Abstract
Background:
Chronic myeloid leukemia (CML) is a clonal myeloproliferative disorder with heterogeneous biological and clinical features. The biomolecular mechanisms of CML response to tyrosine-kinase inhibitors are not fully defined.
Objective:
We undertook a gene expression profiling (GEP) study of selected bone marrow (BM) CD34+/lin- cells of chronic-phase CML patients at diagnosis and after 12 months of TKI nilotinib to investigate molecular signatures characterizing both conditions.
MeSH terms
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Antigens, CD34 / blood
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Bone Marrow Cells / metabolism*
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Bone Marrow Cells / pathology
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Gene Expression Profiling / methods*
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Gene Expression Regulation, Leukemic / drug effects
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Humans
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Leukemia, Myeloid, Chronic-Phase / blood
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Leukemia, Myeloid, Chronic-Phase / drug therapy*
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Leukemia, Myeloid, Chronic-Phase / genetics*
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Leukocyte Count
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Protein-Tyrosine Kinases / therapeutic use
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Pyrimidines / therapeutic use*
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Time Factors
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Treatment Outcome
Substances
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Antigens, CD34
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Pyrimidines
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Protein-Tyrosine Kinases
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nilotinib