Abstract
We investigated the role of lipocalin-2 (LCN-2) and its receptor (SLC22A17) in mediating clonal dominance in a patient with both BCR-ABL and JAK2-V617F mutations. LCN-2 mRNA showed a near 50-fold increase in expression, accompanied by down-regulation of SLC22A17, coinciding with increase in BCR-ABL transcripts, loss of JAK2-V617F and change of clinical phenotype from polycythaemia vera to chronic myeloid leukaemia. These changes were reversed after commencing imatinib mesylate. Consistent with experimental studies, BCR-ABL+ cells express LCN-2 leading to suppression of BCR-ABL- cells and explain their eventual dominance when occurring together with JAK2-V617F.
© 2011 John Wiley & Sons A/S.
Publication types
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Case Reports
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Research Support, Non-U.S. Gov't
MeSH terms
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Acute-Phase Proteins / genetics
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Acute-Phase Proteins / metabolism*
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Fusion Proteins, bcr-abl / genetics*
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Gene Expression Regulation, Leukemic
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Humans
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Janus Kinase 2 / genetics*
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Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics*
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Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism*
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Lipocalin-2
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Lipocalins / genetics
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Lipocalins / metabolism*
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Mutation*
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Organic Cation Transport Proteins / genetics
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Organic Cation Transport Proteins / metabolism
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Phenotype*
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Proto-Oncogene Proteins / genetics
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Proto-Oncogene Proteins / metabolism*
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RNA, Messenger / genetics
Substances
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Acute-Phase Proteins
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LCN2 protein, human
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Lipocalin-2
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Lipocalins
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Organic Cation Transport Proteins
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Proto-Oncogene Proteins
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RNA, Messenger
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SLC22A17 protein, human
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Fusion Proteins, bcr-abl
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Janus Kinase 2