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rdf:type |
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lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0018866,
umls-concept:C0035647,
umls-concept:C0037083,
umls-concept:C0185117,
umls-concept:C0302350,
umls-concept:C0441712,
umls-concept:C0683598,
umls-concept:C0812304,
umls-concept:C1235660,
umls-concept:C1415725,
umls-concept:C1521840,
umls-concept:C1710082,
umls-concept:C2911684
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pubmed:issue |
24
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pubmed:dateCreated |
2010-12-20
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pubmed:abstractText |
Multiple developmental pathways including Notch, Hedgehog, and Wnt are active in malignant brain tumors such as medulloblastoma and glioblastoma (GBM). This raises the possibility that tumors might compensate for therapy directed against one pathway by upregulating a different one. We investigated whether brain tumors show resistance to therapies against Notch, and whether targeting multiple pathways simultaneously would kill brain tumor cells more effectively than monotherapy.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Basic Helix-Loop-Helix...,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic S-Oxides,
http://linkedlifedata.com/resource/pubmed/chemical/GLI1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/HES1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Hedgehog Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Homeodomain Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/MRK 003,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Notch,
http://linkedlifedata.com/resource/pubmed/chemical/Thiadiazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Veratrum Alkaloids,
http://linkedlifedata.com/resource/pubmed/chemical/cyclopamine
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1078-0432
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pubmed:author |
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pubmed:copyrightInfo |
©2010 AACR.
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
16
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6060-70
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pubmed:dateRevised |
2011-5-2
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pubmed:meshHeading |
pubmed-meshheading:21169257-Antineoplastic Combined Chemotherapy Protocols,
pubmed-meshheading:21169257-Basic Helix-Loop-Helix Transcription Factors,
pubmed-meshheading:21169257-Brain Neoplasms,
pubmed-meshheading:21169257-Cell Line, Tumor,
pubmed-meshheading:21169257-Cyclic S-Oxides,
pubmed-meshheading:21169257-Drug Evaluation, Preclinical,
pubmed-meshheading:21169257-Drug Resistance, Neoplasm,
pubmed-meshheading:21169257-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:21169257-Glioblastoma,
pubmed-meshheading:21169257-Hedgehog Proteins,
pubmed-meshheading:21169257-Homeodomain Proteins,
pubmed-meshheading:21169257-Humans,
pubmed-meshheading:21169257-Receptors, Notch,
pubmed-meshheading:21169257-Signal Transduction,
pubmed-meshheading:21169257-Thiadiazoles,
pubmed-meshheading:21169257-Transcription Factors,
pubmed-meshheading:21169257-U937 Cells,
pubmed-meshheading:21169257-Veratrum Alkaloids
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pubmed:year |
2010
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pubmed:articleTitle |
The Notch target Hes1 directly modulates Gli1 expression and Hedgehog signaling: a potential mechanism of therapeutic resistance.
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pubmed:affiliation |
Department of Neuroscience, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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