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A subset of these tumors recur and invade the brain, even after surgery and radiation, resulting in significant disability. There is currently no standard-of-care chemotherapy for meningiomas. As genomic DNA methylation profiling can prognostically stratify these lesions, we sought to determine whether any existing chemotherapies might be effective against meningiomas with high-risk methylation profiles.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>A previously published dataset of meningioma methylation profiles was used to screen for clinically significant CpG methylation events and associated cellular pathways. Based on these results, patient-derived meningioma cell lines were used to test candidate drugs in vitro and in vivo, including efficacy in conjunction with radiotherapy.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>We identified 981 genes for which methylation of mapped CpG sites was related to progression-free survival in meningiomas. Associated molecular pathways were cross-referenced with FDA-approved cancer drugs, which nominated Docetaxel as a promising candidate for further preclinical analyses. Docetaxel arrested growth in 17 meningioma cell sources, representing all tumor grades, with a clinically favorable IC50 values ranging from 0.3 nM to 10.7 mM. The inhibitory effects of this medication scaled with tumor doubling time, with maximal benefit in fast-growing lesions. The combination of Docetaxel and radiation therapy increased markers of apoptosis and double-stranded DNA breaks, and extended the survival of mice engrafted with meningioma cells relative to either modality alone.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Global patterns of DNA methylation may be informative for the selection of chemotherapies against meningiomas, and existing drugs may enhance radiation sensitivity in high-risk cases.<\/jats:p><\/jats:sec>","DOI":"10.1093\/neuonc\/noac206","type":"journal-article","created":{"date-parts":[[2022,8,17]],"date-time":"2022-08-17T13:30:46Z","timestamp":1660743046000},"page":"508-519","source":"Crossref","is-referenced-by-count":6,"title":["Docetaxel targets aggressive methylation profiles and serves as a radiosensitizer in high-risk meningiomas"],"prefix":"10.1093","volume":"25","author":[{"given":"Mark W","family":"Youngblood","sequence":"first","affiliation":[{"name":"Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University , Chicago, Illinois , USA"},{"name":"Northwestern Medicine Malnati Brain Tumor Institute of the Robert H. 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Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University , Chicago, Illinois , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen T","family":"Magill","sequence":"additional","affiliation":[{"name":"Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University , Chicago, Illinois , USA"},{"name":"Northwestern Medicine Malnati Brain Tumor Institute of the Robert H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University , Chicago, Illinois , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sean","family":"Sachdev","sequence":"additional","affiliation":[{"name":"Northwestern Medicine Malnati Brain Tumor Institute of the Robert H. 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