- Volume
- 1
- Issue
- 2
- Pages
- 235-248
- ISSN
- 2662-1347 (ISSN-L)
- PMC
- PMC7328899
- OpenAlex
- W3003119869
- Semantic Scholar
- ab89209b707a91ebe4ac9ce16fd3eeac4c3bdd0b
- Cited by
- 878
- References
- 58
- Citations by year
- 2026: 112 · 2025: 176 · 2024: 152 · 2023: 167 · 2022: 125 · 2021: 87 · 2020: 56 · 2018: 1 · 2015: 1 · 2014: 1
- FWCI
- 54.29
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Nature Cancer (publishedVersion)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Health & Human Services | National Institutes of Health (KL2 TR002542, K08 CA230220, U01 HG008699, U54 HL127366)
- Conquer Cancer Foundation
- Next Generation Fund at the Broad Institute of MIT and Harvard
- Carlos Slim Foundation (Slim Initiative in Genomic Medicine for the Americas
- Topics
- Physical Sciences › Computer Science › Computational Theory and Mathematics › Computational Drug Discovery Methods
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Keywords
- drug repurposing, anticancer agents, cancer cell lines, PRISM, DNA barcoding, vanadium compounds, disulfiram, metallothionein, tepoxalin, growth inhibition
- MeSH terms
- Cell Line, Disulfiram, Humans, Neoplasms, Drug Repositioning
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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