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.
- Antigens, CD34/blood
- Bone Marrow Cells/metabolism
- Gene Expression Profiling/methods
- Gene Expression Regulation, Leukemic/drug effects
- Leukemia, Myeloid, Chronic-Phase/blood
- Leukocyte Count
- Protein-Tyrosine Kinases/therapeutic use
- Pyrimidines/therapeutic use
- Time Factors
- Treatment Outcome