NOTES
Corsello, Steven MNagari, Rohith TSpangler, Ryan DRossen, JordanKocak, MustafaBryan, Jordan GHumeidi, RanadPeck, DavidWu, XiaoyunTang, Andrew AWang, Vickie MBender, Samantha ALemire, EvanNarayan, RajivMontgomery, PhilipBen-David, UriGarvie, Colin WChen, YejiaRees, Matthew GLyons, Nicholas JMcFarland, James MWong, Bang TWang, LiDumont, NancyO'Hearn, Patrick JStefan, EricDoench, John GHarrington, Caitlin NGreulich, HeidiMeyerson, MatthewVazquez, FranciscaSubramanian, AravindRoth, Jennifer ABittker, Joshua ABoehm, Jesse SMader, Christopher CTsherniak, AviadGolub, Todd RengK08 CA230220/CA/NCI NIH HHS/KL2 TR002542/TR/NCATS NIH HHS/U01 HG008699/HG/NHGRI NIH HHS/U54 HL127366/HL/NHLBI NIH HHS/EnglandNat Cancer. 2020 Feb;1(2):235-248. doi: 10.1038/s43018-019-0018-6. Epub 2020 Jan 20.
Abstract
Anti-cancer 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, 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 cell lines' molecular features. Our findings include compounds that killed by inducing PDE3A-SLFN12 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 multi-drug resistance protein 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.