mTORC 2:1 for chemotherapy sensitization in glioblastoma

• Verfasst von: Wick, Wolfgang [VerfasserIn]
• Verfasst von: Blaes, Jonas [VerfasserIn]
• Verfasst von: Weiler, Markus [VerfasserIn]
• Titel: mTORC 2:1 for chemotherapy sensitization in glioblastoma
• Verf.angabe: Wolfgang Wick, Jonas Blaes, and Markus Weiler
• E-Jahr: 2011
• Jahr: November 17, 2011
• Umfang: 2 S.
• Fussnoten: Gesehen am 14.12.2022
• Titel Quelle: Enthalten in: Cancer discovery
• Ort Quelle: Philadelphia, Pa., 2011
• Jahr Quelle: 2011
• Band/Heft Quelle: 1(2011), 6 vom: 16. Nov., Seite 475-476
• ISSN Quelle: 2159-8290
• DOI: doi:10.1158/2159-8290.CD-11-0264
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1827021918

Abstract

mTOR signaling is frequently deregulated in cancer, including brain tumors. Although the signaling of mTOR complex 1 (mTORC1) has been subject to intensive investigations and mTORC1 itself has been a well-established cancer drug target for years, the role of the second complex, mTORC2, remains elusive. Tanaka et al. reveal an EGFRvIII-mTORC2-NFκB signaling cascade and demonstrate that mTORC2 mediates cisplatin resistance through NF-κB in an Akt-independent manner in glioblastoma. Uncovering the role of mTORC2 in chemotherapy resistance in glioblastoma highlights the need for further investigations of mTORC2 inhibition. Cancer Discovery; 1(6); 475-76. ©2011 AACR.Commentary on Tanaka et al., p. 524.