NFKBIA Deletion in Glioblastomas

To the Editor: Aberrant constitutive activation of nuclear factor of κ-light polypeptide gene enhancer in B cells (NF-κB), a transcription factor activated by the epidermal growth factor receptor (EGFR)–signaling pathway, has been detected in glioblastomas. Previous clinical studies have failed to d...

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Veröffentlicht in:The New England journal of medicine 2011-07, Vol.365 (3), p.276-278
Hauptverfasser: Idbaih, Ahmed, Marie, Yannick, Sanson, Marc
Format: Artikel
Sprache:eng
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Zusammenfassung:To the Editor: Aberrant constitutive activation of nuclear factor of κ-light polypeptide gene enhancer in B cells (NF-κB), a transcription factor activated by the epidermal growth factor receptor (EGFR)–signaling pathway, has been detected in glioblastomas. Previous clinical studies have failed to demonstrate the efficacy of therapies that target EGFR. 1 , 2 Bredel et al. (Feb. 17 issue) 3 hypothesized that the therapeutic effects of EGFR inhibition could be circumvented by aberrant activated signaling of this pathway downstream of EGFR. They also reported that deletion of the gene encoding NF-κB inhibitor-α ( NFKBIA ), an inhibitor of the EGFR pathway, is associated with . . .
ISSN:0028-4793
1533-4406
DOI:10.1056/NEJMc1103354