Source:http://linkedlifedata.com/resource/pubmed/id/16778211
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
12
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pubmed:dateCreated |
2006-6-16
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pubmed:abstractText |
Hypereosinophilic syndrome (HES) has recently been recognized as a clonal leukemic lesion, which is due to a specific oncogenic event that generates hyperactive platelet-derived growth factor receptor-alpha-derived tyrosine kinase fusion proteins. In the present work, the effect of retinoids on the leukemic hypereosinophilia-derived EoL-1 cell line and on primary HES-derived cells has been investigated. We show that all-trans-retinoic acid (ATRA) inhibits eosinophil colony formation of HES-derived bone marrow cells and is a powerful inducer of apoptosis of the EoL-1 cell line. Apoptosis was shown in the nanomolar concentration range by phosphatidylserine externalization, proapoptotic shift of the Bcl-2/Bak ratio, drop in mitochondrial membrane potential, activation of caspases, and cellular morphology. Unlike in other ATRA-sensitive myeloid leukemia models, apoptosis was rapid and was not preceded by terminal cell differentiation. Use of isoform-selective synthetic retinoids indicated that retinoic acid receptor-alpha-dependent signaling is sufficient to induce apoptosis of EoL-1 cells. Our work shows that the scope of ATRA-induced apoptosis of malignancies may be wider within the myeloid lineage than thought previously, that the EoL-1 cell line constitutes a new and unique model for the study of ATRA-induced cell death, and that ATRA may have potential for the management of clonal HES.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/FIP1L1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Retinoic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Tretinoin,
http://linkedlifedata.com/resource/pubmed/chemical/mRNA Cleavage and Polyadenylation...,
http://linkedlifedata.com/resource/pubmed/chemical/retinoic acid receptor alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0008-5472
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
66
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6336-44
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:16778211-Apoptosis,
pubmed-meshheading:16778211-Cell Line, Tumor,
pubmed-meshheading:16778211-Drug Hypersensitivity,
pubmed-meshheading:16778211-Eosinophils,
pubmed-meshheading:16778211-HL-60 Cells,
pubmed-meshheading:16778211-Humans,
pubmed-meshheading:16778211-Hypereosinophilic Syndrome,
pubmed-meshheading:16778211-Receptors, Retinoic Acid,
pubmed-meshheading:16778211-Signal Transduction,
pubmed-meshheading:16778211-Stem Cells,
pubmed-meshheading:16778211-Tretinoin,
pubmed-meshheading:16778211-mRNA Cleavage and Polyadenylation Factors
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pubmed:year |
2006
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pubmed:articleTitle |
Apoptosis induction by retinoids in eosinophilic leukemia cells: implication of retinoic acid receptor-alpha signaling in all-trans-retinoic acid hypersensitivity.
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pubmed:affiliation |
Institut National de la Santé et de la Recherche Médicale, UMR-S 718, Institut Universitaire d'Hématologie, University of Paris VII, Paris, France.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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