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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
4
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pubmed:dateCreated |
2010-9-29
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pubmed:abstractText |
Chronic myeloid leukemia (CML) is a clonal multistep myeloproliferative disease originating from and ultimately sustained by a rare population of BCR-ABL(+) cells with multilineage stem cell properties. Imatinib, the most successful of molecular targeted therapies, has revolutionized treatment of patients with CML. Despite this achievement, CML is often not curable, largely due to the innate insensitivity of CML stem cells, particularly when in a quiescent state. This failure of not only imatinib but also the second-generation tyrosine kinase inhibitors (TKIs) frequently leads to relapse upon drug discontinuation. Thus, any curative therapy must eliminate CML stem cells. A comprehensive understanding of the biological properties of CML stem cells and an elucidation of the molecular mechanisms and signaling pathways enabling these CML stem cells to self-renew, combined with insight into the regulation of apoptosis signaling and the mechanisms governing the interaction of CML stem cells with their bone marrow microenvironment, will facilitate the development of therapies for targeting these cells. Here, we discuss the biological properties of CML stem cells and potential strategies to eliminate them.
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pubmed:grant |
http://linkedlifedata.com/resource/pubmed/grant/CA16672,
http://linkedlifedata.com/resource/pubmed/grant/P01 CA049639-09A19007,
http://linkedlifedata.com/resource/pubmed/grant/P01 CA049639-109007,
http://linkedlifedata.com/resource/pubmed/grant/P01 CA049639-119007,
http://linkedlifedata.com/resource/pubmed/grant/P01 CA049639-129007,
http://linkedlifedata.com/resource/pubmed/grant/P01 CA049639-139007,
http://linkedlifedata.com/resource/pubmed/grant/P01 CA049639-149007,
http://linkedlifedata.com/resource/pubmed/grant/P01 CA49639,
http://linkedlifedata.com/resource/pubmed/grant/P30 CA016672-22S29015,
http://linkedlifedata.com/resource/pubmed/grant/P30 CA016672-339044,
http://linkedlifedata.com/resource/pubmed/grant/P30 CA016672-349044,
http://linkedlifedata.com/resource/pubmed/grant/P30 CA016672-34S49044,
http://linkedlifedata.com/resource/pubmed/grant/P30 CA016672-34S59044
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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 |
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1532-8686
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pubmed:author |
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pubmed:copyrightInfo |
Copyright © 2010 Elsevier Inc. All rights reserved.
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pubmed:issnType |
Electronic
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pubmed:volume |
47
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
362-70
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pubmed:dateRevised |
2011-10-3
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pubmed:meshHeading |
pubmed-meshheading:20875553-Antineoplastic Agents,
pubmed-meshheading:20875553-Humans,
pubmed-meshheading:20875553-Interferon-alpha,
pubmed-meshheading:20875553-Leukemia, Myelogenous, Chronic, BCR-ABL Positive,
pubmed-meshheading:20875553-Neoplastic Stem Cells,
pubmed-meshheading:20875553-Piperazines,
pubmed-meshheading:20875553-Protein Kinase Inhibitors,
pubmed-meshheading:20875553-Pyrimidines,
pubmed-meshheading:20875553-Signal Transduction
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pubmed:year |
2010
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pubmed:articleTitle |
The elusive chronic myeloid leukemia stem cell: does it matter and how do we eliminate it?
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pubmed:affiliation |
Section of Molecular Hematology and Therapy, Department of Stem Cell Transplantation and Cellular Therapy, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA. bicarter@mdanderson.org
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Review,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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