Source:http://linkedlifedata.com/resource/pubmed/id/11526598
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3 Suppl 8
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pubmed:dateCreated |
2001-8-29
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pubmed:abstractText |
The cytokine interferon-alfa (IFN-alpha) has substantial activity in chronic myeloid leukemia (CML) and is the nontransplant standard of care for chronic-phase disease. When used as front-line therapy, IFN-alpha induces a state of tumor dormancy and delays progression to advanced phase. Unfortunately, IFN-alpha is associated with substantial toxicity at therapeutic doses. The introduction of pegylated IFN-alpha (PEG-IFN-alpha), a modified form of the protein that permits weekly administration, may alleviate some of the problems observed with IFN-alpha. Combination regimens of IFN-alpha with other drugs such as cytarabine (Ara-C) appear to enhance efficacy and are currently under investigation. The tyrosine kinase inhibitor imatinib mesylate (Gleevec, Novartis Pharmaceuticals Corp, East Hanover, NJ) (formerly STI571) also is efficacious in chronic-phase CML, with a low toxicity profile. However, its potential to cure CML remains unknown even though it achieves frequent cytogenetic responses. To enhance treatment outcome, a combination of IFN-alpha and imatinib mesylate therapies is proposed. Low-dose IFN-alpha may be given after imatinib mesylate-induced remission as a specific immune stimulant to consolidate the remission. Recent data showing a possible additive effect of imatinib mesylate and IFN-alpha suggest that concurrent use of these agents may also be more effective than single use, particularly in advanced stages of CML where imatinib mesylate has activity but resistance develops.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0037-1963
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pubmed:author | |
pubmed:copyrightInfo |
Copyright 2001 by W.B. Saunders Company.
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pubmed:issnType |
Print
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pubmed:volume |
38
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
22-7
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:11526598-Antineoplastic Combined Chemotherapy Protocols,
pubmed-meshheading:11526598-Humans,
pubmed-meshheading:11526598-Interferon-alpha,
pubmed-meshheading:11526598-Leukemia, Myelogenous, Chronic, BCR-ABL Positive,
pubmed-meshheading:11526598-Piperazines,
pubmed-meshheading:11526598-Pyrimidines,
pubmed-meshheading:11526598-Signal Transduction
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pubmed:year |
2001
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pubmed:articleTitle |
Interferon-alfa-based treatment of chronic myeloid leukemia and implications of signal transduction inhibition.
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pubmed:affiliation |
Division of Medicine, Department of Bioimmunotherapy, M.D. Anderson Cancer Center, Houston, TX 77030, USA.
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pubmed:publicationType |
Journal Article,
Review
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