Therapeutic strategies for diffuse midline glioma from high-throughput combination drug screening
Grant L. Lin(Stanford University), Kelli M. Wilson(National Institutes of Health), Michele Ceribelli(National Institutes of Health), Benjamin Z. Stanton(Nationwide Children's Hospital), Pamelyn J. Woo(Stanford University), Sara Kreimer(Stanford University), Elizabeth Y. Qin(Stanford University), Xiaohu Zhang(National Institutes of Health), James Lennon(Stanford University), Surya Nagaraja(Stanford University), Patrick J. Morris(National Institutes of Health), Michael A. Quezada(Stanford University), Shawn Gillespie(Stanford University), Damien Duveau(National Institutes of Health), Aleksandra M. Michalowski(National Institutes of Health), Paul Shinn(National Institutes of Health), Rajarshi Guha(National Institutes of Health), Marc Ferrer(National Institutes of Health), Carleen Klumpp‐Thomas(National Institutes of Health), Sam Michael(National Institutes of Health), Crystal McKnight(National Institutes of Health), Paras S. Minhas(Stanford University), Zina Itkin(National Institutes of Health), Eric H. Raabe(Johns Hopkins University), Lu Chen(National Institutes of Health), Reem Ghanem(Stanford University), Anna C. Geraghty(Stanford University), Lijun Ni(Stanford University), Katrin I. Andreasson(Stanford University), Nicholas A. Vitanza(Stanford University), Katherine E. Warren(National Institutes of Health), Craig J. Thomas(National Institutes of Health), Michelle Monje(California Institute for Regenerative Medicine)
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Abstract
) production via nicotinamide phosphoribosyltransferase (NAMPT) inhibition demonstrated that metabolic catastrophe drives the combination-induced cytotoxicity. This study provides a comprehensive single-agent and combinatorial drug screen for DMG and identifies concomitant HDAC and proteasome inhibition as a promising therapeutic strategy that underscores underrecognized metabolic vulnerabilities in DMG.
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