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rdf:type |
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lifeskim:mentions |
umls-concept:C0027819,
umls-concept:C0031437,
umls-concept:C0033414,
umls-concept:C0205214,
umls-concept:C0271510,
umls-concept:C0580822,
umls-concept:C0851285,
umls-concept:C0965644,
umls-concept:C1332838,
umls-concept:C1333897,
umls-concept:C1547300,
umls-concept:C1548760,
umls-concept:C1550594,
umls-concept:C1704838
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|
pubmed:issue |
5
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|
pubmed:dateCreated |
2006-11-13
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|
pubmed:abstractText |
In neuroblastoma specimens, HIF-2alpha but not HIF-1alpha is strongly expressed in well-vascularized areas. In vitro, HIF-2alpha protein was stabilized at 5% O2 (resembling end capillary oxygen conditions) and, in contrast to the low HIF-1alpha activity at this oxygen level, actively transcribed genes like VEGF. Under hypoxia (1% O2), HIF-1alpha was transiently stabilized and primarily mediated acute responses, whereas HIF-2alpha protein gradually accumulated and governed prolonged hypoxic gene activation. Knockdown of HIF-2alpha reduced growth of neuroblastoma tumors in athymic mice. Furthermore, high HIF-2alpha protein levels were correlated with advanced clinical stage and high VEGF expression and predicted poor prognosis in a clinical neuroblastoma material. Our results demonstrate the relevance of HIF-2alpha in neuroblastoma progression and have general tumor biological implications.
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pubmed:language |
eng
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pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
|
|
pubmed:status |
MEDLINE
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|
pubmed:month |
Nov
|
|
pubmed:issn |
1535-6108
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|
pubmed:author |
pubmed-author:BorgAkeA,
pubmed-author:FredlundErikE,
pubmed-author:GradinKatarinaK,
pubmed-author:Holmquist-MengelbierLindaL,
pubmed-author:LöfstedtTobiasT,
pubmed-author:NavarroSamuelS,
pubmed-author:NilssonHelénH,
pubmed-author:NogueraRosaR,
pubmed-author:PåhlmanSvenS,
pubmed-author:PietrasAlexanderA,
pubmed-author:PoellingerLorenzL,
pubmed-author:Vallon-ChristerssonJohanJ
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|
pubmed:issnType |
Print
|
|
pubmed:volume |
10
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
413-23
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|
pubmed:dateRevised |
2008-11-21
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|
pubmed:meshHeading |
pubmed-meshheading:17097563-Animals,
pubmed-meshheading:17097563-Anoxia,
pubmed-meshheading:17097563-Basic Helix-Loop-Helix Transcription Factors,
pubmed-meshheading:17097563-Child,
pubmed-meshheading:17097563-Female,
pubmed-meshheading:17097563-Gene Expression Profiling,
pubmed-meshheading:17097563-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:17097563-Humans,
pubmed-meshheading:17097563-Hypoxia-Inducible Factor 1, alpha Subunit,
pubmed-meshheading:17097563-Mice,
pubmed-meshheading:17097563-Neoplasm Transplantation,
pubmed-meshheading:17097563-Neuroblastoma,
pubmed-meshheading:17097563-Oligonucleotide Array Sequence Analysis,
pubmed-meshheading:17097563-Oxygen,
pubmed-meshheading:17097563-Phenotype,
pubmed-meshheading:17097563-Procollagen-Proline Dioxygenase,
pubmed-meshheading:17097563-RNA, Messenger,
pubmed-meshheading:17097563-Transcriptional Activation,
pubmed-meshheading:17097563-Tumor Cells, Cultured
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pubmed:year |
2006
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|
pubmed:articleTitle |
Recruitment of HIF-1alpha and HIF-2alpha to common target genes is differentially regulated in neuroblastoma: HIF-2alpha promotes an aggressive phenotype.
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pubmed:affiliation |
Division of Molecular Medicine, Department of Laboratory Medicine, Lund University, University Hospital MAS, SE-205 02 Malmö, Sweden.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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