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rdf:type |
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lifeskim:mentions |
umls-concept:C0004891,
umls-concept:C0007600,
umls-concept:C0023473,
umls-concept:C0035820,
umls-concept:C0205314,
umls-concept:C0252270,
umls-concept:C0441712,
umls-concept:C0651614,
umls-concept:C0679622,
umls-concept:C0683598,
umls-concept:C0906802,
umls-concept:C0939537,
umls-concept:C1552913,
umls-concept:C1709059,
umls-concept:C1710082
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pubmed:issue |
11
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pubmed:dateCreated |
2004-11-12
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pubmed:abstractText |
Acquired resistance to imatinib mesylate (STI571) in chronic myelogenous leukemia (CML) patients has become a serious clinical problem. We previously established STI571-resistant sublines (designated KTR cells) from the CML cell line KT-1. T cell protein tyrosine phosphatase (TC-PTP) was markedly downregulated in all KTR cells compared to parental KT-1 cells. Therefore, we examined whether the suppression of TC-PTP expression might contribute to imatinib mesylate-resistance in KTR 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/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Fusion Proteins, bcr-abl,
http://linkedlifedata.com/resource/pubmed/chemical/Milk Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/PTPN2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Piperazines,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Tyrosine Phosphatase...,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Tyrosine Phosphatases,
http://linkedlifedata.com/resource/pubmed/chemical/Pyrimidines,
http://linkedlifedata.com/resource/pubmed/chemical/STAT5 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators,
http://linkedlifedata.com/resource/pubmed/chemical/imatinib
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0301-472X
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
32
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1057-63
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:15539083-Apoptosis,
pubmed-meshheading:15539083-Cell Line, Tumor,
pubmed-meshheading:15539083-Cell Proliferation,
pubmed-meshheading:15539083-DNA-Binding Proteins,
pubmed-meshheading:15539083-Down-Regulation,
pubmed-meshheading:15539083-Drug Resistance, Neoplasm,
pubmed-meshheading:15539083-Fusion Proteins, bcr-abl,
pubmed-meshheading:15539083-Humans,
pubmed-meshheading:15539083-Leukemia, Myelogenous, Chronic, BCR-ABL Positive,
pubmed-meshheading:15539083-Milk Proteins,
pubmed-meshheading:15539083-Phosphorylation,
pubmed-meshheading:15539083-Piperazines,
pubmed-meshheading:15539083-Protein Tyrosine Phosphatase, Non-Receptor Type 2,
pubmed-meshheading:15539083-Protein Tyrosine Phosphatases,
pubmed-meshheading:15539083-Pyrimidines,
pubmed-meshheading:15539083-STAT5 Transcription Factor,
pubmed-meshheading:15539083-Signal Transduction,
pubmed-meshheading:15539083-Trans-Activators,
pubmed-meshheading:15539083-Transduction, Genetic
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pubmed:year |
2004
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pubmed:articleTitle |
A novel mechanism for imatinib mesylate (STI571) resistance in CML cell line KT-1: role of TC-PTP in modulating signals downstream from the BCR-ABL fusion protein.
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pubmed:affiliation |
Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan.
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pubmed:publicationType |
Journal Article
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