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Cancer Biomark ; 21(1): 41-53, 2017 Dec 12.
Article in English | MEDLINE | ID: mdl-29036785

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.


Subject(s)
Bone Marrow Cells/metabolism , Gene Expression Profiling/methods , Leukemia, Myeloid, Chronic-Phase/drug therapy , Leukemia, Myeloid, Chronic-Phase/genetics , Pyrimidines/therapeutic use , Antigens, CD34/blood , Bone Marrow Cells/pathology , Gene Expression Regulation, Leukemic/drug effects , Humans , Leukemia, Myeloid, Chronic-Phase/blood , Leukocyte Count , Protein-Tyrosine Kinases/therapeutic use , Time Factors , Treatment Outcome
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