Histone deacetylase 10-promoted autophagy as a druggable point of interference to improve the treatment response of advanced neuroblastomas

• Verfasst von: Oehme, Ina [VerfasserIn]
• Verfasst von: Lodrini, Marco [VerfasserIn]
• Verfasst von: Brady, Nathan [VerfasserIn]
• Verfasst von: Witt, Olaf [VerfasserIn]
• Titel: Histone deacetylase 10-promoted autophagy as a druggable point of interference to improve the treatment response of advanced neuroblastomas
• Verf.angabe: Ina Oehme, Marco Lodrini, Nathan R Brady, and Olaf Witt
• E-Jahr: 2013
• Jahr: 08 Oct 2013
• Umfang: 3 S.
• Fussnoten: Gesehen am 29.11.2021
• Titel Quelle: Enthalten in: Autophagy
• Ort Quelle: Abingdon, Oxon : Taylor & Francis, 2005
• Jahr Quelle: 2013
• Band/Heft Quelle: 9(2013), 12, Seite 2163-2165
• ISSN Quelle: 1554-8635
• DOI: doi:10.4161/auto.26450
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: drug resistance
• Sach-SW: HDAC-inhibitor
• Sach-SW: HDAC10
• Sach-SW: lysosome
• Sach-SW: macroautophagy
• Sach-SW: neuroblastoma
• K10plus-PPN: 1779760213

Abstract

Neuroblastoma is the most common extracranial solid tumor in childhood. Despite intense multimodal therapy and many improvements through basic scientific and clinical research, the successful response of advanced-stage patients to chemotherapy remains poor. Autophagy is a cytoprotective mechanism that may help advanced cancer cells survive stressful conditions such as chemotherapy. Here we review our recent findings describing HDAC10 as a promoter of autophagy-mediated survival in neuroblastoma cells and identifying this HDAC isozyme as a druggable regulator of advanced-stage tumor cell survival. These results propose a new and promising way to considerably improve treatment response in the neuroblastoma patient subgroup with the poorest outcome.