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rdf:type |
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lifeskim:mentions |
umls-concept:C0012899,
umls-concept:C0026882,
umls-concept:C0034537,
umls-concept:C0037083,
umls-concept:C0086418,
umls-concept:C0242275,
umls-concept:C0392760,
umls-concept:C0431085,
umls-concept:C0442805,
umls-concept:C1533691,
umls-concept:C1706968,
umls-concept:C1710082
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pubmed:issue |
13
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pubmed:dateCreated |
2006-7-4
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pubmed:abstractText |
It is known that blockage of epidermal growth factor receptor (EGFR)/phosphatidylinositol 3-kinase (PI3K) activity enhances radiation sensitivity of human tumor cells presenting a K-RAS mutation. In the present study, we investigated whether impaired repair of DNA double-strand breaks (DSB) is responsible for the radiosensitizing effect of EGFR and PI3K inhibition in K-RAS mutated (K-RAS(mt)) cells.
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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/2-(4-morpholinyl)-8-phenyl-4H-1-benz...,
http://linkedlifedata.com/resource/pubmed/chemical/9-methoxy-2-methylellipticinium...,
http://linkedlifedata.com/resource/pubmed/chemical/BIBX 1382BS,
http://linkedlifedata.com/resource/pubmed/chemical/Chromones,
http://linkedlifedata.com/resource/pubmed/chemical/Ellipticines,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Morpholines,
http://linkedlifedata.com/resource/pubmed/chemical/Organic Chemicals,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphatidylinositol 3-Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-akt,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Epidermal Growth Factor
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
1078-0432
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
12
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4119-26
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:16818713-Carcinoma,
pubmed-meshheading:16818713-Cell Line, Tumor,
pubmed-meshheading:16818713-Chromones,
pubmed-meshheading:16818713-DNA Repair,
pubmed-meshheading:16818713-Dose-Response Relationship, Drug,
pubmed-meshheading:16818713-Ellipticines,
pubmed-meshheading:16818713-Enzyme Inhibitors,
pubmed-meshheading:16818713-Genes, ras,
pubmed-meshheading:16818713-Humans,
pubmed-meshheading:16818713-Morpholines,
pubmed-meshheading:16818713-Mutation,
pubmed-meshheading:16818713-Organic Chemicals,
pubmed-meshheading:16818713-Phosphatidylinositol 3-Kinases,
pubmed-meshheading:16818713-Proto-Oncogene Proteins c-akt,
pubmed-meshheading:16818713-Radiation Tolerance,
pubmed-meshheading:16818713-Receptor, Epidermal Growth Factor,
pubmed-meshheading:16818713-Signal Transduction,
pubmed-meshheading:16818713-Structure-Activity Relationship
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pubmed:year |
2006
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pubmed:articleTitle |
Blockage of epidermal growth factor receptor-phosphatidylinositol 3-kinase-AKT signaling increases radiosensitivity of K-RAS mutated human tumor cells in vitro by affecting DNA repair.
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pubmed:affiliation |
Divison of Radiobiology and Molecular Environmental Research, Department of Radiation Oncology, University of Tuebingen, Tuebingen, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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