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 MSE 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.
PFS (53% vs 13%, p 5 0,004). Day 100 chimerism does not predict incidence of cGVHD, relapse, or overall survival. Day 56 chimerism result was higher for patient who experienced aGVHD (median 89% vs 78%, p 5 0,048) and was associated with better OS if less than 82.5% (84% vs 53%, p 5 0,01). Conclusion: Limiting CD34 cell dose could lower incidence of cGVHD presumably without influencing relapse incidence and overall survival, while limiting CD3 cell dose could improve survival. Early evaluation of chimerism at day 56 is relevant to identify patients who will experience aGVHD and predict survival.
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