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...
Gespeichert in:
| Hauptverfasser: | , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
November 17, 2011
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| 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 |
MARC
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| 520 | |a 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. | ||
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