Chronic myeloid leukemia (CML) is a pluripotent hematopoietic disorder that is 
currently considered incurable. The tyrosine kinase product of the Philadelphia 
chromosome, P210 BCR-ABL, provided a pathogenetic explanation for the initiation 
of the CML chronic phase and is the molecular therapeutic target for the 
disease. Imatinib mesylate, an orally available BCR-ABL kinase inhibitor, can 
induce haematologic and cytogenetic remission of CML. However, imatinib 
resistance occurs frequently, resulting in relapse. New treatment strategies are 
focusing on resistant CML stem cells and the bone marrow stroma. The 
identification of novel pathways and mechanisms in the bone marrow 
microenvironment could significantly contribute to the development of such 
strategies. In this work, we used a high-resolution label-free MS(E) proteomic 
approach to identify differential protein expression in the CML bone marrow 
plasma of responsive and resistant patients. Oxidative lipid metabolism and 
regulation of the switch from canonical to noncanonical WNT signaling may 
contribute to CML resistance in the bone marrow compartment.