mTORC 2:1 for chemotherapy sensitization in glioblastoma

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 elusi...

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Hauptverfasser: Wick, Wolfgang (VerfasserIn) , Blaes, Jonas (VerfasserIn) , Weiler, Markus (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: November 17, 2011
In: Cancer discovery
Year: 2011, Jahrgang: 1, Heft: 6, Pages: 475-476
ISSN:2159-8290
DOI:10.1158/2159-8290.CD-11-0264
Online-Zugang:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1158/2159-8290.CD-11-0264
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Verfasserangaben:Wolfgang Wick, Jonas Blaes, and Markus Weiler
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Zusammenfassung: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.
Beschreibung:Gesehen am 14.12.2022
Beschreibung:Online Resource
ISSN:2159-8290
DOI:10.1158/2159-8290.CD-11-0264