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 |
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| creator | 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 |
| description | 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. . . . |
| doi_str_mv | 10.1056/NEJMoa1006312 |
| format | Article |
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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. . . .</description><identifier>ISSN: 0028-4793</identifier><identifier>ISSN: 1533-4406</identifier><identifier>EISSN: 1533-4406</identifier><identifier>DOI: 10.1056/NEJMoa1006312</identifier><identifier>PMID: 21175304</identifier><identifier>CODEN: NEJMAG</identifier><language>eng</language><publisher>Waltham, MA: Massachusetts Medical Society</publisher><subject>Biological and medical sciences ; Cancer ; DNA Mutational Analysis ; Gene Amplification ; Gene Deletion ; Gene Expression ; General aspects ; Genes ; Genes, erbB-1 ; Genetics & genetic processes ; Glioblastoma - genetics ; Glioblastoma - mortality ; Génétique & processus génétiques ; Humans ; I-kappa B Proteins - genetics ; Kaplan-Meier Estimate ; Life sciences ; Medical sciences ; Mutation ; Neurology ; NF-KappaB Inhibitor alpha ; Prognosis ; Proteins ; Sciences du vivant ; Tumor Cells, Cultured ; Tumors ; Tumors of the nervous system. Phacomatoses</subject><ispartof>The New England journal of medicine, 2011-02, Vol.364 (7), p.627-637</ispartof><rights>Copyright © 2011 Massachusetts Medical Society. All rights reserved.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2010 Massachusetts Medical Society. 2010</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c521t-a8302bde6b6f170b9b373118883b11d4fc4e8e12753bfbb3008879285e3ab193</citedby><cites>FETCH-LOGICAL-c521t-a8302bde6b6f170b9b373118883b11d4fc4e8e12753bfbb3008879285e3ab193</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.nejm.org/doi/pdf/10.1056/NEJMoa1006312$$EPDF$$P50$$Gmms$$H</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/868663103?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>230,314,777,781,882,2746,2747,26084,27905,27906,52363,54045,64364,64368,72218</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23864447$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21175304$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bredel, Claudia</creatorcontrib><creatorcontrib>Bredel, Markus</creatorcontrib><creatorcontrib>Scholtens, Denise M</creatorcontrib><creatorcontrib>Yadav, Ajay K</creatorcontrib><creatorcontrib>Alvarez, Angel A</creatorcontrib><creatorcontrib>Renfrow, Jaclyn J</creatorcontrib><creatorcontrib>Chandler, James P</creatorcontrib><creatorcontrib>Yu, Irene L.Y</creatorcontrib><creatorcontrib>Carro, Maria S</creatorcontrib><creatorcontrib>Dai, Fangping</creatorcontrib><creatorcontrib>Tagge, Michael J</creatorcontrib><creatorcontrib>Ferrarese, Roberto</creatorcontrib><creatorcontrib>Phillips, Heidi S</creatorcontrib><creatorcontrib>Lukac, Paul J</creatorcontrib><creatorcontrib>Robe, Pierre A</creatorcontrib><creatorcontrib>Weyerbrock, Astrid</creatorcontrib><creatorcontrib>Vogel, Hannes</creatorcontrib><creatorcontrib>Dubner, Steven</creatorcontrib><creatorcontrib>Mobley, Bret</creatorcontrib><creatorcontrib>He, Xiaolin</creatorcontrib><creatorcontrib>Scheck, Adrienne C</creatorcontrib><creatorcontrib>Sikic, Branimir I</creatorcontrib><creatorcontrib>Aldape, Kenneth D</creatorcontrib><creatorcontrib>Chakravarti, Arnab</creatorcontrib><creatorcontrib>Harsh, Griffith R</creatorcontrib><title>NFKBIA Deletion in Glioblastomas</title><title>The New England journal of medicine</title><addtitle>N Engl J Med</addtitle><description>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. . . .</description><subject>Biological and medical sciences</subject><subject>Cancer</subject><subject>DNA Mutational Analysis</subject><subject>Gene Amplification</subject><subject>Gene Deletion</subject><subject>Gene Expression</subject><subject>General aspects</subject><subject>Genes</subject><subject>Genes, erbB-1</subject><subject>Genetics & genetic processes</subject><subject>Glioblastoma - genetics</subject><subject>Glioblastoma - mortality</subject><subject>Génétique & processus génétiques</subject><subject>Humans</subject><subject>I-kappa B Proteins - genetics</subject><subject>Kaplan-Meier Estimate</subject><subject>Life sciences</subject><subject>Medical sciences</subject><subject>Mutation</subject><subject>Neurology</subject><subject>NF-KappaB Inhibitor alpha</subject><subject>Prognosis</subject><subject>Proteins</subject><subject>Sciences du vivant</subject><subject>Tumor Cells, Cultured</subject><subject>Tumors</subject><subject>Tumors of the nervous system. 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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. . . .</abstract><cop>Waltham, MA</cop><pub>Massachusetts Medical Society</pub><pmid>21175304</pmid><doi>10.1056/NEJMoa1006312</doi><tpages>11</tpages></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; ProQuest Central UK/Ireland; New England Journal of Medicine |
| subjects | Biological and medical sciences Cancer DNA Mutational Analysis Gene Amplification Gene Deletion Gene Expression General aspects Genes Genes, erbB-1 Genetics & genetic processes Glioblastoma - genetics Glioblastoma - mortality Génétique & processus génétiques Humans I-kappa B Proteins - genetics Kaplan-Meier Estimate Life sciences Medical sciences Mutation Neurology NF-KappaB Inhibitor alpha Prognosis Proteins Sciences du vivant Tumor Cells, Cultured Tumors Tumors of the nervous system. Phacomatoses |
| title | NFKBIA Deletion in Glioblastomas |
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