NFKBIA Deletion in Glioblastomas

This study shows that the tumor-suppressor gene NFKBIA is deleted in glioblastomas and suggests a degree of mutual exclusivity between these deletions and amplification of EGFR in these tumors. Both NFKBIA deletion and EGFR amplification are associated with poor survival. Glioblastoma multiforme is...

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Veröffentlicht in:The New England journal of medicine 2011-02, Vol.364 (7), p.627-637
Hauptverfasser: Bredel, Claudia, Bredel, Markus, Scholtens, Denise M, Yadav, Ajay K, Alvarez, Angel A, Renfrow, Jaclyn J, Chandler, James P, Yu, Irene L.Y, Carro, Maria S, Dai, Fangping, Tagge, Michael J, Ferrarese, Roberto, Phillips, Heidi S, Lukac, Paul J, Robe, Pierre A, Weyerbrock, Astrid, Vogel, Hannes, Dubner, Steven, Mobley, Bret, He, Xiaolin, Scheck, Adrienne C, Sikic, Branimir I, Aldape, Kenneth D, Chakravarti, Arnab, Harsh, Griffith R
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Sprache:eng
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Zusammenfassung:This study shows that the tumor-suppressor gene NFKBIA is deleted in glioblastomas and suggests a degree of mutual exclusivity between these deletions and amplification of EGFR in these tumors. Both NFKBIA deletion and EGFR amplification are associated with poor survival. Glioblastoma multiforme is the most common and most deadly primary brain tumor. 1 It is a complex disease, in which many signaling pathways are disrupted. 2 – 7 Almost all glioblastomas have excessive activation of the epidermal growth factor receptor (EGFR) pathway, 8 often brought about by amplification (see the Glossary for this and other key terms) or activating mutations of the EGFR oncogene. 9 Alternative mechanisms of the activation of the EGFR pathway may exist in tumors that do not have alterations of EGFR . Nuclear factor of κ-light polypeptide gene enhancer in B-cells (NF-κB) is a transcription factor activated by the EGFR pathway. . . .
ISSN:0028-4793
1533-4406
1533-4406
DOI:10.1056/NEJMoa1006312